TY  - JOUR
AB  - Glutaric aciduria type I (GA-I) is a rare organic aciduria caused by the autosomal recessive inherited deficiency of glutaryl-CoA dehydrogenase (GCDH). GCDH deficiency leads to disruption of L-lysine degradation with characteristic accumulation of glutarylcarnitine and neurotoxic glutaric acid (GA), glutaryl-CoA, 3-hydroxyglutaric acid (3-OHGA). DHTKD1 acts upstream of GCDH, and its deficiency leads to none or often mild clinical phenotype in humans, 2-aminoadipic 2-oxoadipic aciduria. We hypothesized that inhibition of DHTKD1 may prevent the accumulation of neurotoxic dicarboxylic metabolites suggesting DHTKD1 inhibition as a possible treatment strategy for GA-I. In order to validate this hypothesis we took advantage of an existing GA-I (Gcdh(-/-)) mouse model and established a Dhtkd1 deficient mouse model. Both models reproduced the biochemical and clinical phenotype observed in patients. Under challenging conditions of a high lysine diet, only Gcdh(-/-) mice but not Dhtkd1(-/-) mice developed clinical symptoms such as lethargic behaviour and weight loss. However, the genetic Dhtkd1 inhibition in Dhtkd1(-/-)/Gcdh(-/-) mice could not rescue the GA-I phenotype. Biochemical results confirm this finding with double knockout mice showing similar metabolite accumulations as Gcdh(-/-) mice with high GA in brain and liver. This suggests that DHTKD1 inhibition alone is not sufficient to treat GA-I, but instead a more complex strategy is needed. Our data highlights the many unresolved questions within the L-lysine degradation pathway and provides evidence for a so far unknown mechanism leading to glutaryl-CoA.
AU  - Biagosch, C.
AU  - Ediga, R.*
AU  - Hensler, S.
AU  - Faerberboeck, M.
AU  - Kühn, R.
AU  - Wurst, W.
AU  - Meitinger, T.
AU  - Kölker, S.*
AU  - Sauer, S.*
AU  - Prokisch, H.
C1  - 51200
C2  - 43110
CY  - Amsterdam
SP  - 2220-2228
TI  - Elevated glutaric acid levels in Dhtkd1-/Gcdh- double knockout mice challenge our current understanding of lysine metabolism.
JO  - Biochim. Biophys. Acta
VL  - 1863
IS  - 9
PB  - Elsevier Science Bv
PY  - 2017
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - The reactive metabolite methylglyoxal (MG) has been identified as mediator of pain. Scavenging of free MG and the prevention of MG-derived post-translational modifications may provide a useful therapeutic treatment. An arginine-rich, fatty acid coupled, cyclic peptide (CycK(Myr)R4E) with high proteolytic stability and prolonged circulation was developed for the scavenging of MG. It was shown to reduce the formation of albumin-MG adducts in vitro and prevented MG-induced pain by reducing plasma MG levels through the formation of peptide-MG adducts in vivo. CycK(Myr)R4E therefore presents a promising option for the treatment of pain and other diabetic complications associated with high MG levels.
AU  - Brings, S.*
AU  - Fleming, T.*
AU  - de Buhr, S.*
AU  - Beijer, B.*
AU  - Lindner, T.*
AU  - Wischnjow, A.*
AU  - Kender, Z.*
AU  - Peters, V.*
AU  - Kopf, S.*
AU  - Haberkorn, U.*
AU  - Mier, W.*
AU  - Nawroth, P.P.
C1  - 50286
C2  - 42329
SP  - 654-662
TI  - A scavenger peptide prevents methylglyoxal induced pain in mice.
