Seminar: WAVE2 and Tpm3.1: Actin Dynamics, B cell biology, and targeting B-cell lymphomas
Abstract: Activated B cells produce protective antibodies, but aberrant B cell activation can lead to autoimmune disease or B-cell lymphoma. The actin cytoskeleton controls multiple aspects of B cell activation. My PhD has focused on the roles of the WAVE2 and Tpm3.1 proteins in B cells. WAVE2 activates the Arp2/3 complex, which forms branched actin networks. Tpm3.1 recruits’ myosin and stabilizes actin filaments. I showed that siRNA-mediated depletion of WAVE2 decreases B cell spreading on antigen-coated surfaces and reduces B-cell receptor signaling at the immune synapse. Inhibiting Tpm3.1 function reduces B cell spreading and also inhibits the growth and motility of diffuse large B-cell lymphomas (DLBCLs). Hence, Tpm3.1 could be a therapeutic target for treating DLBCL.
LSC 3 (Life Sciences Institute - 2350 Health Sciences Mall) MBIM itsupport@microbiology.ubc.ca America/Vancouver publicSeminar: WAVE2 and Tpm3.1: Actin Dynamics, B cell biology, and targeting B-cell lymphomas
Abstract: Activated B cells produce protective antibodies, but aberrant B cell activation can lead to autoimmune disease or B-cell lymphoma. The actin cytoskeleton controls multiple aspects of B cell activation. My PhD has focused on the roles of the WAVE2 and Tpm3.1 proteins in B cells. WAVE2 activates the Arp2/3 complex, which forms branched actin networks. Tpm3.1 recruits’ myosin and stabilizes actin filaments. I showed that siRNA-mediated depletion of WAVE2 decreases B cell spreading on antigen-coated surfaces and reduces B-cell receptor signaling at the immune synapse. Inhibiting Tpm3.1 function reduces B cell spreading and also inhibits the growth and motility of diffuse large B-cell lymphomas (DLBCLs). Hence, Tpm3.1 could be a therapeutic target for treating DLBCL.