PuSH - Publikationsserver des Helmholtz Zentrums München

Eckey, M.* ; Kuphal, S.* ; Straub, T.* ; Rummele, P.* ; Kremmer, E. ; Bosserhoff, A.K.* ; Becker, P.B.*

Nucleosome remodeler SNF2L suppresses cell proliferation and migration and attenuates Wnt signaling.

Mol. Cell. Biol. 32, 2359-2371 (2012)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
ISWI is an evolutionarily conserved ATPase that catalyzes nucleosome remodeling in different macromolecular complexes. Two mammalian ISWI orthologs, SNF2H and SNF2L, are thought to have specialized functions despite their high sequence similarity. To date, the function of SNF2L in human cells has not been a focus of research. Newly established specific monoclonal antibodies and selective RNA interference protocols have now enabled a comprehensive characterization of loss-of-function phenotypes in human cells. In contrast to earlier results, we found SNF2L to be broadly expressed in primary human tissues. Depletion of SNF2L in He La cells led to enhanced proliferation and increased migration. These phenomena were explained by transcriptome profiling, which identified SNF2L as a modulator of the Wnt signaling network. The cumulative effects of SNF2L depletion on gene expression portray the cell in a state of activated Wnt signaling characterized by increased proliferation and chemotactic locomotion. Accordingly, high levels of SNF2L expression in normal melanocytes contrast with undetectable expression in malignant melanoma. In summary, our data document an inverse relationship between SNF2L expression and features characteristic of malignant cells.
Altmetric
Weitere Metriken?
[➜Einloggen]
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter BETA-CATENIN; GENE-EXPRESSION; CHROMATIN; ISWI; COMPLEX; TRANSCRIPTION; PROTEIN; PATHWAY; CANCER; TARGETS
ISSN (print) / ISBN 0270-7306
e-ISSN 1098-5549
Zeitschrift Molecular and Cellular Biology
Quellenangaben Band: 32, Heft: 13, Seiten: 2359-2371 Artikelnummer: , Supplement: ,
Verlag American Society for Microbiology (ASM)
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)