JO  - Biochim. Biophys. Acta
VL  - 1863
IS  - 3
PY  - 2017
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - The non-coding transcriptome, in particular microRNAs (miRNA), influences cellular survival after irradiation. However, the underlying mechanisms of radiation-induced miRNA expression changes and consequently target expression changes are poorly understood. In this study, we show that ionizing radiation decreases expression of the miR-23a~27a~24-2 cluster through transcriptional regulation by promoter methylation and at the post-transcriptional level by reduced processing through AGO-phosphorylation. Furthermore, we demonstrate that all three mature cluster miRNAs reduce apoptosis by increasing expression of the common target protein XIAP. These findings link a temporal succession of transcriptional and post-transcriptional regulatory mechanisms of the miR~23a~24-2~27a cluster, enabling a dynamic stress response and assuring cellular survival after radiation exposure.
AU  - Heider, T.
AU  - Mutschelknaus, L.
AU  - Radulović, V.
AU  - Winkler, K.
AU  - Kimmel, J.
AU  - Anastasov, N.
AU  - Atkinson, M.J.*
AU  - Mörtl, S.
C1  - 51783
C2  - 43369
CY  - Amsterdam
SP  - 1127-1137
TI  - Radiation induced transcriptional and post-transcriptional regulation of the hsa-miR-23a~27a~24-2 cluster suppresses apoptosis by stabilizing XIAP.
JO  - Biochim. Biophys. Acta
VL  - 1860
IS  - 11
PB  - Elsevier Science Bv
PY  - 2017
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Pulmonary fibrosis (PF) is a chronic progressive lung disease without effective medical treatment options leading to respiratory failure and death within 3–5 years of diagnosis. The pathological process of PF is driven by aberrant wound-healing involving fibroblasts and myofibroblasts differentiated by secreted profibrotic transforming growth factor β (TGF-β1). Classical transient receptor potential 6 (TRPC6), a Na+- and Ca2 +-permeable cation channel, is able to promote myofibroblast conversion of primary rat cardiac and human dermal fibroblasts and TRPC6-deficiency impaired wound healing after injury. To study a potential role of TRPC6 in the development of PF we analyzed lung function, gene and protein expression in wild-type (WT) and TRPC6-deficient (TRPC6 −/−) lungs utilizing a bleomycin-induced PF-model. Fibrotic WT-mice showed a significant higher death rate while bleomycin-treated TRPC6-deficient mice were partly protected from fibrosis as a consequence of a lower production of collagen and an almost normal function of the respiratory system (reduced resistance and elastance compared to fibrotic WT-mice). On a molecular level TGF-β1 induced TRPC6 up-regulation, increased Ca2 + influx and nuclear NFAT localization in WT primary murine lung fibroblasts (PMLFs) resulting in higher stress fiber formation and accelerated contraction rates as compared to treated TRPC6-deficient fibroblasts. Therefore, we conclude that TRPC6 is an important determinant for TGF-β1-induced myofibroblast differentiation during fibrosis and specific channel inhibitors might be beneficial in a future treatment of PF.
AU  - Hofmann, K.*
AU  - Fiedler, S.*
AU  - Vierkotten, S.
AU  - Weber, J.*
AU  - Klee, S.
AU  - Jia, J.
AU  - Zwickenpflug, W.*
AU  - Flockerzi, V.*
AU  - Storch, U.*
AU  - Yildirim, A.Ö.
AU  - Gudermann, T.*
AU  - Königshoff, M.
AU  - Dietrich, A.*
C1  - 50166
C2  - 42332
CY  - Amsterdam
SP  - 560-568
TI  - Classical transient receptor potential 6 (TRPC6) channels support myofibroblast differentiation and development of experimental pulmonary fibrosis.
