[HTML][HTML] Death receptors couple to both cell proliferation and apoptosis
RC Budd - The Journal of clinical investigation, 2002 - Am Soc Clin Investig
RC Budd
The Journal of clinical investigation, 2002•Am Soc Clin InvestigRecent findings suggest that cell death following cytokine withdrawal is dependent not on
proximal caspases but, rather, on those that are more downstream. Thus, mice lacking Fas
or FADD or overexpressing CrmA (which inhibits caspase-8) all inhibit Fas-induced death
but do not block death by cytokine deprivation (22). The reverse is true (that is, Fas-induced
death is unchanged but cytokine withdrawal is impeded) in mice transgenic for Bcl-2, in
knockout animals lacking Bim, and in double knockouts lacking both Bak and Bax (22, 23).
proximal caspases but, rather, on those that are more downstream. Thus, mice lacking Fas
or FADD or overexpressing CrmA (which inhibits caspase-8) all inhibit Fas-induced death
but do not block death by cytokine deprivation (22). The reverse is true (that is, Fas-induced
death is unchanged but cytokine withdrawal is impeded) in mice transgenic for Bcl-2, in
knockout animals lacking Bim, and in double knockouts lacking both Bak and Bax (22, 23).
Recent findings suggest that cell death following cytokine withdrawal is dependent not on proximal caspases but, rather, on those that are more downstream. Thus, mice lacking Fas or FADD or overexpressing CrmA (which inhibits caspase-8) all inhibit Fas-induced death but do not block death by cytokine deprivation (22). The reverse is true (that is, Fas-induced death is unchanged but cytokine withdrawal is impeded) in mice transgenic for Bcl-2, in knockout animals lacking Bim, and in double knockouts lacking both Bak and Bax (22, 23).
The Journal of Clinical Investigation