Molecular mechanisms for apoptosis induced by signaling through the B cell antigen receptor.

Abstract:

:Although the B cell antigen receptor (BCR) transmits survival and activation signals, BCR ligation can induce apoptosis in both immature and mature B cells. BCR-mediated apoptosis is suggested to play a role in self-tolerance by deleting self-reactive B cells. Generation of an apoptotic signal through BCR appears to depend on the composition of the higher order BCR complex and is suggested to occur outside the plasma membrane microdomains, termed lipid rafts. During BCR-mediated apoptosis, mitochondrial dysfunction is induced and is essential for apoptosis, probably by activating both caspases, cysteine proteases that play a central role in apoptosis, and caspase-independent effectors for apoptosis. Although signaling pathways for apoptosis are not yet fully defined in BCR-mediated apoptosis, expression of the proto-oncogene product c-Myc is enhanced upon BCR ligation, and c-Myc appears to mediate BCR ligation-induced apoptosis by causing mitochondrial dysfunction, suggesting that BCR-mediated apoptosis is a form of Myc-induced apoptosis.

journal_name

Int Rev Immunol

authors

Tsubata T

doi

10.3109/08830180109045590

subject

Has Abstract

pub_date

2001-01-01 00:00:00

pages

791-803

issue

6

eissn

0883-0185

issn

1563-5244

journal_volume

20

pub_type

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