TY  - JOUR
AB  - Non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH) and liver fibrosis emerge as progressive liver diseases that accompany metabolic syndrome usually characterized by obesity, insulin resistance and type 2 diabetes. Currently no FDA approved treatments exist for the treatment of NASH and liver fibrosis, which requires a better knowledge of the underlying molecular mechanisms. TSC22D4 belongs to the TSC-22 protein family, the members of which are regulated by inflammatory and stress signals. Interestingly, patients with type 2 diabetes, with NAFLD as well as with NASH all have elevated levels of hepatic TSC22D4 expression. Previous studies with targeted deletion of TSC22D4 specifically in hepatocytes showed that TSC22D4 not only acts as a critical controller of diabetic hyperglycemia, but also contributes to NAFLD/NASH progression. To gain better insight into the development of progressive liver diseases, here we studied the function of TSC22D4 in hepatic stellate cells (HSCs), which play a key role in the pathogenesis of liver fibrosis. Our results indicated that TSC22D4 contributes to TGFβ1-mediated activation of HSCs and promotes their proliferation and migration. RNA-Sequencing analysis revealed that TSC22D4 initiates transcriptional events associated with HSC activation. Overall, our findings establish TSC22D4 as a key hub in the development of liver fibrosis, acting across different cellular compartments. Combinatorial TSC22D4 targeting in both hepatocytes and HSC may thus show superior efficacy against progressive liver disease.
AU  - Sakurai, M.
AU  - Weber, P.
AU  - Wolff, G.
AU  - Wieder, A.
AU  - Szendroedi, J.
AU  - Herzig, S.
AU  - Ekim Üstünel, B.
C1  - 65506
C2  - 52202
SP  - 46-53
TI  - TSC22D4 promotes TGFβ1-induced activation of hepatic stellate cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 618
PY  - 2022
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The MALT1 (Mucosa associated lymphoid tissue lymphoma translocation protein 1) paracaspase couples antigen receptors on lymphocytes to downstream signaling events. Activation of MALT1 is known to involve stimulus-dependent CBM complex formation, that is, the recruitment of BCL10-bound MALT1 to a CARD-Coiled Coil protein. Beyond this canonical, CBM-dependent mechanism of MALT1 activation, recent studies suggest that MALT1 protease activity may be triggered by alternative mechanisms. For instance, the E3-ligase TRAF6 can activate MALT1 proteolytic function and induce MALT1 auto-cleavage. However, the interplay between CBM and TRAF6 with regard to MALT1 activation has remained incompletely elucidated. Here, by generating CRISPR/Cas9-derived knock-out Jurkat T-cells, we show that TRAF6 was dispensable for CARD11/BCL10-dependent MALT1 activation upon T-cell stimulation. However, ectopically-expressed TRAF6 could induce MALT1 activity in Jurkat T-cells devoid of either CARD11 or BCL10. These data provide unequivocal evidence that TRAF6-mediated MALT1 activation does not require the upstream scaffold CARD11 or the interaction between MALT1 and BCL10. Thus, TRAF6 may be part of a previously unidentified non-canonical pathway that triggers MALT1 protease activity independently of canonical CBM signalosomes. (C) 2018 Elsevier Inc. All rights reserved.
AU  - Bardet, M.*
AU  - Seeholzer, T.
AU  - Unterreiner, A.*
AU  - Woods, S.
AU  - Krappmann, D.
AU  - Bornancin, F.*
C1  - 54553
C2  - 45654
CY  - 525 B St, Ste 1900, San Diego, Ca 92101-4495 Usa
SP  - 48-52
TI  - MALT1 activation by TRAF6 needs neither BCL10 nor CARD11.
JO  - Biochem. Biophys. Res. Commun.
VL  - 506
IS  - 1
PB  - Academic Press Inc Elsevier Science
PY  - 2018
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Heterozygous missense mutations in the human VCP gene cause inclusion body myopathy associated with Paget disease of bone and fronto-temporal dementia (IBMPFD) and amyotrophic lateral sclerosis (ALS). The exact molecular mechanisms by which VCP mutations cause disease manifestation in different tissues are incompletely understood. In the present study, we report the comprehensive analysis of a newly generated R155C VCP knock-in mouse model, which expresses the ortholog of the second most frequently occurring human pathogenic VCP mutation. Heterozygous R155C VCP knock-in mice showed decreased plasma lactate, serum albumin and total protein concentrations, platelet numbers, and liver to body weight ratios, and increased oxygen consumption and CD8+/Ly6C + T-cell fractions, but none of the typical human IBMPFD or ALS pathologies. Breeding of heterozygous mice did not yield in the generation of homozygous R155C VCP knock-in animals. Immunoblotting showed identical total VCP protein levels in human IBMPFD and murine R155C VCP knock-in tissues as compared to wild-type controls. However, while in human IBMPFD skeletal muscle tissue 70% of the total VCP mRNA was derived from the mutant allele, in R155C VCP knock-in mice only 5% and 7% mutant mRNA were detected in skeletal muscle and brain tissue, respectively. The lack of any obvious IBMPFD or ALS pathology could thus be a consequence of the very low expression of mutant VCP. We conclude that the increased and decreased fractions of the R155C mutant VCP mRNA in man and mice, respectively, are due to missense mutation-induced, divergent alterations in the biological half-life of the human and murine mutant mRNAs. Furthermore, our work suggests that therapy approaches lowering the expression of the mutant VCP mRNA below a critical threshold may ameliorate the intrinsic disease pathology.
AU  - Clemen, C.S.*
AU  - Winter, L.*
AU  - Strucksberg, K.H.*
AU  - Berwanger, C.*
AU  - Türk, M.*
AU  - Kornblum, C.*
AU  - Florin, A.*
AU  - Aguilar-Pimentel, J.A.
AU  - Amarie, O.V.
AU  - Becker, L.
AU  - Garrett, L.
AU  - Hans, W.
AU  - Moreth, K.
AU  - Neff, F.
AU  - Pingen, L.
AU  - Rathkolb, B.
AU  - Rácz, I.*
AU  - Rozman, J.
AU  - Treise, I.
AU  - Fuchs, H.
AU  - Gailus-Durner, V.
AU  - Hrabě de Angelis, M.
AU  - Vorgerd, M.*
AU  - Eichinger, L.*
AU  - Schröder, R.*
C1  - 54126
C2  - 45273
CY  - 525 B St, Ste 1900, San Diego, Ca 92101-4495 Usa
SP  - 2770-2777
TI  - The heterozygous R155C VCP mutation: Toxic in humans! Harmless in mice?
JO  - Biochem. Biophys. Res. Commun.
VL  - 503
IS  - 4
PB  - Academic Press Inc Elsevier Science
PY  - 2018
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Dendrite morphogenesis is a complex but well-orchestrated process. Various studies reported the involvement of alteration in dendrite morphology in different brain disorders, including neuropsychiatric disorders. Initially, beta B2-crystallin (gene symbol: Crybb2/CRYBB2) has been described as a structural protein of the ocular lens. Mutations of the corresponding gene, Crybb2, lead to cataract. Recent studies in mice suggested that mutations in Crybb2 cause alterations in hippocampal morphology and function, albeit its function in hippocampal neuron development remained elusive. In the current study, we found that Crybb2 contributes to dendritogenesis in vitro and in vivo. Furthermore, screening of previous data on differential expression-arrays, we found Tmsb4X up-regulated in Crybb2 mutants mouse brain. Additionally, Tmsb4X was co-expressed with Crybb2 at actin-enriched cell ruffles. Over-expression of Tmsb4X in cultured hippocampal neurons inhibited dendritogenesis, which phenocopied Crybb2 knockdown. The current study uncovers a new function of Crybb2 in brain development, especially in dendritogenesis, and the possible interplay partner Tmsb4X involved in this process. (C) 2018 Elsevier Inc. All rights reserved.
AU  - Sun, M.*
AU  - Ahmad, N.*
AU  - Zhang, R.*
AU  - Graw, J.
C1  - 53600
C2  - 44716
CY  - 525 B St, Ste 1900, San Diego, Ca 92101-4495 Usa
SP  - 123-130
TI  - Crybb2 associates with Tmsb4X and is crucial for dendrite morphogenesis.
JO  - Biochem. Biophys. Res. Commun.
