![]() |
Volumn 4, Issue , 2013, Pages
|
TNF can activate RIPK3 and cause programmed necrosis in the absence of RIPK1.
|
Author keywords
[No Author keywords available]
|
Indexed keywords
CASPASE 8;
CASPASE INHIBITOR;
PEPTIDE CHLOROMETHYL KETONE;
PROTEIN BAK;
PROTEIN BAX;
QUINOLINE DERIVATIVE;
QUINOLINE VAL ASP(OME) CH2 OPH;
QUINOLINE-VAL-ASP(OME)-CH2-OPH;
RECEPTOR INTERACTING PROTEIN SERINE THREONINE KINASE;
RECOMBINANT PROTEIN;
RIPK1 PROTEIN, MOUSE;
RIPK3 PROTEIN, MOUSE;
TUMOR NECROSIS FACTOR ALPHA;
TUMOR NECROSIS FACTOR RECEPTOR 1;
TUMOR NECROSIS FACTOR RECEPTOR ASSOCIATED DEATH DOMAIN PROTEIN;
ANIMAL;
APOPTOSIS;
ARTICLE;
BIOSYNTHESIS;
CELL LINE;
DRUG EFFECT;
FIBROBLAST;
GENETICS;
METABOLISM;
MOUSE;
NECROSIS;
PATHOLOGY;
AMINO ACID CHLOROMETHYL KETONES;
ANIMALS;
APOPTOSIS;
BCL-2 HOMOLOGOUS ANTAGONIST-KILLER PROTEIN;
BCL-2-ASSOCIATED X PROTEIN;
CASPASE 8;
CASPASE INHIBITORS;
CELL LINE;
FIBROBLASTS;
MICE;
NECROSIS;
QUINOLINES;
RECEPTOR-INTERACTING PROTEIN SERINE-THREONINE KINASES;
RECEPTORS, TUMOR NECROSIS FACTOR, TYPE I;
RECOMBINANT PROTEINS;
TNF RECEPTOR-ASSOCIATED DEATH DOMAIN PROTEIN;
TUMOR NECROSIS FACTOR-ALPHA;
|
EID: 84878964122
PISSN: None
EISSN: 20414889
Source Type: None
DOI: 10.1038/cddis.2012.201 Document Type: Article |
Times cited : (126)
|
References (0)
|