J Immunol. 1999 Sep 1;163(5):2378-81.

Cutting edge: a novel mechanism for rescue of B cells from CD95/Fas-mediated apoptosis.External

Catlett, I. M., Bishop, G. A.,
--- - Department of Microbiology, Graduate Program in Immunology, University of Iowa, Veterans Affairs Medical Center, Iowa City 52242, USA.
CD95-induced apoptosis contributes to the maintenance of homeostasis in both B and T lymphocyte-mediated immunity. B cells increase CD95 expression in response to activation signals and become susceptible to CD95-induced apoptosis. Protection from CD95-mediated death signals can be induced in mature B cells by signals delivered through the B cell Ag receptor. In this paper we demonstrate for the first time that rescue from apoptosis can occur independently of de novo protein synthesis. This rescue from apoptosis prevents activation of caspase 8, the apical caspase in the CD95 death pathway, and CD95-FADD (Fas-associated death domain containing protein) association does not occur normally. Thus B cell activation signals can biochemically modify proximal elements of the CD95 death pathway and regulate the sensitivity of cells to apoptosis induction at an early stage in programmed cell death.
PMID: 10452970External
Arrow2 In vitro interaction Arrow2 In vivo interaction Arrow2 Characterization Arrow2 Functional role Arrow2 top
In vivo interaction
  Endogenous
expression
Overexpression DD1 DD2 Reference
Family DD1 DD2 Method Species Region Species Region
DD FADD Link Fas Co-immunoprecipitation A20 Murine B cell 10452970
(Link: click this icon to show interactions only between the two corresponding DDs)