VL  - 503
IS  - 1
PB  - Academic Press Inc Elsevier Science
PY  - 2018
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Hepatitis B virus (HBV) infection is one of the major health problems in the world. Transgelin-2 (TAGLN2) expression has been revealed to be significantly altered in previous studies concerning HBV-host interaction. The present study investigated TAGLN2 expression patterns in HBV related hepatocellular carcinoma (HCC) tissues and its role in HBV transcription and replication. We collected 59 HBV related HCC tissue samples, their adjacent non-tumoral tissues and 16 normal livers to make the tissue microarray. TAGLN2 protein was detected by immunohistochemistry and the transcriptional levels of TAGLN2, HBc, HBs and HBx were detected by qRT-PCR. Then we investigated the function of TAGLN2 on HBV transcription and replication in vitro by ectopic expressing or knocking down TAGLN2 in HepG2 and HepG2.2.15 cell lines. We further studied the effect of HBx on TAGLN2 expression with a Tet-on HBx expressing cell line. TAGLN2 protein expression was lower in normal livers and HBV-HCC tissues comparing to adjacent non-tumoral tissues. The transcriptional levels of TAGLN2 in HBV-HCC tissues and their adjacent tissues were positively related to that of HBc, HBs and HBx (P < 0.05). Ectopic expression of TAGLN2 in vitro could enhance HBV transcription and replication while suppressing TAGLN2 had the contrary effect. TAGLN2 could be induced by HBx in a dose-dependent manner. Our data demonstrated that TAGLN2 might be an HBx induced positive host factor involved in HBV transcription and replication and HBx related liver fibrosis and tumorigenesis.
AU  - Yu, Y.
AU  - He, Z.*
AU  - Cao, Y.*
AU  - Tang, H.*
AU  - Huang, F.*
C1  - 49218
C2  - 33593
CY  - San Diego
SP  - 1051-1058
TI  - TAGLN2, a novel regulator involved in Hepatitis B virus transcription and replication.
JO  - Biochem. Biophys. Res. Commun.
VL  - 477
IS  - 4
PB  - Academic Press Inc Elsevier Science
PY  - 2016
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - More and more industrial chemistry reactions relies on green technologies. Enzymes are finding increasing use in diverse chemical processes. Epoxidized vegetable oils have recently found applications as plasticizers and additives for PVC production. We report here an unusual activity of the M. globosa lipase (SMG1) that is able to catalyze epoxidation of alkenes. SMG1 catalyzes formation of peroxides from long chain carboxylic acids that subsequently react with double bonds of alkenes to produce epoxides. The SMG1 is selective towards carboxylic acids and active also as a mutant lacking hydrolase activity. Moreover we present previously unobserved mechanism of catalysis that does not rely on acyl-substrate complex nor tetrahedral intermediate. Since SMG1 lipase is activated by allosteric change upon binding to the lipophilic-hydrophilic phase interface we reason that it can be used to drive the epoxidation in the lipohilic phase exclusively.
AU  - Wang, X.*
AU  - Tang, Q.*
AU  - Popowicz, G.M.
AU  - Yang, B.*
AU  - Wang, Y.*
C1  - 43873
C2  - 36616
CY  - San Diego
SP  - 392-396
TI  - A mechanistic study into the epoxidation of carboxylic acid and alkene in a mono, di-acylglycerol lipase.
JO  - Biochem. Biophys. Res. Commun.
VL  - 460
IS  - 2
PB  - Academic Press Inc Elsevier Science
PY  - 2015
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Mutations in type I collagen genes (COL1A1/2) typically lead to Osteogenesis imperfecta, the most common heritable cause of skeletal fractures and bone deformation in humans. Heterozygous Col1a1, animals with a dominant mutation in the terminal C-propeptide domain of type I collagen develop typical skeletal hallmarks and internal hemorrhages starting from 6day after birth. The disease progression for Aga2/+ mice, however, is not uniform differing between severe phenotype lethal at the 6-11th day of life, and moderate-to-severe one with survival to adulthood. Herein we investigated whether a new modality that combines X-ray computer tomography with fluorescence tomography in one hybrid system can be employed to study internal bleedings in relation to bone fractures and obtain insights into disease progression. The disease phenotype was characterized on Aga2/+ vs. wild type mice between 6 and 9days postnatal. Anatomical and functional findings obtained in-vivo were contrasted to the ex-vivo appearance of the same tissues under cryo-slicing.
AU  - Ermolayev, V.
AU  - Cohrs, C.M.
AU  - Mohajerani, P.
AU  - Ale, A.B.F
AU  - Hrabě de Angelis, M.
AU  - Ntziachristos, V.
C1  - 23300
C2  - 31020
SP  - 389-393
TI  - Ex-vivo assessment and non-invasive in vivo imaging of internal hemorrhages in Aga2/+ mutant mice.
JO  - Biochem. Biophys. Res. Commun.
VL  - 432
IS  - 2
PB  - Elsevier Academic Press
PY  - 2013
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - LRRK2 is one of the most important genetic contributors to Parkinson's disease (PD). Point mutations in this gene cause an autosomal dominant form of PD, but to date no cellular phenotype has been consistently linked with mutations in each of the functional domains (ROC, COR and Kinase) of the protein product of this gene. In this study, primary fibroblasts from individuals carrying pathogenic mutations in the three central domains of LRRK2 were assessed for alterations in the autophagy/lysosomal pathway using a combination of biochemical and cellular approaches. Mutations in all three domains resulted in alterations in markers for autophagy/lysosomal function compared to wild type cells. These data highlight the autophagy and lysosomal pathways as read outs for pathogenic LRRK2 function and as a marker for disease, and provide insight into the mechanisms linking LRRK2 function and mutations.
AU  - Manzoni, C.*
AU  - Mamais, A.*
AU  - Dihanich, S.*
AU  - McGoldrick, P.*
AU  - Devine, M.J.*
AU  - Zerle, J.
AU  - Kara, E.*
AU  - Taanman, J.W.*
AU  - Healy, D.G.*
AU  - Marti-Masso, J.F.*
AU  - Schapira, A.H.*
AU  - Plun-Favreau, H.*
AU  - Tooze, S.*
AU  - Hardy, J.*
AU  - Bandopadhyay, R.*
AU  - Lewis, P.A.*
C1  - 28541
C2  - 33432
SP  - 862-866
TI  - Pathogenic Parkinson's disease mutations across the functional domains of LRRK2 alter the autophagic/lysosomal response to starvation.
JO  - Biochem. Biophys. Res. Commun.
VL  - 441
IS  - 4
PB  - Academic Press - Elsevier
PY  - 2013
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Purpose: beta-Muricholic acid (beta mcA) is a trihydroxylated bile acid that constitutes the major bile acid in rat and mouse. beta MCA is more hydrophilic than ursodeoxycholic acid and has been evaluated for dissolution of cholesterol gallstones. Since it is unknown if beta MCA has beneficial effects on hepatocyte cell death we determined the effect of tauro-beta MCA (T beta MCA) on apoptosis in vitro. Methods: Human Ntcp-transfected HepG2 cells and primary hepatocytes from rat and mouse were incubated with the proapoptotic glycochenodeoxycholic acid (GCDCA) as well as the free fatty acid palmitate in the absence and presence of T beta MCA. Apoptosis was quantified using caspase 3/7-assays and after Hoechst 33342 staining. The mitochondrial membrane potential (MMP) was measured fluorometrically using JC-1 (5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-benzimidazol-carbocyaniniodide). Immunoblotting was performed against the proapoptotic Bcl-2-protein Bax. Results: In Ntcp-HepG2 cells, GCDCA markedly increased apoptosis after 4 h. Co-incubation with T beta MCA reduced apoptosis to 49% (p < 0.01 vs. GCDCA, each; n = 6). While GCDCA (100 mu mol/L) reduced the MMP to 34% after 6 h, combination treatment with T beta MCA restored the MMP to control levels at all time points (n = 4). T beta MCA also restored breakdown of the MMP induced by palmitate. GCDCA induced a translocation of Bax from the cytosol to mitochondria that was inhibited by simultaneous treatment with T beta MCA in eqimolar concentrations. Conclusions: T beta MCA restricts hepatocellular apoptosis induced by low micromolar concentrations of GCDCA or palmitate via inhibition of Bax translocation to mitochondria and preservation of the MMP. Thus, further studies are warranted to evaluate a potential use of T beta MCA in ameliorating liver injury in cholestasis.
AU  - Denk, G.U.*
AU  - Kleiss, C.P.*
AU  - Wimmer, R.*
AU  - Vennegeerts, T.*
AU  - Reiter, F.P.*
AU  - Schulz, S.
AU  - Zischka, H.
AU  - Rust, C.*
C1  - 8564
C2  - 30188
SP  - 758-764
TI  - Tauro-β-muricholic acid restricts bile acid-induced hepatocellular apoptosis by preserving the mitochondrial membrane potential.
JO  - Biochem. Biophys. Res. Commun.
VL  - 424
IS  - 4
PB  - Elsevier Science
PY  - 2012
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - There is an increasing interest in the integration of hybrid bio-semiconductor systems for the non-invasive evaluation of physiological parameters. High quality gallium nitride and its alloys show promising characteristics to monitor cellular parameters. Nevertheless, such applications not only request appropriate sensing capabilities but also the biocompatibility and especially the biofunctionality of materials. Here we show extensive biocompatibility studies of gallium nitride and, for the first time, a biofunctionality assay using ionizing radiation. Analytical sensor devices are used in medical settings, as well as for cell-and tissue engineering. Within these fields, semiconductor devices have increasingly been applied for online biosensing on a cellular and tissue level. Integration of advanced materials such as gallium nitride into these systems has the potential to increase the range of applicability for a multitude of test devices and greatly enhance sensitivity and functionality. However, for such applications it is necessary to optimize cell-surface interactions and to verify the biocompatibility of the semiconductor. In this work, we present studies of mouse fibroblast cell activity grown on gallium nitride surfaces after applying external noxa. Cell-semiconductor hybrids were irradiated with X-rays at air kerma doses up to 250 mGy and the DNA repair dynamics, cell proliferation, and cell growth dynamics of adherent cells were compared to control samples. The impact of ionizing radiation on DNA, along with the associated cellular repair mechanisms, is well characterized and serves as a reference tool for evaluation of substrate effects. The results indicate that gallium nitride does not require specific surface treatments to ensure biocompatibility and suggest that cell signaling is not affected by micro-environmental alterations arising from gallium nitride-cell interactions. The observation that gallium nitride provides no bio-functional influence on the cellular environment confirms that this material is well suited for future biosensing applications without the need for additional chemical surface modification.
