The availability of inducer members for heterodimerization with Bcl-2 or Bcl-xL may be regulated by signals generated by the binding of cytokines. Bad is a proapoptotic member of the Bcl-2 family and is sequestered in the cytosol when cytokines are present. Upon removal of cytokines, Bad becomes dephosphorylated at specific serine residues, dissociates from and heterodimerizes with Bcl-xL.
Bad phosphorylation and reassociation with can be induced by addition of cytokines. Furthermore, hyper-phosphorylated Bad does not bind to Bcl-xL. These results suggest that the cytokine-engaged receptor prevents apoptosis by inducing the phosphorylation of the apoptotic-inducing members of the Bcl-2 family, thereby making them unavailable for dimerization with Bcl-2 or Bcl-xL.
The identity of the kinase pathway that couples cytokine receptor binding to phosphorylation of the pro-apoptotic Bcl-2 family members is under intense study.
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Activated protein kinase B PKB has been shown to prevent the apoptotic cell death of Rat-1 cells that are induced by c- myc. PI3K is active when cytokines are bound to their receptors reviewed in ref.
The Bcl-2 family may also be central to another type of apoptosis induction. Bcl-2 overexpression prevents free radical-induced lipid peroxidation. Studies using in vitro assays of apoptosis have shown that activation of the cysteine protease CPP32 is dependent on the release of cytochrome c from the mitochondria.
It is possible that cytosolic cytochrome c propagates or initiates free radical production. Although the mechanism for activation of apoptosis by these events is unknown, the findings suggest a function for the Bcl-2 family in regulating free radical damage. Bcl-xL forms pores in artificial membranes 38 and have a crystal structure similar to the B-subunit of diphtheria toxin.
Thus, Bcl-xL and Bcl-2 have the potential to translocate materials across membranes.
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Mitochondrial membrane pore formation and subsequent loss of mitochondrial transmembrane potential has been found to be one of the earliest cellular events associated with apoptosis. All Rights Reserved. Skip to main content. Figure 1. Figure 2. Activationof apoptosis on withdrawal of cytokine.enter
Cytokine-related Mechanisms of Apoptosis: R&D Systems
Panel A shows cell with cytokine and panel B shows cell without cytokine. References Thompson, C. Oppenheim, R.
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Downregulation of HtrA1 promotes resistance to anoikis and peritoneal dissemination of ovarian cancer cells.