JO  - Biochim. Biophys. Acta
VL  - 1863
IS  - 2
PB  - Elsevier Science Bv
PY  - 2017
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - An alcohol-based non-crosslinking tissue fixative, PAXgene Tissue System, has been proposed as alternative fixation method to formalin, providing superior and morphological preservation. To date, metabolites have not been assessed in PAXgene-fixed tissues. The study focuses on a comparison between PAXgene and standard formalin fixation for metabolomic analysis by MALDI mass spectrometry imaging. Therefore, fifty-six samples from seven mice organs were fixed with PAXgene (PFPE) or formalin (FFPE), embedded in paraffin, and processed to a tissue microarray. PAXgene was able to spatially preserve metabolites in organs achieving an overlap of common metabolites ranging from 34 to 78% with FFPE. Highly similar signal intensities and visualization of molecules demonstrated negligible differences for metabolite imaging on PFPE compared to FFPE tissues. In addition, we performed proteomic analysis of intact proteins and peptides derived from enzymatic digestion. An overlap of 33 to 58% was found between FFPE and PFPE tissue samples in peptide analysis with a higher number of PFPE-specific peaks. Analysis of intact proteins achieved an overlap in the range of 0 to 28% owing to the poor detectability of cross-linked proteins in formalin-fixed tissues. Furthermore, metabolite and peptide profiles obtained from PFPE tissues were able to correctly classify organs independent of the fixation method, whereas a distinction of organs by protein profiles was only achieved by PAXgene fixation. Finally, we applied MALDI MSI to human biopsies by sequentially analyzing metabolites and peptides within the same tissue section. Concerning prospective studies, PAXgene can be used as an alternative fixative for multi-omic tissue analysis.
AU  - Urban, C.
AU  - Buck, A.
AU  - Siveke, J.T.*
AU  - Lordick, F.*
AU  - Luber, B.*
AU  - Walch, A.K.
AU  - Aichler, M.
C1  - 52093
C2  - 43706
CY  - Amsterdam
SP  - 51-60
TI  - PAXgene fixation enables comprehensive metabolomic and proteomic analyses of tissue specimens by MALDI MSI.
JO  - Biochim. Biophys. Acta
VL  - 1862
IS  - 1
PB  - Elsevier Science Bv
PY  - 2017
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Analysis of the cellular mechanisms of metabolic disorders, including type 2 diabetes mellitus, is complicated by the large number of reactions and interactions in metabolic networks. Metabolic control analysis with appropriate modularization is a powerful method for simplifying and analyzing these networks. To analyze control of cellular energy metabolism in adherent cell cultures of the INS-1 832/13 pancreatic β-cell model we adapted our microscopy assay of absolute mitochondrial membrane potential (δψM) to a fluorescence microplate reader format, and applied it in conjunction with cell respirometry. In these cells the sensitive response of δψM to extracellular glucose concentration drives glucose-stimulated insulin secretion. Using metabolic control analysis we identified the control properties that generate this sensitive response. Force-flux relationships between δψM and respiration were used to calculate kinetic responses to δψM of processes both upstream (glucose oxidation) and downstream (proton leak and ATP turnover) of δψM. The analysis revealed that glucose-evoked δψM hyperpolarization is amplified by increased glucose oxidation activity caused by factors downstream of δψM. At high glucose, the hyperpolarized δψM is stabilized almost completely by the action of glucose oxidation, whereas proton leak also contributes to the homeostatic control of δψM at low glucose. These findings suggest a strong positive feedback loop in the regulation of β-cell energetics, and a possible regulatory role of proton leak in the fasting state. Analysis of islet bioenergetics from published cases of type 2 diabetes suggests that disruption of this feedback can explain the damaged bioenergetic response of β-cells to glucose.
AU  - Gerencser, A.A.*
AU  - Mookerjee, S.A.*
AU  - Jastroch, M.
AU  - Brand, M.D.*
C1  - 50191
C2  - 42243
CY  - Amsterdam
SP  - 1054-1065
TI  - Positive feedback amplifies the response of mitochondrial membrane potential to glucose concentration in clonal pancreatic beta cells.
