BCAR3 Blocking Peptide – The purity is >90%,tested by HPLC and MS. Purity

Breast tumors are initially dependent on estrogens for growth and progression and can be inhibited by anti-estrogens such as tamoxifen. However, breast cancers progress to become anti-estrogen resistant. Breast cancer anti-estrogen resistance gene 3 was identified in the search for genes involved in the development of estrogen resistance. The gene encodes a component of intracellular signal transduction that causes estrogen-independent proliferation in human breast cancer cells. The protein contains a putative src homology 2 (SH2) domain, a hall mark of cellular tyrosine kinase signaling molecules, and is partly homologous to the cell division cycle protein CDC48. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2012]

BCAR3: a ubiquitously expressed regulator of R-Ras activity that has been implicated in breast cancer. A GDP exchange factor whose overexpression confers antiestrogen resistance, activates Rac, PAK1, and the cyclin D1. Can accelerate the degradation of IRS-1, thus regulating signaling through the insulin receptor. When overexpressed, it confers anti-estrogen resistance in breast cancer cell lines. May also be regulated by cellular adhesion to extracellular matrix proteins. Up-regulated by interleukin-1-alpha and TNF-beta in thymus cortical reticular cell lines (mouse).Two alternatively spliced human isoforms have been described.

Protein type: GEFs, Ras; GEFs; Motility/polarity/chemotaxis; Adaptor/scaffold

Chromosomal Location of Human Ortholog: 1p22.1

Molecular Function: protein binding; guanyl-nucleotide exchange factor activity

Biological Process: response to drug; small GTPase mediated signal transduction; lens morphogenesis in camera-type eye; signal transduction; positive regulation of peptidyl-serine phosphorylation; positive regulation of GTPase activity