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Luscher-Firzlaff, J.* ; Gawlista, I.* ; Vervoorts, J.* ; Kapelle, K.* ; Braunschweig, T.* ; Walsemann, G.* ; Rodgarkia-Schamberger, C.* ; Schuchlautz, H.* ; Dreschers, S.* ; Kremmer, E. ; Lilischkis, R.* ; Cerni, C.* ; Wellmann, A.* ; Lüscher, B.*

The human trithorax protein hASH2 functions as an oncoprotein.

Cancer Res. 68, 749-758 (2008)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Regulation of chromatin is an important aspect of controlling promoter activity and gene expression. Posttranslational modifications of core histones allow proteins associated with gene transcription to access chromatin. Closely associated with promoters of actively transcribed genes, trimethylation of histone H3 at lysine 4 (H3K4me3) is a core histone mark set by several protein complexes. Some of these protein complexes contain the trithorax protein ASH2 combined with the MLL oncoproteins. We identified human ASH2 in a complex with the oncoprotein MYC. This finding, together with the observation that hASH2 interacts with MLL, led us to test whether hASH2 itself is involved in transformation. We observed that hASH2 cooperates with Ha-RAS to transform primary rat embryo fibroblasts (REF). Furthermore, transformation of REFs by MYC and Ha-RAS required the presence of rAsh2. In an animal model, the hASH2/Ha-RAS-transformed REFs formed rapidly growing tumors characteristic of fibrosarcomas that, compared with tumors derived from MYC/Ha-RAS transformed cells, were poorly differentiated. This finding suggests that ASH2 functions as an oncoprotein. Although hASH2 expression at the mRNA level was generally not deregulated, hASH2 protein expression was increased in most human tumors and tumor cell lines. In addition, knockdown of hASH2 inhibited tumor cell proliferation. Taken together, these observations define hASH2 as a novel oncoprotein.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2008
HGF-Berichtsjahr 2008
ISSN (print) / ISBN 0008-5472
e-ISSN 1538-7445
Zeitschrift Cancer Research
Quellenangaben Band: 68, Heft: 3, Seiten: 749-758 Artikelnummer: , Supplement: ,
Verlag American Association for Cancer Research (AACR)
Verlagsort Philadelphia, Pa.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
PSP-Element(e) G-501700-003
DOI 10.1158/0008-5472.CAN-07-3158
Scopus ID 38849117845
Erfassungsdatum 2008-11-21
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