AU  - Hofstetter, M.
AU  - Howgate, J.*
AU  - Schmid, M.
AU  - Schoell, S.*
AU  - Sachsenhauser, M.*
AU  - Adigüzel, D.
AU  - Stutzmann, M.*
AU  - Sharp, I.D.*
AU  - Thalhammer, S.
C1  - 8549
C2  - 30178
SP  - 348-353
TI  - In vitro bio-functionality of gallium nitride sensors for radiation biophysics.
JO  - Biochem. Biophys. Res. Commun.
VL  - 424
IS  - 2
PB  - Elsevier
PY  - 2012
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Gene expression analysis is frequently used to analyze the response to viral infection, and 18S RNA, SHDA and GAPDH represent popular house keeping genes (HKGs) often used to normalize gene expression. Here we describe the first systematic selection and evaluation of suitable HKGs for gene expression analysis in chicken embryo fibroblasts (CEF) infected with NDV adapted to the guidelines from Gorzelniak and Ferguson. Our results indicate that ACTB, HPRT1 and HMBS were valuable and stable HKGs, while 18S RNA, GAPDH and SHDA are considerably regulated during the course of infection and thus precluded for normalization. Normalizing the infection dependent gene IFN-a and the infection independent gene B2M to inappropriate HKGs consequently misleads to significant errors in estimating their regulations. Our study emphasizes that even the most popular HKGs like 18S RNA and GAPDH can lead to divergent and inaccurate data interpretation of significant magnitude if not carefully analyzed for stability before.
AU  - Yin, R.
AU  - Liu, X.*
AU  - Liu, C.*
AU  - Ding, Z.*
AU  - Zhang, X.*
AU  - Tian, F.
AU  - Liu, W.*
AU  - Yu, J.*
AU  - Li, L.*
AU  - Hrabě de Angelis, M.
AU  - Stöger, T.
C1  - 6618
C2  - 28980
CY  - San Diego, CA
SP  - 537-540
TI  - Systematic selection of housekeeping genes for gene expression normalization in chicken embryo fibroblasts infected with Newcastle disease virus.
JO  - Biochem. Biophys. Res. Commun.
VL  - 413
IS  - 4
PB  - Academic Press
PY  - 2011
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The category A agent, botulinum neurotoxin (BoNT), is the most toxic molecule known to mankind. The endopeptidase activity of light chain domain of BoNT is the cause for the inhibition of the neurotransmitter release and the flaccid paralysis that leads to lethality in botulism. Currently, antidotes are not available to reverse the flaccid paralysis caused by BoNT. In the present study, we have identified three RNA aptamers through SELEX-process, which bind strongly to the light chain of type A BoNT (BoNT/A) and inhibit the endopeptidase activity, with IC50 in low nM range. Inhibition kinetic studies reveal low nM K-1 and non-competitive nature of their inhibition. Aptamers are unique group of molecules as therapeutics, and this is first report of their development as an antidote against botulism. These data on K-1 and IC50 strongly suggest that the aptamers have strong potential as antidotes that can reverse the symptom caused by BoNT/A.
AU  - Chang, T.W.*
AU  - Blank, M.
AU  - Janardhanan, P.*
AU  - Singh, B.R.*
AU  - Mello, C.*
AU  - Blind, M.*
AU  - Cai, S.W.*
C1  - 5781
C2  - 28262
CY  - San Diego
SP  - 854-860
TI  - In vitro selection of RNA aptamers that inhibit the activity of type A botulinum neurotoxin.
JO  - Biochem. Biophys. Res. Commun.
VL  - 396
IS  - 4
PB  - Academic Press Inc. Elsevier Sci.
PY  - 2010
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) is a highly specific and sensitive technique for the quantification of gene expression on the mRNA levels. But use of unconfirmed housekeeping genes (HKGs) could lead to misinterpretation of the expression of genes of interest (GOI). In this study, the stability and suitability of 11 frequently used housekeeping genes, namely 18S rRNA, ACTB, B2M, CYPA, GADPH, GUSB, HMBS, HPRT1, RPL13A, SDHA and TBP in 36 lung tissues isolated from either wild-type (WT) mice or p50 knock out (p50-/-) mice or p105 knock-out (p105-/-) mice which were treated with either carbon nanoparticle (CNP) or H(2)O or non-treated, have been validated by geNorm, NormFinder and BestKeeper programs. The expression levels of ACTB, GUSB and RPL13A were the most constant in lung tissues across three genotypes and three kinds of treatments. A set of three most stable genes is found sufficient to be used as housekeeping genes for lung tissues in studies of similar design.
AU  - Yin, R.
AU  - Tian, F.
AU  - Frankenberger, B.
AU  - Hrabě de Angelis, M.
AU  - Stöger, T.
C1  - 4873
C2  - 27474
SP  - 531-536
TI  - Selection and evaluation of stable housekeeping genes for gene expression normalization in carbon nanoparticle-induced acute pulmonary inflammation in mice.
JO  - Biochem. Biophys. Res. Commun.
VL  - 399
IS  - 4
PB  - Elsevier
PY  - 2010
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The mitochondrial 12S rRNA is considered a hotspot for mutations associated with nonsyndromic (NSHL) and aminoglycoside-induced hearing loss (AIHL). Although aminoglycoside ototoxicity is the most common cause of bilateral vestibular dysfunction, the conceivable role of 12S rRNA mutations has never been systematically investigated. We sequenced the 12S rRNA of 66 patients with bilateral vestibulopathy (BV) with (n = 15) or without (n = 51) prior exposure to aminoglycosides, as well as 155 healthy controls with intact vestibular function (sport pilots), and compared these to 2704 published sequences (Human Mitochondrial Genome Database). No mutations with a confirmed pathogenicity were found (A1555G, C1494T), but four mutations with a hitherto tentative status were detected (T669C, C960del, C960ins, T961G). Due to their predominant occurrence in patients without aminoglycoside exposure, their detection in controls and a weak evolutionary conservation, their pathogenic role in vestibulocochlear dysfunction remains provisional.
AU  - Elstner, M.*
AU  - Schmidt, C.*
AU  - Zingler, V.C.*
AU  - Prokisch, H.
AU  - Bettecken, T.
AU  - Elson, J.L.*
AU  - Rudolph, G.*
AU  - Bender, A.*
AU  - Halmagyi, GM.*
AU  - Brandt, T.*
AU  - Strupp, M.*
AU  - Klopstock, T.
C1  - 5380
C2  - 28283
SP  - 379-383
TI  - Mitochondrial 12S rRNA susceptibility mutations in aminoglycoside-associated and idiopathic bilateral vestibulopathy.
JO  - Biochem. Biophys. Res. Commun.
VL  - 377
IS  - 2
PB  - Elsevier
PY  - 2008
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - SRC family kinases (SFKs) are involved in the activation of phosphatidylinositol-3-kinase (PI3K). In addition, the activity of this lipid kinase can be regulated by the DNA repair protein NBS1. Here, we describe a disturbed expression of some members of the non-receptor tyrosine kinase family in lymphoblastoid cell lines generated from cells of Nijmegen breakage syndrome (NBS) patients. Especially, only minor amounts of the kinases LCK and HCK are expressed in the NBS1(-/-) cell lines as compared to the consanguineous NBS1(+/-) cells. We demonstrate that SFK activity is important for a proper activation of PI3K in these cells and that it is reduced in NBS1(-/-) cells. We provide evidence that the observed reduced PI3K activity in NBS lymphoblasts is caused by an impaired expression of the SFKs LCK and/or HCK. Thus, our data establish a new function for the NBS1 protein as a regulator of PI3K activity via SFK members.
AU  - Sagan, D.
AU  - Eckardt-Schupp, F.
AU  - Eicholtz-Wirth, H.
C1  - 592
C2  - 25748
SP  - 181-186
TI  - Reduced expression of SRC family kinases decreases PI3K activity in NBS1-/- lymphoblasts.
JO  - Biochem. Biophys. Res. Commun.
