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Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis
The results indicate that BID is a mediator of mitochondrial damage induced by Casp8, and coexpression of BclxL inhibits all the apoptotic changes induced by tBID. Expand
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
It is demonstrated that necroptosis contributes to delayed mouse ischemic brain injury in vivo through a mechanism distinct from that of apoptosis and offers a new therapeutic target for stroke with an extended window for neuroprotection. Expand
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Pulse chase and arrest of autophagy at the pre‐proteolysis stage reveal that fission followed by selective fusion segregates dysfunctional mitochondria and permits their removal by autophagic. Expand
Identification of RIP1 kinase as a specific cellular target of necrostatins.
Necroptosis is a cellular mechanism of necrotic cell death induced by apoptotic stimuli in the form of death domain receptor engagement by their respective ligands under conditions where apoptotic execution is prevented and necrostatins are established as the first-in-class inhibitors of RIP1 kinase, the key upstream kinase involved in the activation of necroptosis. Expand
Autophagy in cell death: an innocent convict?
The visualization of autophagosomes in dying cells has led to the belief that autophagy is a nonapoptotic form of programmed cell death. This concept has now been evaluated using cells and organismsExpand
The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1β-converting enzyme
It is proposed that the CED-3 protein acts as a cysteine protease in the initiation of programmed cell death in C. elegans and that cysteINE proteases also function in programmed cell deaths in mammals. Expand
Apoptosis in the nervous system
The principal molecular components of the apoptosis programme in neurons include Apaf-1 (apoptotic protease-activating factor 1) and proteins of the Bcl-2 and caspase families, which regulate neuronal apoptosis through the action of critical protein kinase cascades. Expand
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed. Expand
A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress.
Salubrinal demonstrates the feasibility of selective pharmacological targeting of cellular dephosphorylation events and suggests that selective chemical inhibitors of eIF2alpha deph phosphorylation may be useful in diseases involving ER stress or viral infection. Expand
Mechanisms of pre‐apoptotic calreticulin exposure in immunogenic cell death
Depletion of PERK, caspase‐8 or SNAREs had no effect on cell death induced by anthracyclines, yet abolished the immunogenicity of cell death, which could be restored by absorbing recombinant CRT to the cell surface. Expand