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E2F transcription factor 5, p130-binding

The protein encoded by this gene is a member of the E2F family of transcription factors. The E2F family plays a crucial role in the control of cell cycle and action of tumor suppressor proteins and is also a target of the transforming proteins of small DNA tumor viruses. The E2F proteins contain several evolutionarily conserved domains that are present in most members of the family. These domains include a DNA binding domain, a dimerization domain which determines interaction with the differentiation regulated transcription factor proteins (DP), a transactivation domain enriched in acidic amino acids, and a tumor suppressor protein association domain which is embedded within the transactivation domain. This protein is differentially phosphorylated and is expressed in a wide variety of human tissues. It has higher identity to E2F4 than to other family members. Both this protein and E2F4 interact with tumor suppressor proteins p130 and p107, but not with pRB. Alternative splicing results in multiple variants encoding different isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: E2F4, E2F1, CD43, PCNA, pRb
Papers using E2F5 antibodies
Abnormal epidermal differentiation and impaired epithelial-mesenchymal tissue interactions in mice lacking the retinoblastoma relatives p107 and p130
Toppari Jorma et al., In Reproductive Biology and Endocrinology, 2002
... from Lab Vision Corporation, a mouse monoclonal antibody against E2F-3 from Upstate, a mouse monoclonal antibody against E2F-5 from Santa Cruz Biotechnology, Inc., rabbit polyclonal antibodies ...
Papers on E2F5
MicroRNA-34a targets FMNL2 and E2F5 and suppresses the progression of colorectal cancer.
Liang et al., Guangzhou, China. In Exp Mol Pathol, Aug 2015
FMNL2 and E2F5 were identified as direct targets of miR-34a.
pRb2/p130 localizes to the cytoplasm in diffuse gastric cancer.
Giordano et al., Napoli, Italy. In J Cell Physiol, Apr 2015
pRb2/p130 is a key tumor suppressor, whose oncosuppressive activity has mainly been attributed to its ability to negatively regulate cell cycle by interacting with the E2F4 and E2F5 transcription factors.
miR-98 delays skeletal muscle differentiation by down-regulating E2F5.
Polesskaya et al., Gif-sur-Yvette, France. In Biochem J, Mar 2015
We conclude that miR-98 regulates muscle differentiation by altering the expression of the transcription factor E2F5 and, in turn, of multiple E2F5 targets.
The effects of soy supplementation on gene expression in breast cancer: a randomized placebo-controlled study.
Norton et al., Kettering, United Kingdom. In J Natl Cancer Inst, 2014
This signature was characterized by overexpression (>2-fold) of cell cycle transcripts, including those that promote cell proliferation, such as FGFR2, E2F5, BUB1, CCNB2, MYBL2, CDK1, and CDC20 (P < .01).
Multicilin drives centriole biogenesis via E2f proteins.
Kintner et al., Los Angeles, United States. In Genes Dev, 2014
Here we show that Multicilin acts by forming a ternary complex with E2f4 or E2f5 and Dp1 that binds and activates most of the genes required for centriole biogenesis, while other cell cycle genes remain off.
Role of the Na ⁺/K ⁺/2Cl⁻ cotransporter NKCC1 in cell cycle progression in human esophageal squamous cell carcinoma.
Otsuji et al., Kyoto, Japan. In World J Gastroenterol, 2014
Pathway analysis showed that the top-ranked canonical pathway was the G2/M DNA damage checkpoint regulation pathway, which involves MAD2L1, DTL, BLM, CDC20, BRCA1, and E2F5.
Promising roles of mammalian E2Fs in hepatocellular carcinoma.
Li et al., Hefei, China. In Cell Signal, 2014
Eight members, E2F1 E2F8 have been recognized of this family so far, and the members of this family are generally divided into activator E2F (E2F1--E2F3a), repressor E2F (E2F3b--E2F5) and inhibitor E2F (E2F6--E2F8) subclasses based on their structur-e and function.
A multi-resource data integration approach: identification of candidate genes regulating cell proliferation during neocortical development.