VL  - 377
IS  - 1
PB  - Elsevier
PY  - 2008
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The ascorbate pools of the extracellular respiratory lining fluids and the plant apoplast are currently considered as part of the first line of defence against ambient ozone. Ozone is in fact rapidly decomposed by ascorbate, but the only product identified so far (singlet oxygen) is toxic. Peroxy-l-threonic and peroxy-oxalic acids are now derived as further decomposition products on the basis of Criegee-type ozone chemistry. These secondary toxicants may resemble known ozone induced transmitter molecules by participating in signalling events affecting plant and animal innate immunity.
AU  - Sandermann, H.
C1  - 3266
C2  - 25116
SP  - 271-274
TI  - Ecotoxicology of ozone: Bioactivation of extracellular ascorbate.
JO  - Biochem. Biophys. Res. Commun.
VL  - 366
IS  - 2
PB  - Elsevier
PY  - 2008
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - DNA double strand breaks (DSBs) pose a severe hazard to the genome as erroneous rejoining of DSBs can lead to mutation and cancer. Here, we have investigated the correlation between X irradiation-induced gamma-H2AX foci, theoretically induced DSBs, and the minimal number of mis-rejoined DNA breaks (MNB) in irradiated lymphocytes obtained from two healthy humans by painting of the whole chromosome complement by spectral karyotyping. There were less gamma-H2AX foci/dose than theoretically expected, while misrepair, as expressed by MNB/gamma-H2AX focus, was similar at 0.5 and 1Gy but 3.6-fold up at 3Gy. Hence, our results suggest that X-ray-induced gamma-H2AX foci in G0 lymphocyte nuclei contain more than one DSB and that the increasing number of DSBs per gamma-H2AX repair factory lead to an increased rate of misrepair.
AU  - Scherthan, H.*
AU  - Hieber, L.
AU  - Braselmann, H.
AU  - Meineke, V.*
AU  - Zitzelsberger, H.
C1  - 1339
C2  - 25408
SP  - 694-697
TI  - Accumulation of DSBs in gamma-H2AX domains fuel chromosomal aberrations.
JO  - Biochem. Biophys. Res. Commun.
VL  - 371
IS  - 4
PB  - Elsevier
PY  - 2008
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The crucial role of the biopolymer "Von Willebrand factor" (VWF) in blood platelet binding is tightly regulated by the shear forces to which the protein is exposed in the blood flow. Under high-shear conditions, VWFs ability to immobilize blood platelets is strongly increased due to a change in conformation which at sufficient concentration is accompanied by the formation of ultra large VWF bundles (ULVWF). However, little is known about the dynamic and mechanical properties of such bundles. Combining a surface acoustic wave (SAW) based microfluidic reactor with an atomic force microscope (AFM) we were able to study the relaxation of stretched VWF bundles formed by hydrodynamic stress. We found that the dynamical response of the network is well characterized by stretched exponentials, indicating that the relaxation process proceeds through hopping events between a multitude of minima. This finding is in accordance with current ideas of VWF self-association. The longest relaxation time does not show a clear dependence on the length of the bundle, and is dominated by the internal conformations and effective friction within the bundle.
AU  - Steppich, D.M.*
AU  - Angerer, J.I.*
AU  - Opfer, J.*
AU  - Sritharan, K.*
AU  - Schneider, S.W.*
AU  - Thalhammer, S.
AU  - Wixforth, A.*
AU  - Alexander-Katz, A.*
AU  - Schneider, M.F.*
C1  - 384
C2  - 25637
SP  - 507-512
TI  - Relaxation of ultralarge VWF bundles in a microfluidic-AFM hybrid reactor.
JO  - Biochem. Biophys. Res. Commun.
VL  - 369
IS  - 2
PB  - Elsevier
PY  - 2008
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Mutations in the human ABCA3 gene, encoding an ABC-transporter, are associated with respiratory failure in newborns and pediatric interstitial lung disease. In order to study disease mechanisms, a transgenic mouse model with a disrupted Abca3 gene was generated by targeting embryonic stem cells. While heterozygous animals developed normally and were fertile, individuals homozygous for the altered allele (Abca3-/-) died within one hour after birth from respiratory failure, ABCA3 protein being undetectable. Abca3-/- newborns showed atelectasis of the lung in comparison to a normal gas content in unaffected or heterozygous littermates. Electron microscopy demonstrated the absence of normal lamellar bodies in type II pneumocytes. Instead, condensed structures with apparent absence of lipid content were found. We conclude that ABCA3 is required for the formation of lamellar bodies and lung surfactant function. The phenotype of respiratory failure immediately after birth corresponds to the clinical course of severe ABCA3 mutations in human newborns.
AU  - Hammel, M.*
AU  - Michel, G.
AU  - Hoefer, C.
AU  - Klaften, M.
AU  - Müller-Höcker, J.*
AU  - Hrabě de Angelis, M.
AU  - Holzinger, A.*
C1  - 4638
C2  - 24448
SP  - 947-951
TI  - Targeted inactivation of the murine Abca3 gene leads to respiratory failure in newborns with defective lamellar bodies.
JO  - Biochem. Biophys. Res. Commun.
VL  - 359
IS  - 4
PB  - Elsevier
PY  - 2007
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The CD155 ligand CD96 is an immunoglobulin-like protein tentatively allocated to the repertoire of human NK receptors. We report here that the CD96/CD155-interaction is preserved between man and mouse although both receptors are only moderately conserved in amino acid sequence. Moreover, murine CD96 (mCD96) binds to nectin-1, a receptor related to CD155. Applying newly generated monoclonal antibodies specifically recognizing mCD96, an expression profile is revealed resembling closely that of human CD96 (hCD96) on cells of hematopoietic origin. A panel of anti-mCD96 but also recently established anti-mCD155 antibodies effectively prevents formation of CD96/CD155-complexes. This was exploited to demonstrate that the only available receptor for mCD96 present on thymocytes is mCD155. Moreover, T cell adhesion to insect cells expressing mCD155 is blocked by these antibodies depending on the T cell subtype. These results suggest a function of the CD96/CD155-adhesion system in T cell biology.
AU  - Seth, S.*
AU  - Maier, M.K.*
AU  - Qiu, Q.*
AU  - Ravens, I.*
AU  - Kremmer, E.
AU  - Forster, R.*
AU  - Bernhardt, G.*
C1  - 4226
C2  - 25706
SP  - 959-965
TI  - The murine pan T cell marker CD96 is an adhesion receptor for CD155 and nectin-1.
JO  - Biochem. Biophys. Res. Commun.
VL  - 364
IS  - 4
PB  - Elsevier
PY  - 2007
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - This study was carried out to determine the elastic properties of single collagen type I fibrils with the use of atomic force microscopy (AFM). Native collagen fibrils were formed by self-assembly in vitro characterized with the AFM. To confirm the inner assembly of the collagen fibrils, the AFM was used as a microdissection tool. Native collagen type I fibrils were dissected and the inner core uncovered. To determine the elastic properties of collagen fibrils the tip of the AFM was used as a nanoindentor by recording force-displacement curves. Measurements were done on the outer shell and in the core of the fibril. The structural investigations revealed the banding of the shell also in the core of native collagen fibrils. Nanoindentation experiments showed the same Young's modulus on the shell as well as in the core of the investigated native collagen fibrils. In addition, the measurements indicate a higher adhesion in the core of the collagen fibrils compared to the shell.
AU  - Strasser, S.*
AU  - Zink, A.*
AU  - Janko, M.*
AU  - Heckl, W.M.*
AU  - Thalhammer, S.
C1  - 3911
C2  - 24247
SP  - 27-32
TI  - Structural investigations on native collagen type I fibrils using AFM.
JO  - Biochem. Biophys. Res. Commun.
VL  - 354
IS  - 1
PB  - Elsevier
PY  - 2007
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Little is known about determinants regulating expression of Mannan-binding lectin associated serine protease-2 (MASP-2), the effector component of the lectin pathway of complement activation. Comparative bioinformatic analysis of the MASP2 promoter regions in human, mouse, and rat, revealed conservation of two putative Stat binding sites, termed StatA and StatB. Site directed mutagenesis specific for these sites was performed. Transcription activity was decreased 5-fold when StatB site was mutated in the wildtype reporter gene construct. Gel retardation and competition assays demonstrated that proteins contained in the nuclear extract prepared from HepG2 specifically bound double-stranded StatB oligonucleotides. Supershift analysis revealed Stat3 to be the major specific binding protein. We conclude that Stat3 binding is important for MASP2 promoter activity.
AU  - Unterberger, C.
AU  - Hanson, S.*
AU  - Klingenhoff, A.*
AU  - Oesterle, D.*
AU  - Frankenberger, M.
AU  - Endo, Y.*
AU  - Matsushita, M.*
AU  - Fujita, T.*
AU  - Schwaeble, W.*
AU  - Weiss, E.H.*
AU  - Ziegler-Heitbrock, L.
AU  - Stover, C.*
C1  - 4224
C2  - 25086
SP  - 1022-1025
TI  - Stat3 is involved in control of MASP2 gene expression.
JO  - Biochem. Biophys. Res. Commun.
VL  - 364
IS  - 4
PB  - Elsevier
PY  - 2007
SN  - 0006-291X
ER  - 

TY  - JOUR
AU  - Gires, O.