JO  - Biochim. Biophys. Acta
VL  - 1863
IS  - 5
PB  - Elsevier Science Bv
PY  - 2016
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Metabolomics studies of human plasma demonstrate a correlation of lower plasma lysophosphatidylcholines (LPC) concentrations with insulin resistance, obesity, and inflammation. This relationship is not unraveled on a molecular level. Here we investigated the effects of the abundant LPC(16:0) and LPC(18:1) on human skeletal muscle cells differentiated to myotubes. Transcriptome analysis of human myotubes treated with 10μM LPC for 24h revealed enrichment of up-regulated peroxisome proliferator-activated receptor (PPAR) target transcripts, including ANGPTL4, PDK4, PLIN2, and CPT1A. The increase in both PDK4 and ANGPTL4 RNA expression was abolished in the presence of either PPARδ antagonist GSK0660 or GSK3787. The induction of PDK4 by LPCs was blocked with siRNA against PPARD. The activation of PPARδ transcriptional activity by LPC was shown as PPARδ-dependent luciferase reporter gene expression and enhanced DNA binding of the PPARδ/RXR dimer. On a functional level, further results show that the LPC-mediated activation of PPARδ can reduce fatty acid-induced inflammation and ER stress in human skeletal muscle cells. The protective effect of LPC was prevented in the presence of the PPARδ antagonist GSK0660. Taking together, LPCs can activate PPARδ, which is consistent with the association of high plasma LPC levels and PPARδ-dependent anti-diabetic and anti-inflammatory effects.
AU  - Klingler, C.
AU  - Zhao, X.*
AU  - Adhikary, T.*
AU  - Li, J.*
AU  - Xu, G.*
AU  - Häring, H.U.
AU  - Schleicher, E.*
AU  - Lehmann, R.
AU  - Weigert, C.
C1  - 49684
C2  - 40872
CY  - Amsterdam
SP  - 1980-1992
TI  - Lysophosphatidylcholines activate PPARδ and protect human skeletal muscle cells from lipotoxicity.
JO  - Biochim. Biophys. Acta
VL  - 1861
IS  - 12
PB  - Elsevier Science Bv
PY  - 2016
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - We have isolated a Pinus sylvestris cDNA encoding a globular protein of 474 amino acids with a predicted molecular weight of 52,995 Da. The deduced amino acid sequence showed 41.9% identity and 13.6% similarity to mammalian cytosolic 3-hydroxy-3-methylglutaryl-CoA-synthase (HMGS). Treatment of Scots pine seedlings with ozone resulted in a transient increase of a 1.95 kb transcript, whereas a 1.2 kb mRNA decreased transiently, indicating a possible influence of ozone on isoprenoid biosynthesis.
AU  - Wegener, A.
AU  - Gimbel, W.
AU  - Werner, T.
AU  - Hani, J.
AU  - Ernst, D.
AU  - Sandermann, H.
C1  - 46468
C2  - 0
SP  - 247-252
TI  - Molecular cloning of ozone-inducible protein from Pinus sylvestris L. with high sequence similarity to vertebrate 3-hydroxy-3-methylglutaryl-CoA-synthase.
JO  - Biochim. Biophys. Acta
VL  - 1350
IS  - 3
PY  - 1997
SN  - 0006-3002
ER  - 

TY  - JOUR
AU  - Sandermann, H.
C1  - 20663
C2  - 13878
SP  - 130-133
TI  - Induction of Lipid-Protein Mismatch by Xenobiotics with General Membrane Targets.
JO  - Biochim. Biophys. Acta
VL  - 1150
PY  - 1993
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Northern blot analysis of rat RNA from cell lines and isolated organs with a specific rat cDNA probe detected two GTP cyclohydrolase I mRNA species of approx. 1.4 and 3.6 kb. The ratio between these two species varies between 0.6 and 2.4 in different rat organs. Using primers derived from highly conserved regions in the rat and Escherichia coli cDNA sequences a human GTP cyclohydrolase I probe was obtained by means of reverse transcription and PCR (polymerase chain reaction). The human PCR product consisting of 555 bp was cloned and sequenced. It shows a 92% identity with the published sequence of the rat gene. The analysis of various human cell lines with this specific probe shows only one species of GTP cyclohydrolase I mRNA with an approximate size of 3.6 kb.
AU  - Gütlich, M.
AU  - Schott, K.
AU  - Werner, T.
AU  - Bacher, A.
