ArticleThe EMBO journal1998
TAFII105 mediates activation of anti-apoptotic genes by NF-kappaB.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 79 citations in OpenAlex.
- ARMC5 is part of an RPB1-specific ubiquitin ligase implicated in adrenal hyperplasia.Nucleic acids research · 2022Article
- Genome reading by the NF-κB transcription factors.Nucleic acids research · 2019Review
- X-linked Dystonia-Parkinsonism patient cells exhibit altered signaling via nuclear factor-kappa B.Neurobiology of disease · 2017Article
- The Process and Regulatory Components of Inflammation in Brain Oncogenesis.Biomolecules · 2017Review
- Targeting TBP-Associated Factors in Ovarian Cancer.Frontiers in oncology · 2014Review
- Estrogen responsiveness of the TFIID subunit TAF4B in the normal mouse ovary and in ovarian tumors.Biology of reproduction · 2013Article
- Analysis of the RelA:CBP/p300 interaction reveals its involvement in NF-κB-driven transcription.PLoS biology · 2013Article
- Impact of constitutional copy number variants on biological pathway evolution.BMC evolutionary biology · 2013Article
- Article
- Shifting players and paradigms in cell-specific transcription.Molecular cell · 2009Review
- Structural changes in TAF4b-TFIID correlate with promoter selectivity.Molecular cell · 2008Article
- TAF4 inactivation in embryonic fibroblasts activates TGF beta signalling and autocrine growth.The EMBO journal · 2005Article
- TAF9b (formerly TAF9L) is a bona fide TAF that has unique and overlapping roles with TAF9.Molecular and cellular biology · 2005Article
- Core promoter binding by histone-like TAF complexes.Molecular and cellular biology · 2005Article
- To be, or not to be: NF-kappaB is the answer--role of Rel/NF-kappaB in the regulation of apoptosis.Oncogene · 2003Review
- Mechanism of rapid transcriptional induction of tumor necrosis factor alpha-responsive genes by NF-kappaB.Molecular and cellular biology · 2002Article
- Redundant role of tissue-selective TAF(II)105 in B lymphocytes.Molecular and cellular biology · 2002Article
- Prodos is a conserved transcriptional regulator that interacts with dTAF(II)16 in Drosophila melanogaster.Molecular and cellular biology · 2001Article
- The glucocorticoid receptor inhibits NFkappaB by interfering with serine-2 phosphorylation of the RNA polymerase II carboxy-terminal domain.Genes & development · 2000Article
- Glucocorticoids repress NF-kappaB-driven genes by disturbing the interaction of p65 with the basal transcription machinery, irrespective of coactivator levels in the cell.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor NF-kappaB is important for expression of genes involved in immune responses, viral infections, cytokine signaling and stress. In addition NF-kappaB plays a crucial role in protecting cells from TNF-alpha-induced apoptotic stimuli, presumably by activating anti-apoptotic genes. Here we report that the sub-stoichiometric TFIID subunit TAFII105 is essential for activation of anti-apoptotic genes in response to TNF-alpha, serving as a transcriptional coactivator for NF-kappaB. The putative coactivator domain of TAFII105 interacts with the activation domain of the p65/RelA member of the NF-kappaB family, and further stimulates p65-induced transcription in human 293 cells. Moreover, inhibition of TAFII105 activity by overexpression of a dominant negative mutant of TAFII105 decreased NF-kappaB transcriptional activity and severely reduced cell survival in response to TNF-alpha. Similarly, expression of anti-sense TAFII105 RNA sensitized the cells to TNF-alpha cytotoxicity. These results suggest that TAFII105 is involved in activation of anti-apoptotic genes by NF-kappaB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.