Breast Cancer Anti-Estrogen Resistance 3 Proteins (BCAR3)

Human Breast Cancer Anti-Estrogen Resistance 3 (BCAR3) interaction partners

1. BCAR3 is an essential interactor and mediator of HEF1-induced migration.

2. BCAR3 acts as a putative suppressor of breast cancer progression by inhibiting the prometastatic TGFbeta/Smad signaling pathway in invasive breast tumors.

3. BCAR1 and BCAR3 scaffolding proteins have roles in cell signaling and antiestrogen resistance

4. Taken together, these results demonstrated that BCAR3 plays an important role in the signaling pathways of insulin leading to cell cycle progression and cytoskeleton reorganization, but not GLUT4 translocation.

5. BCAR3 promotes cell motility by regulating actin cytoskeletal and adhesion remodeling in invasive breast cancer cells.

6. BCAR3 expression may regulate Src signaling in a BCAR3-p130(cas) complex-dependent fashion by altering the ability of the Src SH3 domain to bind the p130(cas) SBD

7. BCAR3-p130Cas complex formation is not required for BCAR3-mediated anti-estrogen resistance, Rac activation or discohesion of epithelial breast cancer cells

8. 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

9. AND-34 activates phosphatidylinositol 3-kinase and induces anti-estrogen resistance in a SH2 and GDP exchange factor-like domain-dependent manner

10. BCAR3 and NSP1 are more highly expressed than SH2D3C (SHEP1) in breast cancer cells, and the expression patterns suggest differential roles for the three genes during breast cancer progression.

11. BCAR3 induces anti-estrogen resistance in breast tumor cell lines by altering cell-cell/cell-matrix interactions and cyclin D1 promoter activity.

12. the spatial and temporal regulation of BCAR3/p130(Cas) interactions within the cell is important for controlling breast cancer cell motility

13. BCAR3 protein, through its SH2 domain, is involved in the signaling pathways of EGF leading to cell cycle progression; BCAR3 itself is part of a mitogenic signaling pathway.

14. The expression of breast cancer anti-estrogen resistance 3 results in basal serine phosphorylation of Crk-Associated Substrate Protein that normally occurs during adhesion of breast cancer cells to fibronectin.

Mouse (Murine) Breast Cancer Anti-Estrogen Resistance 3 (BCAR3) interaction partners

1. The first spontaneous mutation in the Bcar3 gene associated with lens extrusion cataracts.

2. data presented here suggest that Bcar3 could play a role in testis development

3. many BCAR3-mediated signaling events in epithelial and mesenchymal cells are independent of p130Cas association

4. p130Cas- and HEF1-associated AND-34 may regulate B cell adhesion and motility through a Cdc42-mediated signaling pathway.

5. 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)

6. AND-34-mediated signaling is required for maintenance of the structural integrity of the adult ocular lens.

Xenopus laevis Breast Cancer Anti-Estrogen Resistance 3 (BCAR3) interaction partners

1. bcar3 gene is expressed downstream of Gata2 during gastrulation, and is co-expressed with gata2 but is more broadly expressed during later development; its binding partner, bcar1 shows overlapping expression patterns