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Breast tumors are initially dependent on estrogens for growth and progression and can be inhibited by anti-estrogens such as tamoxifen. Additionally we are shipping BCAR3 Antibodies (47) and BCAR3 Proteins (4) and many more products for this protein.
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data presented here suggest that Bcar3 could play a role in testis development
many BCAR3-me (show BCAR1 ELISA Kits)diated signaling events in epithelial and mesenchymal cells are independent of p130 (show AKT1 ELISA Kits)Cas association
p130Cas (show BCAR1 ELISA Kits)- and HEF1 (show NEDD9 ELISA Kits)-associated AND-34 may regulate B cell adhesion and motility through a Cdc42 (show CDC42 ELISA Kits)-mediated signaling pathway.
study presents a pluridisciplinary approach, including small-angle X-ray scattering, that provides first insights into the structure of the complex formed between BCAR3 and human enhancer of filamentation 1 (HEF1 (show NEDD9 ELISA Kits))
BCAR3 is an essential interactor and mediator of HEF1 (show NEDD9 ELISA Kits)-induced migration.
BCAR3 acts as a putative suppressor of breast cancer progression by inhibiting the prometastatic TGFbeta (show TGFB1 ELISA Kits)/Smad (show SMAD1 ELISA Kits) signaling pathway in invasive breast tumors.
BCAR1 (show BCAR1 ELISA Kits) and BCAR3 scaffolding proteins have roles in cell signaling and antiestrogen resistance
Taken together, these results demonstrated that BCAR3 plays an important role in the signaling pathways of insulin (show INS ELISA Kits) leading to cell cycle progression and cytoskeleton reorganization, but not GLUT4 (show SLC2A4 ELISA Kits) translocation.
BCAR3 promotes cell motility by regulating actin cytoskeletal and adhesion remodeling in invasive breast cancer cells.
BCAR3 expression may regulate Src (show SRC ELISA Kits) signaling in a BCAR3-p130(cas (show BCAR1 ELISA Kits)) complex-dependent fashion by altering the ability of the Src (show SRC ELISA Kits) SH3 domain (show ITSN1 ELISA Kits) to bind the p130(cas (show BCAR1 ELISA Kits)) SBD (show TRAPPC4 ELISA Kits)
BCAR3-p130Cas (show BCAR1 ELISA Kits) complex formation is not required for BCAR3-mediated anti-estrogen resistance, Rac (show AKT1 ELISA Kits) activation or discohesion of epithelial breast cancer cells
the c-Src/Cas/BCAR3 signaling axis is a prominent regulator of c-Src activity, which in turn controls cell behaviors that lead to aggressive and invasive breast tumor phenotypes
AND-34 activates phosphatidylinositol 3-kinase and induces anti-estrogen resistance in a SH2 and GDP exchange factor-like domain-dependent manner
BCAR3 and NSP1 are more highly expressed than SH2D3C (SHEP1 (show SH2D3C ELISA Kits)) in breast cancer cells, and the expression patterns suggest differential roles for the three genes during breast cancer progression.
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.
breast cancer anti-estrogen resistance 3
, breast cancer antiestrogen resistance 3
, breast cancer anti-estrogen resistance protein 3
, breast cancer anti-estrogen resistance protein 3-like
, p130Cas-binding protein AND-34
, SH2 domain-containing protein 3B
, breast cancer antiestrogen resistance 3 protein
, dJ1033H22.2 (breast cancer anti-estrogen resistance 3)
, novel SH2-containing protein 2