AU  - Mack, B.*
AU  - Rauch, J.
AU  - Matthias, C.*
C1  - 5331
C2  - 23943
SP  - 252-259
TI  - CK8 correlates with malignancy in leukoplakia and carcinomas of the head and neck.
JO  - Biochem. Biophys. Res. Commun.
VL  - 343
PY  - 2006
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Prions as causative agents of transmissible spongiform encephalopathies have been well investigated in experimental and modelling work. However, little is known about the molecular pathogenesis of prion-induced encephalopathies, the role of co-factors, and the interaction of prions with cellular components. We investigated the influence of prion infection on expression of murine endogenous retroviruses (ERVs), which compose approximately 10% of the mouse genome. Hypothalamic neuronal cells (GT1) and neuroblastoma cells (N2a) were examined. Both cell lines can be persistently infected with mouse adapted prion strains, i.e., RML. Using a mammalian retrovirus-specific DNA microarray and quantitative PCR methods, we compared the expression profiles of ERVs in prion-infected, uninfected, and anti-prion compound-treated murine neuronal cell lines, including clonal cell populations. The results suggest that prion infection influences ERV expression in neuronal cell lines, that this influence is cell line-specific, ERV-specific, and responsive to anti-prion compound treatment.
AU  - Stengel, A.
AU  - Bach, C.
AU  - Vorberg, I.*
AU  - Frank, O.*
AU  - Gilch, S.*
AU  - Lutzny, G.*
AU  - Seifarth, W.*
AU  - Erfle, V.
AU  - Maas, E.*
AU  - Schätzl, H.*
AU  - Leib-Mösch, C.
AU  - Greenwood, A.D.
C1  - 4439
C2  - 24128
SP  - 825-831
TI  - Prion infection influences murine endogenous retrovirus expression in neuronal cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 343
PY  - 2006
SN  - 0006-291X
ER  - 

TY  - JOUR
AU  - Gires, O.
AU  - Andratschke, M.
AU  - Schmitt, B.
AU  - Mack, B.
AU  - Schaffrik, M.
C1  - 4306
C2  - 23056
SP  - 1154-1162
TI  - Cytokeratin 8 associates with the external leaflet of plasma membranes in tumour cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 328
PY  - 2005
SN  - 0006-291X
ER  - 

TY  - JOUR
AU  - Rauch, J.*
AU  - Ahlemann, M.*
AU  - Schaffrik, M.*
AU  - Mack, B.*
AU  - Ertongur, S.*
AU  - Andratschke, M.*
AU  - Zeidler, R.*
AU  - Lang, S.*
AU  - Gires, O.
C1  - 3225
C2  - 22027
SP  - 156-162
TI  - Allogenic antibody-mediated identification of head and neck cancer antigens.
JO  - Biochem. Biophys. Res. Commun.
VL  - 323
PY  - 2004
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Mutations in the SALL1 gene on chromosome 16q12.1 cause Townes–Brocks syndrome (TBS). This autosomal dominantly inherited disorder is characterized by typical malformations of the thumbs, the ears, and the anus, and also commonly affects the kidneys and other organ systems. SALL1 has recently been shown to localize to chromocenters and other heterochromatin foci in murine fibroblasts and to interact with the telomere-repeat-binding factor TRF1/PIN2. Here, we show that the ubiquitin-conjugating enzyme 2I (UBE2I), the human homolog of S. cerevisiae UBC9, and the small ubiquitin-like modifier-1 (SUMO-1) interact with SALL1 in the yeast two-hybrid system. The interaction of SALL1 and UBE2I was confirmed in a glutathione S-transferase (GST) pull-down experiment. In an in vitro assay, it could be demonstrated that SALL1 is covalently modified by at least two SUMO-1 molecules in the presence of UBA2/AOS1 and UBE2I. Mutation of lysine 1086 of SALL1 to arginine abrogates SALL1 sumoylation, suggesting the presence of a polymeric SUMO-1 chain in the wild type state.
AU  - Netzer, C.*
AU  - Bohlander, S.K.
AU  - Rieger, L.*
AU  - Müller, S.*
AU  - Kohlhase, J.*
C1  - 22207
C2  - 20916
SP  - 870-876
TI  - Interaction of the developmental regulator SALL1 with UBE2I and SUMO-1.
JO  - Biochem. Biophys. Res. Commun.
VL  - 296
IS  - 4
PY  - 2002
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Protein material was extracted from amyloid-rich sections of formalin-fixed and paraffin-embedded heart tissue from an individual with senile systemic amyloidosis, known to contain wild-type transthyretin as major amyloid fibril protein. Amino acid sequence analysis of tryptic peptides of this material revealed in addition to transthyretin sequences, also amino acid sequence corresponding to an N-terminal fragment of apolipoprotein A-IV. In immunohistochemistry, an antiserum to a synthetic apolipoprotein A-IV peptide labeled amyloid specifically. This peptide formed spontaneously amyloid-like fibrils in vitro and enhanced fibril formation from wild-type transthyretin. We conclude that several apolipoproteins, including apolipoprotein A-IV, may be important minor amyloid constituents, promoting fibril formation.
AU  - Bergström, J.*
AU  - Murphy, C.*
AU  - Eulitz, M.
AU  - Weiss, D.T.*
AU  - Westermark, G.T.*
AU  - Solomon, A.*
AU  - Westermark, P.*
C1  - 21827
C2  - 20045
SP  - 903-908
TI  - Codeposition of Apolipoprotein A-IV and Transthyretin in Senile Systemic (ATTR) Amyloidosis.
JO  - Biochem. Biophys. Res. Commun.
VL  - 285
IS  - 4
PY  - 2001
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - A 2-kb promoter fragment of SIX3, a human transcription factor essential for vertebrate eye development, has been characterized in a gene reporter assay system. The peak of activity implies the 2-kb sequence of SIX3, whereas 5′-deletion constructs of the promoter decreases successively to 60% of the activity starting from the entire promoter. In contrast, cutting off 300 bp of the 3′ promoter extinguishes its activity completely. Coexpression experiments of different other transcription factors illuminate the regulation of SIX3 during eye development: Pax6 activates the −703/−349 SIX3 promoter threefold, and PROX1 even eightfold. In contrast, Msx2 represses the entire SIX3 promoter. Furthermore, Six3 is regulated by its own negative feedback loop. In conclusion, SIX3 expression underlies a complex regulation, which is an important part to understand the network of transcription factors during eye development.A 2-kb promoter fragment of SIX3, a human transcription factor essential for vertebrate eye development, has been characterized in a gene reporter assay system. The peak of activity implies the 2-kb sequence of SIX3, whereas 5′-deletion constructs of the promoter decreases successively to 60% of the activity starting from the entire promoter. In contrast, cutting off 300 bp of the 3′ promoter extinguishes its activity completely. Coexpression experiments of different other transcription factors illuminate the regulation of SIX3 during eye development: Pax6 activates the −703/−349 SIX3 promoter threefold, and PROX1 even eightfold. In contrast, Msx2 represses the entire SIX3 promoter. Furthermore, Six3 is regulated by its own negative feedback loop. In conclusion, SIX3 expression underlies a complex regulation, which is an important part to understand the network of transcription factors during eye development.
AU  - Lengler, J.
AU  - Graw, J.
C1  - 21713
C2  - 19906
SP  - 372-376
TI  - Regulation of the Human SIX3 Gene Promoter.
JO  - Biochem. Biophys. Res. Commun.
VL  - 287
IS  - 2
PY  - 2001
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Four ABC half transporters (ALDP, ALDRP, PMP70, and PMP69) have been identified in the mammalian peroxisomal membrane but no function has been unambiguously assigned to any of them. To date X-linked adrenoleukodystrophy (X-ALD) is the only human disease known to result from a defect of one of these ABC transporters, ALDP. Using the yeast two-hybrid system and in vitro GST pull-down assays, we identified the peroxin PEX19p as a novel interactor of ALDP, ALDRP, and PMP70. The cytosolic farnesylated protein PEX19p was previously shown to be involved in an early step of the peroxisomal biogenesis. The PEX19p interaction occurs in an internal N-terminal region of ALDP which we verified to be important for proper peroxisomal targeting of this protein. Farnesylated wild-type PEX19p and a farnesylation-deficient mutant PEX19p did not differ in their ability to bind to ALDP. Our data provide evidence that PEX19p is a cytosolic acceptor protein for the peroxisomal ABC transporters ALDP, PMP70, and ALDRP and might be involved in the intracellular sorting and trafficking of these proteins to the peroxisomal membrane.
AU  - Gloeckner, C.J.
AU  - Mayerhofer, P.U.*
AU  - Landgraf, P.*
AU  - Muntau, A.C.*
AU  - Holzinger, A.*
AU  - Gerber, J.-K.
AU  - Kammerer, S.*
AU  - Adamski, J.
AU  - Roscher, A.A.*
C1  - 10337
C2  - 22331
SP  - 144-150
TI  - Human adrenoleukodystrophy protein and related peroxisomal ABC transporters interact with the peroxisomal assembly protein PEX19p.
