New to MyHealth?
Manage Your Care From Anywhere.
Access your health information from any device with MyHealth. You can message your clinic, view lab results, schedule an appointment, and pay your bill.
ALREADY HAVE AN ACCESS CODE?
DON'T HAVE AN ACCESS CODE?
NEED MORE DETAILS?
MyHealth for Mobile
Transgene expression of bcl-x(L) permits anti-immunoglobulin (Ig)-induced proliferation in xid B cells
Transgene expression of bcl-x(L) permits anti-immunoglobulin (Ig)-induced proliferation in xid B cells JOURNAL OF EXPERIMENTAL MEDICINE Solvason, N., Wu, W. W., Kabra, N., Lund-Johansen, F., Roncarolo, M. G., Behrens, T. W., Grillot, D. A., Nunez, G., Lees, E., Howard, M. 1998; 187 (7): 1081-1091Abstract
Mutations in the tyrosine kinase, Btk, result in a mild immunodeficiency in mice (xid). While B lymphocytes from xid mice do not proliferate to anti-immunoglobulin (Ig), we show here induction of the complete complement of cell cycle regulatory molecules, though the level of induction is about half that detected in normal B cells. Cell cycle analysis reveals that anti-Ig stimulated xid B cells enter S phase, but fail to complete the cell cycle, exhibiting a high rate of apoptosis. This correlated with a decreased ability to induce the anti-apoptosis regulatory protein, Bcl-xL. Ectopic expression of Bcl-xL in xid B cells permitted anti-Ig induced cell cycle progression demonstrating dual requirements for induction of anti-apoptotic proteins plus cell cycle regulatory proteins during antigen receptor mediated proliferation. Furthermore, our results link one of the immunodeficient traits caused by mutant Btk with the failure to properly regulate Bcl-xL.
View details for Web of Science ID 000073075900011
View details for PubMedID 9529324