AU  - Ziegler, I.
C1  - 40598
C2  - 38756
SP  - 133-140
TI  - Species and tissue specificity of mammalian GTP cyclohydrolase I messenger RNA.
JO  - Biochim. Biophys. Acta
VL  - 1171
IS  - 2
PY  - 1992
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - (6R)-5,6,7,8-Tetrahydrobiopterin is produced by stimulated human T lymphocytes, and is known to affect various aspects of interleukin-2-directed T cell proliferation. Using an increased apparent affinity of interleukin 2 receptor to interleukin 2 as a measure of activity, this study explores whether other 6-substituted pterins might have the same effect, and what structural features are necessary for activity. Of the compounds tested, only the T-lymphocyte-derived (6R)-5,6,7,8-tetrahydrobiopterin was active. The diastereomeric (6S)-5,6,7,8-tetrahydrobiopterin was inactive, as were 7,8-dihydrobiopterin, sepiapterin, 5,6,7,8-tetrahydroneopterin, 6,7-dimethyl-5,6,7,8-tetrahydropterin and 6-hydroxymethylpterin. 7,8-Dihydroneopterin and neopterin were also found to be inactive. It follows that neither of these compounds participates in the feedback modulation of IL-2 receptor affinity, although both of them can be detected upon IFN-γ stimulation of human monocytes/macrophages. A computer-based molecular modelling study of (6R)-5,6,7,8-tetrahydrobiopterin and (6R)-5,6,7,8-tetrahydroneopterin revealed substantial differences in overall shape between the two molecules, with certain features figuring prominently in the low-energy conformers of (6R)-5,6,7,8-tetrahydrobiopterin.
AU  - Ziegler, I.
AU  - Borchert, M.E.
AU  - Heaney, F.M.
AU  - Davis, A.P.
AU  - Boyle, P.H.
C1  - 40599
C2  - 13544
SP  - 330-334
TI  - Structural requirements for the modulatory effect of 6-substituted pterins on interleukin 2 receptor binding.
JO  - Biochim. Biophys. Acta
VL  - 1135
IS  - 3
PY  - 1992
SN  - 0006-3002
ER  - 

TY  - JOUR
AU  - Sandermann, H.
AU  - Duncan, T.M.
C1  - 19257
C2  - 12328
SP  - 235-240
TI  - Lipid-dependent Membrane Enzymes. Kinetic Modelling of the Activation of Protein Kinase C by Phosphatidylserine.
JO  - Biochim. Biophys. Acta
VL  - 1069
PY  - 1991
SN  - 0006-3002
ER  - 

TY  - JOUR
AU  - Sandermann, H.
AU  - Duncan, T.M.
C1  - 19553
C2  - 12654
TI  - Lipid-dependent Membrane Enzymes. Kinetic Modelling of the Activation of Protein Kinase C by Phosphatidylserine.
JO  - Biochim. Biophys. Acta
PY  - 1991
SN  - 0006-3002
ER  - 

TY  - JOUR
AU  - Beck-Speier, I.
AU  - Mishra, A.
AU  - Luippold, G.B.
AU  - Godleski, J.J.
C1  - 18337
C2  - 11528
TI  - Effect of Sulfite on the Stimulation of Human Neutrophils.
JO  - Biochim. Biophys. Acta
PY  - 1990
SN  - 0006-3002
ER  - 

TY  - JOUR
AU  - Bors, W.
AU  - Wachtveitl, J.
AU  - Saran, M.
C1  - 17453
C2  - 10360
TI  - The Mechanism of Cytochrome c Reduction by Alkyl Radicals. Evidence for Multiple Reaction Pathways.