JO  - Biochem. Biophys. Res. Commun.
VL  - 271
IS  - 1
PY  - 2000
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The putative precursor molecule of a human AL type amyloid fibril protein was isolated from an ultrafiltrate after hemofiltration. Subsequennt separation of this protein was achieved by high performance liquid chromatography (HPLC) after reduction and carboxymethylation of the disulfide bonds. The protein was separated into several fractions which were further analyzed by automatic amino acid sequence determination. It was deduced from the sequence data that the precursor molecule is an immunoglobulin L-chain of the λ-type. The V-region of this protein is most closely related to the proteins of subgroup II. Internal splits occurred in the molecule after lysine residues in positions 110, 129 and 179. The predominant fragment commences with either serine or alanine in position 9 and extends to a serine in position 65 of the V-region. Tryptic peptides generated from the fragments cover nearly the entire V- and C-region of the L-chain, with the exception of positions 1-8, from which no peptide has been isolated.
AU  - Eulitz, M.
AU  - Linke, R.P.
C1  - 40419
C2  - 40028
SP  - 1427-1434
TI  - The precursor molecule of A Vλ II-immunoglobulin light chain-derived amyloid fibril protein circulates precleaved.
JO  - Biochem. Biophys. Res. Commun.
VL  - 194
IS  - 3
PY  - 1993
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Human and murine chromatin was differentially labeled by hybridization with DNA probes that bind to species-specific satellite DNA. The targets for in situ hybridization were the mouse-specific major or gamma satellite DNA and the human alpha satellite DNA. These sequences typically are localized at or near the chromosome centromeres, and remain their tight localization throughout the cell cycle. DNA probes were synthesized in vitro by primer directed DNA amplification using the polymerase chain reaction. In typical applications like the differentiation of cells derived from chimeric animals or the characterization of chromosomes in somatic cell hybrids, the two DNA probes are differently labeled and detected using label-specific reagents that fluoresce at different wavelengths. The rapid technique for chromatin discrimination described here combines high specificity with unprecedented signal intensity.
AU  - Weier -, H.U.G.*
AU  - Zitzelsberger, H.
AU  - Gray, J.W.*
C1  - 40514
C2  - 38796
SP  - 1313-1319
TI  - Differential staining of human and murine chromatin in situ by hybridization with species-specific satellite DNA probes.
JO  - Biochem. Biophys. Res. Commun.
VL  - 182
IS  - 3
PY  - 1992
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - HL-60 cells produce an autostimulatory growth factor. Since the stimulatory effect of HL-60 conditioned medium is only observed in the absence of exogenous transferrin we have assayed HL-60 cells for the production of transferrin and found that they produce polypeptides which react with transferrin antibodies. 35S-methionine labelling, immunoprecipitation and subsequent separation by SDS-gel electrophoresis reveals the presence of a major transferrin related 41 +/- 2 kDa species released by HL-60 cells. Physiological levels of iron salts completely abolish the requirement of exogenous transferrin which indicates that the endogenous transferrin related polypeptides in the presence of exogenous inorganic iron salts are sufficient for the proliferation of HL-60 cells provided insulin or related growth factors are present. The addition of transferrin receptor antibodies inhibits the stimulatory action of the endogenous transferrin related activity.
AU  - Dittmann, K.H.
AU  - Petrides, P.E.
C1  - 19111
C2  - 12167
SP  - 473-478
TI  - A 41 kDa Transferrin Related Molecule Acts as an Autocrine Growth Factor for HL-60 Cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 176
IS  - 1
PY  - 1991
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The natural killer-like cell line YT constitutively expresses GTP-cyclohydrolase activity whereas 6-pyruvoyltetrahydropterin synthase and sepiapterin reductase are absent. The product, dihydroneopterin triphosphate, is dephosphorylated and oxidized causing neopterin to accumulate in the cells. The activities of the H 4biopterin synthesizing enzymes are not controlled by IFN-γ or the synergistic action of both IFN-γ and IL-2 as has been shown for monocytes/macrophages (Huber C. et al. (1984) J. Exp. Med. 160, 310) and CD4 + T cells, respectively (Ziegler I. et al. (1990) J. Biol. Chem. 265, 17026). Sepiapterin reductase specifically is induced by incubation of the cells with sepiapterin, leaving GTP-cyclohydrolase, 6-pyruvoyltetrahydropterin synthase and other enzymes related to pteridine metabolism (dihydropteridine reductase, dihydrofolate reductase) unaffected. The data indicate that H 4biopterin synthesis is individually regulated in the diverse cellular components of the immune system.
AU  - Schott, K.
AU  - Yodoi, J.
AU  - Schwulera, U.
AU  - Ziegler, I.
C1  - 40744
C2  - 38962
SP  - 1430-1436
TI  - Control of pteridine biosynthesis in the natural killer-like cell line YT.
JO  - Biochem. Biophys. Res. Commun.
VL  - 176
IS  - 3
PY  - 1991
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - A chimeric provirus in which the 5'LTR of a complete biologically active Mouse Mammary Tumour Virus (MMTV) proviral DNA has been replaced with the Rous Sarcoma Virus LTR has been constructed. Upon transfection into permissive cells, this provirus directs the synthesis of the MMTV gag and env structural proteins, but is impaired in packaging of the RNAs that encode these proteins. Supertransfection of these cells with MMTV based vector constructs results in the production of infectious recombinant virus at a higher efficiency than with previously described helper cell lines. Such a retroviral vector system based on MMTV will allow the study of the effects of conditional expression of inserted genes upon infected cells.
AU  - Salmons, B.
AU  - Moritz-Legrand, S.
AU  - Garcha, I.
AU  - Günzburg, W.H.
C1  - 17854
C2  - 10770
SP  - 1191-1198
TI  - Construction and characterization of a packaging cell line for MMTV-based conditional retroviral vectors.
JO  - Biochem. Biophys. Res. Commun.
VL  - 159
IS  - 3
PY  - 1989
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Established osteoblast-like (OB) cells infected with the bone tumor-inducing C-type retrovirus OA MuLV remained nontumorigenic over 104 cell culture passages. DNA histograms revealed a new cell population with a stem line peak at 5c. A second OA MuLV-infected OB cell line underwent neoplastic transformation with increasing passage level. These cells showed diffuse aneuploidy. Stepwise linear discriminant analysis of the chromatin structure of control, OA MuLV-infected, and FBR osteosarcoma virus-transformed cell lines resulted in various levels of discrimination ranging between 79.6% for control cells versus nontumorigenic OA MuLV-infected cells, and 96.6% for nontumorigenic OA MuLV-infected cells versus FBR osteosarcoma virus-transformed cells. OA MuLV-infected tumorigenic cells and FBR osteosarcoma virus-transformed cells were discriminated at a 93.6% level.
AU  - Schmid, J.
AU  - Aubele, M.
AU  - Jütting, U.
AU  - Rodenacker, K.
AU  - Luz, A.
AU  - Erfle, V.
AU  - Burger, G.
C1  - 18896
C2  - 11256
SP  - 728-735
TI  - Computer-assisted Imaging Cytometry of Nuclear Chromatin Reveals Bone Tumor Virus Infection and Neoplastic Transformation of Adherent Osteoblast-like Cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 164
IS  - 2
PY  - 1989
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Established osteoblast-like (OB) cells infected with the bone tumor-inducing C-type retrovirus OA MuLV remained nontumorigenic over 104 cell culture passages. DNA histograms revealed a new cell population with a stem line peak at 5c. A second OA MuLV-infected OB cell line underwent neoplastic transformation with increasing passage level. These cells showed diffuse aneuploidy. Stepwise linear discriminant analysis of the chromatin structure of control, OA MuLV-infected, and FBR osteosarcoma virus-transformed cell lines resulted in various levels of discrimination ranging between 79.6% for control cells versus nontumorigenic OA MuLV-infected cells, and 96.6% for nontumorigenic OA MuLV-infected cells versus FBR osteosarcoma virus-transformed cells. OA MuLV-infected tumorigenic cells and FBR osteosarcoma virus-transformed cells were discriminated at a 93.6% level.
AU  - Schmidt, J.*
AU  - Aubele, M.
AU  - Jütting, U.
AU  - Rodenacker, K.
AU  - Luz, A.*
AU  - Erfle, V.F.*
AU  - Burger, G.T.
C1  - 42060
C2  - 11256
SP  - 728-735
TI  - Computer-assisted imaging cytometry of nuclear chromatin reveals bone tumor virus infection and neoplastic transformation of adherent osteoblast-like cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 164
IS  - 2
PY  - 1989
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Urinary stones with amyloid structure, obtained from uremic patients, were analyzed according to molecular weight, amino acid sequence, and antigenic content. A major protein of approximately 7 kD, designated AB protein, was isolated by size exclusion using HPLC in 60% formic acid. AB protein reacted in immunodiffusion only with an antiserum to β2-microglobulin, with β2m spurring over AB protein. N-terminal amino acid sequence analysis defined two fragments homologous to β2m. One fragment commenced with Ile at position 7 and the other with Ser at position 20, with a cleavage point subsequent to a lysyl residue in both. It is concluded that β2m is a precursor of urinary amyloid stones and intratubular concretions of patients with preterminal and terminal renal failure; limited proteolysis is involved in AB amyloid generation.
