High impact information on Bcar3

• Synergistic promotion of c-Src activation and cell migration by Cas and AND-34/BCAR3 [1].
• Consistent with this, a subpopulation of AND-34 overexpressing B cells have long filamentous actin-containing cellular extensions [2].
• The carboxyl-terminal guanine nucleotide exchange factor domain of AND-34, as well as the activity of its putative target Rap1, contribute to these events [1].
• As previously reported for lymphoid cells transfected with constitutively active Cdc42, AND-34 overexpression inhibits SDF-1alpha-induced B cell polarization [2].
• Efficient binding to AND-34 required both the Src-binding domain and a flanking carboxyl-terminal region of p130(Cas) [3].

Biological context of Bcar3

• Fifteen minutes of serum stimulation of vanadate-pretreated AND-34-1-transfected NIH3T3 fibroblasts induces tyrosine phosphorylation of AND-34 as well as coprecipitating 95-, 125-, and 130-kDa proteins [4].
• Anti-CD3 epsilon treatment induces up-regulation of the AND-34 mRNA levels in total thymic RNA but not in RNA from purified thymocytes, suggesting that this transcript is derived from a thymic stromal cell population [4].

Anatomical context of Bcar3

• IL-1 and TNF increase AND-34 transcript levels in thymic cortical reticular, thymic nurse, and fibroblast cell lines [4].
• AND-34, a novel p130Cas-binding thymic stromal cell protein regulated by adhesion and inflammatory cytokines [4].
• In the thymic cortical reticular cell line, IL-1 and TNF induce a protein of the predicted 93-kDa size reactive with anti-AND-34 peptide antisera [4].

Associations of Bcar3 with chemical compounds

• Consistent with such an association, AND-34 tyrosine phosphorylation is induced following adherence of trypsinized fibroblasts to fibronectin or poly-L -lysine-coated surfaces [4].

References