AATF (Apoptosis Antagonizing Transcription Factor)

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Nucleolar AATF regulates c-Jun–mediated apoptosis

The AP-1 transcription factor c-Jun has been shown to be essential for stress-induced apoptosis in several models. However, the molecular mechanisms underlying the proapoptotic activity of c-Jun are poorly understood. We identify the apoptosis-antagonizing transcription factor (AATF) as a novel nucleolar stress sensor, which is required as a cofactor for c-Jun-mediated apoptosis. Overexpression...

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TSG101 interacts with apoptosis-antagonizing transcription factor and enhances androgen receptor-mediated transcription by promoting its monoubiquitination.

Apoptosis-antagonizing transcription factor (AATF), also termed Che-1, was identified as interacting protein of Dlk/ZIP kinase and RNA polymerase II, respectively. Che-1 has additionally been shown to bind Rb, thereby activating transcription factor E2F and promoting cell cycle progression. Moreover, AATF enhances steroid receptor-mediated transactivation in a hormone- and dose-dependent manner...

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Che-ating death: CHE1/AATF protects from p53-mediated apoptosis.

The tumour suppressor p53 directs cells towards different fates depending on the cell type and the stimulus. The decision to direct a cell towards apoptosis rather than cell-cycle arrest or senescence has important implications for tumour suppression in normal cells and drug response in tumour cells. Cells that undergo senescence and growth arrest can persist and contribute to organismal ageing...

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AATF/Che-1 acts as a phosphorylation-dependent molecular modulator to repress p53-driven apoptosis.

Following genotoxic stress, cells activate a complex signalling network to arrest the cell cycle and initiate DNA repair or apoptosis. The tumour suppressor p53 lies at the heart of this DNA damage response. However, it remains incompletely understood, which signalling molecules dictate the choice between these different cellular outcomes. Here, we identify the transcriptional regulator apoptos...

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The transcription factor Zbtb7b promotes CD4 expression by antagonizing Runx-mediated activation of the CD4 silencer.

The persistence of CD4 expression is a key event distinguishing the differentiation of MHC class II-restricted thymocytes into CD4 T cells from that of MHC class I-restricted thymocytes into CD8 T cells. The zinc finger transcription factor Zbtb7b (or cKrox or Thpok) is normally expressed in MHC class II-restricted thymocytes and promotes CD4 lineage choice. When expressed in MHC class I-restri...

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ژورنال

عنوان ژورنال: Atlas of Genetics and Cytogenetics in Oncology and Haematology

سال: 2011

ISSN: 1768-3262

DOI: 10.4267/2042/38401