AU  - Linke, R.P.
AU  - Bommer, J.
AU  - Ritz, E.R.
AU  - Waldherr, R.
AU  - Eulitz, M.
C1  - 42116
C2  - 38380
SP  - 665-671
TI  - Amyloid kidney stone of uremic patients consist of Beta2-microglobulin fragments.
JO  - Biochem. Biophys. Res. Commun.
VL  - 136
IS  - 2
PY  - 1986
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Lectin stimulation of human peripheral blood mononuclear cells causes an increase in neopterin, biopterin, 6-hydroxymethylpterin and 6-formylpterin, as was determined by HPLC after iodine oxidation of the acid extract. After 72 h, pteridines peak at levels 5-10-fold as compared to resting cells. Levels decline to initial values during the following 24 h. Changes in pteridine proportions indicate that the synthesis of tetrahydrobiopterin proceeding from dihydroneopterin triphosphate is controlled during the process of lymphocyte activation. The release of both cellular neopterin and biopterin, but not of 6-hydroxymethylpterin and its aldehyde, is controlled by interferon-γ.
AU  - Ziegler, I.
C1  - 41598
C2  - 38237
SP  - 404-411
TI  - Synthesis and interferon-γ controlled release of pteridines during activation of human peripheral blood mononuclear cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 132
IS  - 1
PY  - 1985
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Hydroxyurea induces DNA repair replication in the cytochrome P-450-containing C2Rev7 rat hepatoma cell line. Repair is severalfold increased by pretreatment of the cells with dexamethasone, which induces cytochrome P-450-dependent monooxygenase activities in these cells. In the dedifferentiated hepatoma line H5, which strongly expresses cytochrome P-448 but no cytochrome P-450-dependent enzyme activities, hydroxyurea is not genotoxic. The results support the notion that the formation of genotoxic metabolites from hydroxyurea is mediated by a cytochrome P-450-dependent enzyme.
AU  - Andrae, U.
C1  - 41877
C2  - 38334
SP  - 409-415
TI  - Evidence for the involvement of cytochrome P-450-dependent monooxygenase(S) in the formation of genotoxic metabolites from N-hydroxyurea.
JO  - Biochem. Biophys. Res. Commun.
VL  - 118
IS  - 2
PY  - 1984
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Phosphorylation of purified yeast fructose-1,6-bisphosphatase was studied using purified preparations from yeast of two different cyclic AMP-independent protein kinases and a cyclic AMP-dependent protein kinase. Incorporation of 32P into fructose-1,6-bisphosphatase could be demonstrated only with the cyclic AMP-dependent protein kinase. Phosphorylation of fructose-1,6-bisphosphatase was stimulated by 3 μM fructose-2,6-bisphosphate and inhibited by 1 mM 5′-AMP.
AU  - Pohlig, G.*
AU  - Wingender-Drissen, R.*
AU  - Noda, T.*
AU  - Holzer, H.
C1  - 40904
C2  - 38465
SP  - 317-324
TI  - Cyclic AMP and fructose-2,6-bisphosphate stimulated in vitro phosphorylation of yeast fructose-1,6-bisphosphatase.
JO  - Biochem. Biophys. Res. Commun.
VL  - 115
IS  - 1
PY  - 1983
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Aphidicolin, an inhibitor of the α-polymerase in mammalian cells, at a concentration of 0.5 μg/ml, is shown to enable cells which are growing exponentially and synchronized in the S-phase of the cell cycle, to repair potentially lethal damage caused by exposure to either x-rays or UV light. The drug holds cells up in the S-phase which may serve to allow time for repair and could prevent fixation of damage which may occur when the cells progress through the cell cycle. The possible involvement of α- and β-polymerase in repair of potentially lethal damage is discussed.
AU  - Iliakis, G.E.
AU  - Nüsse, M.
C1  - 41302
C2  - 38667
SP  - 1209-1214
TI  - Aphidicolin promotes repair of potentially lethal damage in irradiated mammalian cells synchronized in S-phase.
JO  - Biochem. Biophys. Res. Commun.
VL  - 104
IS  - 4
PY  - 1982
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Previous in vivo experiments have shown that simultaneously with the glucose-induced inactivation of yeast fructose-1,6-bisphosphatase a phosphorylation of serine residues of the enzyme occurs. The inactivation of fructose-1,6-bisphosphatase dependent on ATP, Mg++ and cyclic AMP is now demonstrated in a cell-free yeast extract suggesting the existence of a cyclic AMP-dependent fructose-1,6-bisphosphatase kinase. When glucose is added to intact yeast cells within 30 sec the cyclic AMP concentration increases from 0.7 to 3 nmol per g wet weight. This observation suggests that upon addition of glucose to yeast cells cyclic AMP functions as the mediating signal for the protein kinase catalyzed phosphorylation of fructose-1,6-bisphosphatase. The levels of glucose-6-phosphate and fructose-6-phosphate also show a transient rise with a maximum 15 to 30 sec after the addition of glucose to yeast cells, i.e. shortly before the observed increase of the cyclic AMP concentration. Thus, the sugar phosphates may function as allosteric effectors which stimulate adenylate cyclase and/or inhibit cyclic AMP phosphodiesterase thereby leading to a transient rise of the cyclic AMP levels, which in turn may be the signal for the phosphorylation of fructose-1,6-bisphosphatase.
AU  - Purwin, C.
AU  - Leidig, F.
AU  - Holzer, H.
C1  - 42152
C2  - 38282
SP  - 1482-1489
TI  - Cyclic AMP-dependent phosphorylation of fructose-1,6-bisphosphatase in yeast.
JO  - Biochem. Biophys. Res. Commun.
VL  - 107
IS  - 4
PY  - 1982
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Fructose-1,6-bisphosphatase was precipitated with purified rabbit antiserum from extracts of 32P-orthophosphate labelled yeast cells, submitted to SDS polyacrylamide gel electrophoresis, extracted from the gels and counted for radioactivity due to 32P incorporation. Fructose-1,6-bisphosphatase from glucose starved yeast cells contained a very low 32P label. During 3 min treatment of the glucose starved cells with glucose the 32P-label increased drastically. Subsequent incubation of the cells in an acetate containing, glucose-free medium led to a label which was again low. Analysis for phosphorylated amino acids in the immunpprecipitated fructose-1,6-bisphosphatase protein from the 3 min glucose-inactivated cells exhibited phospho-serine as the only labelled phosphoamino acid. These data demonstrate a phosphorylation of a serine residue of fructose-1,6-bisphosphatase during this 3 min glucose treatment of glucose starved cells. A concomitant about 60 % inactivation of the enzyme had been shown to occur. The data in addition show a release of the esterified phosphate from the enzyme upon incubation of cells in a glucose-free medium, a treatment which leads to peactivation of enzyme activity. A protein kinase and a protein phosphatase catalysing this metabolic interconversion of fructose-1,6-bisphosphatase are postulated. It is assumed that metabolites accumulating after the addition of glucose exert a positive effect on the kinase activity and/or have a negative effect on the phosphatase activity. A role of the enzymic phosphorylation of fructose-1,6-bisphosphatase in the initiation of complete proteolysis of the enzyme during "catabolite inactivation" is discussed.
AU  - Müller, D.
AU  - Holzer, H.
C1  - 41241
C2  - 38556
SP  - 926-933
TI  - Regulation of fructose-1,6-bisphosphatase in yeast by phosphorylation/dephosphorylation.
JO  - Biochem. Biophys. Res. Commun.
VL  - 103
IS  - 3
PY  - 1981
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Addition of glucose to glucose-derepressed yeast cells causes disappearance of 60 % of the activity of fructose-1,6-bisphosphatase within 3 to 5 min. Reversibility of this "catabolite inactivation" reaction in a glucose-free medium is independent on de novo protein synthesis. The pH-optima of fructose-1,6-bisphosphatase activity in gel-filtrated crude extracts were shown to be 8.25 for the enzyme from derepressed cells and 8.8 for the enzyme from cells treated with glucose for 4 min. In studies with |3H| - leucine labelled glucose-derepressed cells the protein cross reacting with antibodies against fructose-1,6-bisphosphatase did not disappear within the first 10 min after addition of glucose. These findings suggest that the glucose induced rapid inactivation of the enzyme is the result of a covalent modification which decreases the fructose-1,6-bisphosphatase activity and changes the pH-activity profile of the enzyme, but does not change its immunological reactivity to antibodies. It is concluded that the covalent modification renders the enzyme susceptible to proteinases and thereby initiates its selective proteolysis.
AU  - Tortora, P.
AU  - Birtel, M.
AU  - Lenz, A.-G.
AU  - Holzer, H.
C1  - 41775
C2  - 38572
SP  - 688-695
TI  - Glucose-dependent metabolic interconversion of fructose-1,6-bisphosphatase in yeast.