JO  - Biochim. Biophys. Acta
PY  - 1988
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Feeding a 0.05% polychlorinated biphenyl-supplemented diet to rats resulted in an increase of liver 3-hydroxy-3-methylglutaryl coenzyme A reductase activity within 9 days, followed by a decrease towards normal levels. Polychlorinated biphenyls were incorporated into the microsomal membrane. There was a concomitant decrease in the cholesterol/phospholipid ratio in the microsomal fraction. Immunotitration studies strongly suggested that polychlorinated biphenyls modulate preexisting 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by changing the lipid environment of the enzyme. 32P-labeled cDNA probes were used to study the levels of mRNA coding for 3-hydroxy-3-methylglutaryl coenzyme A reductase during polychlorinated biphenyl feeding. Northern dot hybridization experiments showed an increase in the amount of this mRNA. This stimulation correlated with the increase in the activity of the enzyme but was more pronounced. The data suggest that polychlorinated biphenyls act on the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity by enzyme-lipid interaction and at the transcriptional level.
AU  - Jenke, H.S.
C1  - 42571
C2  - 36588
SP  - 85-93
TI  - Polychlorinated biphenyls interfere with the regulation of hydroxymethylglutaryl-coenzyme A reductase activity in rat liver via enzyme-lipid interaction and at the transcriptional level.
JO  - Biochim. Biophys. Acta
VL  - 837
IS  - 1
PY  - 1985
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - The influence of 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) and several other pesticides on the physical state of membrane phospholipids was investigated using model lipids. The thermal dependence of fluorescence intensity of the probe parinaric acid in dipalmitoylphosphatidylcholine liposomes and lipid vesicles of mixed composition were recorded. DDT was incorporated into the liposomal bilayer. The insecticide lowered the phase transition temperature and broadened the the temperature range of the transition. The effects were concentration-dependent. The results may be interpreted as a sort of blurred and facilitated phase transition of bilayer lipids caused by intercalation of DDt between fatty acyl chains of membrane phospholipids.
AU  - Buff, K.
AU  - Berndt, J.
C1  - 41750
C2  - 38575
SP  - 205-212
TI  - Interaction of DDT (1,1,1-trichloro-2,2-bis(p-chlorophenyl)-ethane) with liposomal phospholipids.
JO  - Biochim. Biophys. Acta
VL  - 643
IS  - 1
PY  - 1981
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - The substrate specificity of proteinase B (EC 3.4.22.9) from Baker's yeast was studied. Experiments with unblocked synthetic peptides indicated that the enzyme has no aminopeptidase activity. The proteinase cleaves trypsin substrates like Bz-Arg-OEt, Bz-Arg-pNA and Bz-Ile-Glu-Gly-Arg-pNA and chymotrypsin substrates like Ac-Tyr-OEt and Bz-Tyr-pNA. The Km value for Ac-Tyr-OEt is similar to that of chymotrypsin A, but the catalytic activity per mol proteinase B amounts to only 1 20 that of chymotrypsin A. Km and kcat for Bz-Arg-OEt are 1 50 and 1 7 as high as the corresponding values determined for trypsin. Proteinase B cleaved the oxidized insulin B chain with an initial rapid cleavage step at Leu(15)-Tyr(16) and Phe(24)-Phe(25). Slower hydrolysis was observed at Gln(4)-His(5), Leu(11)-Val(12) Tyr(16)-Leu(17), Leu(17)-Val(18), Arg(22)-Gly(23) and Phe(25)-Tyr(26). These results suggest that the specificity of proteinase B is comparable to the specificity of porcine chymotrypsin C as well as of trypsin. When the hexapeptide Leu-Trp-Met-Arg-Phe-Ala was used as a substrate for proteinase B, the enzyme preferentially attacked at Arg-Phe and more slowly at Trp-Met.
AU  - Kominami, E.
AU  - Hoffschulte, H.K.
AU  - Leuschel, L.
AU  - Maier, K.L.
AU  - Holzer, H.
C1  - 41073
C2  - 38545
SP  - 136-141
TI  - The substrate specificity of proteinase B from Baker's yeast.
