ArticleCell cycle (Georgetown, Tex.)2010
KLF8 recruits the p300 and PCAF co-activators to its amino terminal activation domain to activate transcription.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- KLF12 transcriptionally regulates PD-L1 expression in non-small cell lung cancer.Molecular oncology · 2023Article
- Demethylase-independent roles of LSD1 in regulating enhancers and cell fate transition.Nature communications · 2023Article
- Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- TRAF2 Knockdown in Nasopharyngeal Carcinoma Induced Cell Cycle Arrest and Enhanced the Sensitivity to Radiotherapy.BioMed research international · 2020Article
- Bioselection Reveals miR-99b and miR-485 as Enhancers of Adenoviral Oncolysis in Pancreatic Cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Regulation of Krüppel-like factor 8 by the NEDD4 E3 ubiquitin ligase.American journal of translational research · 2019Article
- Krüppel-like factor 8 regulates VEGFA expression and angiogenesis in hepatocellular carcinoma.Scientific reports · 2018Article
- Krüppel-like factor 8 induces epithelial-to-mesenchymal transition and promotes invasion of pancreatic cancer cells through transcriptional activation of four and a half LIM-only protein 2.Oncology letters · 2017Article
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- ERK2 phosphorylates Krüppel-like factor 8 protein at serine 48 to maintain its stability.American journal of cancer research · 2016Article
- Identification of epidermal growth factor receptor and its inhibitory microRNA141 as novel targets of Krüppel-like factor 8 in breast cancer.Oncotarget · 2015Article
- Small hairpin RNA-mediated Krüppel-like factor 8 gene knockdown inhibits invasion of nasopharyngeal carcinoma.Oncology letters · 2015Article
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- KLF8 and FAK cooperatively enrich the active MMP14 on the cell surface required for the metastatic progression of breast cancer.Oncogene · 2014Article
- Kruppel-like factor 15 is a critical regulator of cardiac lipid metabolism.The Journal of biological chemistry · 2014Article
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- Downregulated Krüppel-like factor 8 is involved in decreased trophoblast invasion under hypoxia-reoxygenation conditions.Reproductive sciences (Thousand Oaks, Calif.) · 2014Article
- Kruppel-like factor 15 is critical for vascular inflammation.The Journal of clinical investigation · 2013Article
- Generation of mice deficient in both KLF3/BKLF and KLF8 reveals a genetic interaction and a role for these factors in embryonic globin gene silencing.Molecular and cellular biology · 2013Article
- Krüppel-like factor 8 overexpression is correlated with angiogenesis and poor prognosis in gastric cancer.World journal of gastroenterology · 2013Article
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4 authors at 2 institutions in 2 countries.
Funding
Abstract
Krüppel-like factor 8 (KLF8) regulates critical cellular processes including cell cycle progression, transformation, epithelial-to-mesenchymal transition, migration and invasion by either repressing or activating target gene promoters. As a repressor, KLF8 recruits the CtBP co-repressor via its PVDLS repression motif. However, how KLF8 acts as an activator has not been determined. Here we report the identification of both the KLF8 activation domain and associated co-activators. By site-directed mutagenesis and cyclin D1 promoter reporter assays using both mouse fibroblasts and human epithelial cells, we determined that deletion of residues 100-260 or mutation of Q118-Q248 abolished KLF8 transactivity. this transactivity was dramatically reduced in p300(-/-), CBP(-/-) or PCAF(-/-) cells and could be restored by re-expressing p300 or PCAF, but not CBP. Co-immunoprecipitation analyses demonstrated that KLF8 interacted with these co-activators whereas the Q118N-Q248N mutant did not. Chromatin immunoprecipitation experiments showed that KLF8 promoted histone acetylation at the promoter whereas the Q118N-Q248N mutant had a dramatic loss of this function. Western blotting revealed that unlike wild-type KLF8 the Q118N-Q248N was no longer able to upregulate cyclin D1 protein level. BrdU incorporation assays showed that the Q118N-Q248N mutant also lost the ability to promote DNA synthesis. Taken together, these results identified the KLF8 activation domain located between residues 101-260 where the well-conserved Q118 and Q248 are essential for recruiting p300 and PCAF to activate target gene transcription.
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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.