|Other Names||Transcription factor E2F2, E2F-2, E2F2|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Transcription activator that binds DNA cooperatively with DP proteins through the E2 recognition site, 5'-TTTC[CG]CGC- 3' found in the promoter region of a number of genes whose products are involved in cell cycle regulation or in DNA replication. The DRTF1/E2F complex functions in the control of cell-cycle progression from g1 to s phase. E2F2 binds specifically to RB1 in a cell-cycle dependent manner.|
|Tissue Location||Highest level of expression is found in placenta, low levels are found in lung. Found as well in many immortalized cell lines derived from tumor samples|
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E2F2 is a member of the E2Ffamily of transcription factors. The E2F family plays a crucialrole in the control of cell cycle and action of tumor suppressorproteins and is also a target of the transforming proteins of smallDNA tumor viruses. The E2F proteins contain several evolutionallyconserved domains found in most members of the family. Thesedomains include a DNA binding domain, a dimerization domain whichdetermines interaction with the differentiation regulatedtranscription factor proteins (DP), a transactivation domainenriched in acidic amino acids, and a tumor suppressor proteinassociation domain which is embedded within the transactivationdomain. This protein and another 2 members, E2F1 and E2F3, have anadditional cyclin binding domain. This protein binds specificallyto retinoblastoma protein pRB in a cell-cycle dependent manner, andit exhibits overall 46% amino acid identity to E2F1. [provided byRefSeq].
Revenko, A.S., et al. Mol. Cell. Biol. 30(22):5260-5272(2010)Hayami, S., et al. Mol. Cancer 9, 59 (2010) :Chen, J., et al. Cancer Causes Control 20(9):1769-1777(2009)Cunningham, J.M., et al. Br. J. Cancer 101(8):1461-1468(2009)Lal, A., et al. Mol. Cell 35(5):610-625(2009)
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