JO  - Biochim. Biophys. Acta
VL  - 661
IS  - 1
PY  - 1981
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Lipid-depleted yeast, grown anaerobically, contains only very low amounts of sterols. The hydroxymethylglutaryl-CoA reductase activity, the regulatory enzyme of sterol synthesis in yeast, is also low. Aeration of such cells in a buffer containing a carbon source induces hydroxymethylglutaryl-CoA reductase activity and increases sterol synthesis. The velocity of the increase depends on the carbon source present during the aeration period. Glucose and sugars that are easily converted to glucose were found to be most effective. A supplement of unsaturated fatty acids during anaerobic growth causes a several-fold greater velocity of the enzyme induction and of sterol biosynthesis. Linolenic acid (30 microM) accelerated sterol biosynthesis about 7-fold. Activities of galactokinase and galactose-1-phosphate uridyltransferase, which are involved in the conversion of galactose to glucose, increased several-fold in the supplemented cells within 6 h of aeration, concomitantly with stimulation of sterol synthesis from galactose. It is suggested that the stimulation of enzyme induction and sterol biosynthesis in fatty acid supplemented cells is due to a completion of the protein-synthesizing apparatus during cell growth. A markedly enhanced capacity of these cells to incorporate leucine into acid-precipitable protein supports this assumption.
AU  - Boll, M.
AU  - Löwel, M.
AU  - Berndt, J.
C1  - 41628
C2  - 38836
SP  - 429-439
TI  - Effect of unsaturated fatty acids on sterol biosynthesis in yeast.
JO  - Biochim. Biophys. Acta
VL  - 620
IS  - 3
PY  - 1980
SN  - 0006-3002
ER  - 

TY  - JOUR
AU  - Bors, W.
AU  - Michel, C.
AU  - Saran, M.
AU  - Lengfelder, E.
C1  - 41349
C2  - 35708
SP  - 162-172
TI  - The involvement of oxygen radicals during the autoxidation of adrenalin.
JO  - Biochim. Biophys. Acta
VL  - 540
IS  - 1
PY  - 1978
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - A two cluster (4Fe4S) ferredoxin and a rubredoxin have been isolated from the sulfur-reducing bacterium Desulfuromonas acetoxidans. Their amino acid compositions are reported and compared to those of other iron-sulfur proteins. The ferredoxin contains 8 cysteine residues, 8 atoms of iron and 8 atoms of labile sulfur per molecule; its minimum molecular weight is 6163. The protein exhibits an absorbance ratio of A385 A283 = 0.74. Storage results in a bleaching of the chromophore; the denatured ferredoxin is reconstitutable with iron and sulfide. The instability temperature is 52°C. The rubredoxin does not differ markedly from rubredoxins from other anaerobic bacteria.
AU  - Probst, I.
AU  - Moura, J.J.G.*
AU  - Moura, I.*
AU  - Bruschi, M.H.*
AU  - Le Gall, J.Y.*
C1  - 42009
C2  - 35823
SP  - 38-44
TI  - Isolation and characterization of a rubredoxin and an (8Fe-8S) ferredoxin from Desulfuromonas acetoxidans.
JO  - Biochim. Biophys. Acta
VL  - 502
IS  - 1
PY  - 1978
SN  - 0006-3002
ER  - 

TY  - JOUR
AB  - Rhodopseudomonas capsulata Kb1 utilizes glucose via the Entner-Doudoroff pathway and fructose via the Embden-Meyerhof pathway. In this bacterium, 1-phosphofructokinase (EC 2.7.1.56) is the key enzyme of the Embden-Meyerhof pathway and is induced by fructose but not by glucose. This enzyme could also be demonstrated in various species of phototrophic bacteria after growth in fructose-salts medium.
AU  - Conrad, R.S.
AU  - Schlegel, H.G.
C1  - 42536
C2  - 35524
SP  - 221-225
TI  - Different pathways for fructose and glucose utilization in Rhodopseudomonas capsulata and demonstration of 1-phosphofructokinase in phototrophic bacteria.
JO  - Biochim. Biophys. Acta
VL  - 358
IS  - 1
PY  - 1974
SN  - 0006-3002
ER  -