Role of chromodomain helicase DNA-binding protein 2 in DNA damage response signaling and tumorigenesis
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چکیده
منابع مشابه
Chromodomain helicase/ATPase DNA binding protein 1-like protein expression predicts poor prognosis in nasopharyngeal carcinoma
Nasopharyngeal carcinoma (NPC) is a malignancy with a high metastatic ability. Recent studies have implicated the role of chromodomain helicase/ATPase DNA binding protein 1-like (CHD1L) gene as a novel oncogene; however, the functional role of CHD1L in NPC remains unknown. The aim of this study was to evaluate the clinical significance of CHD1L positivity in NPC. CHD1L protein expression was ex...
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Serum response factor (SRF) is a widely expressed protein that plays a key role in the regulation of smooth muscle differentiation, proliferation, migration, and apoptosis. It is generally accepted that one mechanism by which SRF regulates these diverse functions is through pathway-specific cofactor interactions. A novel SRF cofactor, chromodomain helicase DNA binding protein 8 (CHD8), was isol...
متن کاملDNA damage and tumorigenesis.
Asacomplexpathologicprocess,tumorigenesishas involved various regulating mechanisms at molecular and cellular levels, particularly tightly related to DNA damage. In previous issues of JMCB, we have published several papers highlighting the relationship between tumorigenesis and DNA damage. As a guest editor, Dr Shen has organized a special issue on genomic instability and cancer (Shen, 2011). I...
متن کاملAcetyltransferase p300 collaborates with chromodomain helicase DNA-binding protein 4 (CHD4) to facilitate DNA double-strand break repair.
Chromatin remodelling is critical for repairing DNA damage and maintaining genomic integrity. Previous studies have reported that histone acetyltransferase p300 and ATP-dependent chromatin remodeler chromodomain helicase DNA-binding protein 4 (CHD4) functions, respectively, in DNA double-strand breaks (DSBs) repair. But the physiological significance of their interaction remains elusive. Here, ...
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ژورنال
عنوان ژورنال: Oncogene
سال: 2009
ISSN: 0950-9232,1476-5594
DOI: 10.1038/onc.2008.440