JO  - Biochem. Biophys. Res. Commun.
VL  - 100
IS  - 2
PY  - 1981
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The occurrence of the proteinase A inhibitors 2 and 3 was investigated in wild type strains of Saccharomycescerevisiae and Saccharomycescarlsbergensis as well as in several strains of commercial baker's yeast. Haploid and diploid strains of Saccharomycescerevisiae contain only proteinase A inhibitor 3 whereas in Saccharomycescarlsbergensis only proteinase A inhibitor 2 is found. Strains of commercial baker's yeast contain either proteinase A inhibitor 3 or both inhibitors in a constant ratio of 1:3. Single cell cultures isolated from a strain of commercial baker's yeast also contain a mixture of the two inhibitors. Therefore, baker's yeast is not a mixture of two different cell types but the genome for both inhibitors is present in each single cell. In general, the results indicate that the occurrence of the two proteinase A inhibitors is determined genetically and, therefore, they may be called “isoinhibitors”. © 1980, All rights reserved.
AU  - Meußdoerffer, F.
C1  - 51635
C2  - 0
SP  - 423-429
TI  - Occurrence of proteinase a isoinhibitors in wild type yeast strains and commercial baker's yeast.
JO  - Biochem. Biophys. Res. Commun.
VL  - 97
IS  - 2
PY  - 1980
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Cell lines derived from Reuber H-4-II-E hepatoma cells and their hybrids that differ in the expression of liver-specific functions are shown to contain different forms of monooxygenases. According to the specificity toward the substrates benzo(a)pyrene, aldrin and chenodeoxycholic acid, the kinetics of the epoxidation of aldrin, the response to inducers, such as benz(a)anthracene and dexamethasone, and the in vitro modifier 7,8-benzoflavone, the monooxygenases predominating in differentiated cell lines belong to the cytochrome P-450-dependent enzyme(s), those in the less differentiated lines belong to the cytochrome P-448-dependent form(s).
AU  - Wiebel, F.J.
AU  - Wolff, T.
AU  - Lambiotte, M.
C1  - 41863
C2  - 38846
SP  - 466-472
TI  - Presence of cytochrome P-450- and cytochrome P-448-dependent monooxygenase functions in hepatoma cell lines.
JO  - Biochem. Biophys. Res. Commun.
VL  - 94
IS  - 2
PY  - 1980
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The amino acid sequence of proteinase B inhibitor 1 (IB1) from bakers' yeast has been established by automated Edman degradation up to position 42. A comparison with the sequence of proteinase B inhibitor 2 (IB2) revealed two differences: LEU-32 and GLU-34 in IB2 are replaced by VAL-32 and LYS-34 in IB1. Identity of the COOH-terminal region of IB1 with that of IB2 was proved by degradation with the carboxypeptidases A and Y. Furthermore, a chymotryptic peptide was isolated from each of the 74 residues containing inhibitors. The two fragments, ranging from position 42 to the COOH termini of the inhibitors, were found to be identical with respect to electrophoretical mobility, end groups, amino acid composition and peptide pattern after tryptic digestion. It is concluded, that the two inhibitor sequences are identical beyond position 42. IB1 and IB2 are isoinhibitors, because they are coded by different genes.
AU  - Maier, K.L.
AU  - Müller, H.R.*
AU  - Tesch, R.*
AU  - Witt, I.*
AU  - Holzer, H.
C1  - 40936
C2  - 38541
SP  - 1390-1398
TI  - Amino acid sequence of yeast proteinase B inhibitor 1 comparison with inhibitor 2.
JO  - Biochem. Biophys. Res. Commun.
VL  - 91
IS  - 4
PY  - 1979
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The tetraamine occurring in Euglena gracilis, previously believed to be spermine, is shown to be norspermine [N, N′-bis (3-aminopropyl)-1,3-diaminopropane]. Proof of identity was established by HPLC, HPCC and mass spectrometric investigations.
AU  - Kneifel, H.
AU  - Schuber, F.J.*
AU  - Aleksijevic, A.*
AU  - Grove, J.R.*
C1  - 41840
C2  - 35790
SP  - 42-46
TI  - Occurrence of norspermine in Euglena gracilis.
JO  - Biochem. Biophys. Res. Commun.
VL  - 85
IS  - 1
PY  - 1978
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The flavin component of soluble hydrogenase (hydrogen: NAD+ oxidoreductase, EC 1.12.1.2) from Alcaligenes eutrophus was identified as FMN by thin layer chromatography in two solvent systems and by binding studies with apoflavodoxin from Megasphaera elsdenii. The flavin of hydrogenase reacted rapidly with apoflavodoxin with almost complete quenching of the fluorescence at 525 nm. Quantitative determination of FMN was performed by fluorimetric titration with a standardized solution of apoflavodoxin. From the determined FMN content of different enzyme preparations and from the percentage of stimulation of hydrogenase activity by exogenous FMN it is concluded that hydrogenase contains 2 FMN per molecule.
AU  - Schneider, K.A.
AU  - Schlegel, H.G.
C1  - 41337
C2  - 35705
SP  - 564-571
TI  - Identification and quantitative determination of the flavin component of soluble hydrogenase from Alcaligenes eutrophus.
JO  - Biochem. Biophys. Res. Commun.
VL  - 84
IS  - 3
PY  - 1978
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - The α-isopropylmalate synthase (EC 4.1.3.12) from AlcaligeneseutrophusH 16 was inactivated by EDTA in a time-dependent reaction. Only the addition of Mn++ plus dithiothreitol could restore the activity. The substrate, α-ketoisovalerate, prevented the inactivation; the feedback inhibitor, leucine, and it's antagonist, valine, increased the rate of inactivation. Except for α,α′-bipyridyl, chelating reagents, other than EDTA had no effect on the enzyme stability. It is suggested that the α-isopropylmalate synthase is a metallo enzyme - the evidence points to Mn++ as the metal ion - and that this enzyme uses a mechanism of catalysis which differs from that of the analogous malate synthase (EC 4.1.3.2) and citrate synthase (EC 4.1.3.4).
AU  - Wiegel, J.W.
C1  - 41779
C2  - 38109
SP  - 907-912
TI  - Mn++-specific reactivation of edta inactivated α-isopropylmalate synthase from Alcaligenes eutrophusH 16.
JO  - Biochem. Biophys. Res. Commun.
VL  - 82
IS  - 3
PY  - 1978
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - In exponentially growing cells of Saccharomyces, cerevisiae, cycloheximide stimulated intracellular protein degradation to the same extent as did starvation for required amino acids. By using inhibitors of macromolecular synthesis and temperature-sensitive mutants defective in different steps of RNA and protein synthesis it could be demonstrated, that this stimulation of protein degradation was directly related to the inhibition of protein synthesis per se, but not connected to the cessation of ribosomal RNA synthesis or to the inhibition of cell growth.
AU  - Betz, H.
C1  - 42684
C2  - 35587
SP  - 114-120
TI  - Inhibition of protein synthesis stimulates intracellular protein degradation in growing yeast cells.
JO  - Biochem. Biophys. Res. Commun.
VL  - 72
IS  - 1
PY  - 1976
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - Anaerobically cultured yeast cells have a very low HMG-CoA reductase activity and a low sterol content. When these cells are transfered to phosphate buffer containing 1.2 % glucose and held under aerobic conditions, the specific activity of the HMG-CoA reductase increases up to sixfold within 8 hrs. The increase in the reductase activity is paralled by an increase in the sterol content. This induction of HMG-CoA reductase in resting yeast cells is inhibited by cycloheximide indicating that a de novo synthesis of enzyme protein is mediated by glucose under aerobic conditions. It appears that the regulation of sterol synthesis in yeast is closely connected with the aerobic glucose metabolism.
AU  - Berndt, J.
AU  - Boll, M.
AU  - Löwel, M.
AU  - Gaumert, R.
C1  - 41948
C2  - 35369
SP  - 843-848
TI  - Regulation of sterol biosynthesis in yeast: Induction of 3-hydroxy-3-methylglutaryl-CoA reductase by glucose.
JO  - Biochem. Biophys. Res. Commun.
VL  - 51
IS  - 4
PY  - 1973
SN  - 0006-291X
ER  - 

TY  - JOUR
AB  - After exhaustion of citrate in the growth medium, the citrate lyase of Rhodopseudomonas,gelatinosa is inactivated by deacetylation. Upon addition of citrate to a suspension of cells containing inactive enzyme the lyase is reactivated. The discovery of Buckel, Buschmeier and Eggerer (1), that deacetylation causes loss of activity of purified citrate lyase from Klebsiella,aerogenes, therefore, seems to be the basis of a regulatory mechanism of biological significance.
AU  - Giffhorn, F.
AU  - Beuscher, N.
AU  - Gottschalk, G.
C1  - 42300
C2  - 35580
SP  - 467-472
TI  - Regulation of citrate lyase activity in Rhodopseudomonas gelatinosa.
JO  - Biochem. Biophys. Res. Commun.
VL  - 49
IS  - 2
PY  - 1972
SN  - 0006-291X
ER  -