Nowakowski et al., Tallahassee, United States. In Front Neurosci, 2013
We used a mouse in situ hybridization dataset (The Allen Institute for Brain Science) to identify 13 genes (Cdon, Celsr1, Dbi, E2f5, Eomes, Hmgn2, Neurog2, Notch1, Pcnt, Sox3, Ssrp1, Tead2, Tgif2) with high correlation of expression in the proliferating cells of the VZ of the neocortex at early stages of development (E15.5).
Role of skeletal muscle in palate development.
Kablar et al., Halifax, Canada. In Histol Histopathol, 2013
A cDNA microarray analysis revealed differentially expressed genes in the cleft palate of amyogenic mouse fetuses and suggested candidate molecules with a novel function in palatogenesis (e.g., Tgfbr2, Bmp7, Trim71, E2f5, Ddx5, Gfap, Sema3f).
A potential oncogenic role of the commonly observed E2F5 overexpression in hepatocellular carcinoma.
Chung et al., Seoul, South Korea. In World J Gastroenterol, 2011
Data indicate that E2F5 is commonly overexpressed in primary hepatocellular carcinomas and show that E2F5 knockdown significantly repressed the growth of HCC cells.
The E2F5 repressor is an activator of E6/E7 transcription and of the S-phase entry in HPV18-associated cells.
Thierry et al., Singapore, Singapore. In Oncogene, 2010
Diverting the function of E2F5 from a cell-cycle repressor into an activator might contribute to the higher oncogenic potential of HPV18 when compared with other high-risk HPV types.
Tumor suppression by ARF: gatekeeper and caretaker.
Raychaudhuri et al., Chicago, United States. In Cell Cycle, 2010
While the regulation of the activator E2Fs is related to cell cycle arrest, there is evidence that the regulation of the repressors, E2F4 and E2F5, is significant in maintaining genomic stability.
E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer.
Choolani et al., Singapore, Singapore. In Bmc Cancer, 2009
cell-cycle regulatory protein E2F5 might play a significant role in epithelial ovarian cancer pathogenesis
Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome.
Osamura et al., Isehara, Japan. In Br J Cancer, 2009
Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome.
Analysis of the relevance of e2fs and their target genes with rat liver regeneration.
Xu et al., In Indian J Gastroenterol, 2008
E2F transcription factor genes and their 34 target genes have a role in liver regeneration.
Inactivation of E2F3 results in centrosome amplification.
Leone et al., Columbus, United States. In Cancer Cell, 2003
Loss of E2F3, but not E2F1, E2F2, E2F4, or E2F5 results in unregulated cyclin E-dependent kinase activity, defects in nucleophosmin B association with centrosomes, and premature centriole separation and duplication.
Regulation of E2F transcription by cyclin E-Cdk2 kinase mediated through p300/CBP co-activators.
La Thangue et al., Glasgow, United Kingdom. In Nat Cell Biol, 2000
Here we show that E2F-5 is phosphorylated by the cyclin E-Cdk2 complex, which functions in the late G1 phase, but not by the early-G1-phase-acting cyclin D-CDK complex.
Regulation of the G1/S transition phase in mesangial cells by E2F1.
Marumo et al., Tokyo, Japan. In Kidney Int, 1999
The E2F family consists of a group of five closely related proteins (E2F1 through E2F5).
Upregulation of E2F transcription factors in chemically induced mouse skin tumors.
Mukhtar et al., Cleveland, United States. In Int J Oncol, 1999
Western blot analysis data showed 3.0- to 7.6-fold upregulation of E2F-1, E2F-2, E2F-3, E2F-4 and E2F-5 in tumors compared to normal epidermis.
E2F-1 functions in mice to promote apoptosis and suppress proliferation.
Greenberg et al., Boston, United States. In Cell, 1996
Members of the E2F transcription factor family (E2F-1-E2F-5) are believed to be critical positive regulators of cell cycle progression in eukaryotes although the in vivo functions of the individual E2Fs have not been elucidated.
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