Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics
The Ced-3/interleukin 1beta converting enzyme-like homolog Mch6 and the lamin-cleaving enzyme Mch2alpha are substrates for the apoptotic mediator CPP32
A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain
Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt
A novel mechanism of TRAF signaling revealed by structural and functional analyses of the TRADD-TRAF2 interaction
Dexamethasone protects auditory hair cells against TNFalpha-initiated apoptosis via activation of PI3K/Akt and NFkappaB signaling
FLAME-1, a novel FADD-like anti-apoptotic molecule that regulates Fas/TNFR1-induced apoptosis
Essential roles of Atg5 and FADD in autophagic cell death: dissection of autophagic cell death into vacuole formation and cell death
Involvement of Noxa in cellular apoptotic responses to interferon, double-stranded RNA, and virus infection
TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex
Translational induction of the inhibitor of apoptosis protein HIAP2 during endoplasmic reticulum stress attenuates cell death and is mediated via an inducible internal ribosome entry site element
Ordering the cytochrome c-initiated caspase cascade: hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 in a caspase-9-dependent manner
Localization of dynein light chains 1 and 2 and their pro-apoptotic ligands
DISC (Primary complex) FADD, CASP8, CASP10
Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death
Tumor necrosis factor-alpha induces Bax-Bak interaction and apoptosis, which is inhibited by adenovirus E1B 19K
The death domain kinase RIP has an essential role in DNA damage-induced NF-kappa B activation
The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4
The receptor for the cytotoxic ligand TRAIL
Overview of cell death signaling pathways
Death-associated protein kinase phosphorylates ZIP kinase, forming a unique kinase hierarchy to activate its cell death functions
Solution structure of the RAIDD CARD and model for CARD/CARD interaction in caspase-2 and caspase-9 recruitment
Survival activity of Bcl-2 homologs Bcl-w and A1 only partially correlates with their ability to bind pro-apoptotic family members
ROCK1 phosphorylates and activates zipper-interacting protein kinase
Caspase-3 is required for alpha-fodrin cleavage but dispensable for cleavage of other death substrates in apoptosis
Direct binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADD
Structure of the heterodimeric complex between CAD domains of CAD and ICAD
Acinus is a caspase-3-activated protein required for apoptotic chromatin condensation
Apollon ubiquitinates SMAC and caspase-9, and has an essential cytoprotection function
Characterization of Fas (Apo-1, CD95)-Fas ligand interaction
BOD (Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with diverse antiapoptotic Bcl-2 members
X-linked IAP is a direct inhibitor of cell-death proteases
The distinct roles of TRAF2 and RIP in IKK activation by TNF-R1: TRAF2 recruits IKK to TNF-R1 while RIP mediates IKK activation
A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD
IAP family proteins--suppressors of apoptosis
Nonionic detergents induce dimerization among members of the Bcl-2 family
Caspase-10 is an initiator caspase in death receptor signaling
HtrA2 cleaves Apollon and induces cell death by IAP-binding motif in Apollon-deficient cells
Activation of JNK1, RSK2, and MSK1 is involved in serine 112 phosphorylation of Bad by ultraviolet B radiation
The X-ray structure of a BAK homodimer reveals an inhibitory zinc binding site
Underphosphorylated BAD interacts with diverse antiapoptotic Bcl-2 family proteins to regulate apoptosis
PIDD mediates NF-kappaB activation in response to DNA damage
Uncoordinated regulation of stress fibers and focal adhesions by DAP kinase
Delineation of the caspase-9 signaling cascade
The c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspases
The serine protease Omi/HtrA2 is released from mitochondria during apoptosis. Omi interacts with caspase-inhibitor XIAP and induces enhanced caspase activity
Ubiquitin-protein ligase activity of X-linked inhibitor of apoptosis protein promotes proteasomal degradation of caspase-3 and enhances its anti-apoptotic effect in Fas-induced cell death
Phospholipase C-gamma 2 couples Bruton's tyrosine kinase to the NF-kappaB signaling pathway in B lymphocytes
TRAF2 phosphorylation modulates tumor necrosis factor alpha-induced gene expression and cell resistance to apoptosis
Molecular cloning of ILP-2, a novel member of the inhibitor of apoptosis protein family
The membrane-associated inhibitor of apoptosis protein, BRUCE/Apollon, antagonizes both the precursor and mature forms of Smac and caspase-9
CRADD, a novel human apoptotic adaptor molecule for caspase-2, and FasL/tumor necrosis factor receptor-interacting protein RIP
Phosphorylation and activation of myosin by Rho-associated kinase (Rho-kinase)
A serine protease, HtrA2, is released from the mitochondria and interacts with XIAP, inducing cell death
Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3
Eukaryotic translation initiation factor 4G is targeted for proteolytic cleavage by caspase 3 during inhibition of translation in apoptotic cells
BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis
Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis
Caspase-2 is localized at the Golgi complex and cleaves golgin-160 during apoptosis
The pro-apoptotic function of death-associated protein kinase is controlled by a unique inhibitory autophosphorylation-based mechanism
Molecular mechanisms of nonmuscle myosin-II regulation
Loss of Bif-1 suppresses Bax/Bak conformational change and mitochondrial apoptosis
Dual role of BRUCE as an antiapoptotic IAP and a chimeric E2/E3 ubiquitin ligase
ZIP kinase identified as a novel myosin regulatory light chain kinase in HeLa cells
IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs
Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins
Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors
Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
Identification of amino acid residues important for ligand binding to Fas
Cleavage of lamin A by Mch2 alpha but not CPP32: multiple interleukin 1 beta-converting enzyme-related proteases with distinct substrate recognition properties are active in apoptosis
DFF, a heterodimeric protein that functions downstream of caspase-3 to trigger DNA fragmentation during apoptosis
JAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis
The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex
DAP5 promotes cap-independent translation of Bcl-2 and CDK1 to facilitate cell survival during mitosis
Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway
The anti-apoptotic activity of XIAP is retained upon mutation of both the caspase 3- and caspase 9-interacting sites
TRAIL receptors 1 (DR4) and 2 (DR5) signal FADD-dependent apoptosis and activate NF-kappaB
Nuclear caspase-3 and caspase-7 activation, and poly(ADP-ribose) polymerase cleavage are early events in camptothecin-induced apoptosis
The caspase-cleaved DAP5 protein supports internal ribosome entry site-mediated translation of death proteins
In vitro selection and characterization of Bcl-X(L)-binding proteins from a mix of tissue-specific mRNA display libraries
FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis
Anatomy of TRAF2. Distinct domains for nuclear factor-kappaB activation and association with tumor necrosis factor signaling proteins
Identification of a new form of death-associated protein kinase that promotes cell survival
Molecular cloning and characterization of Bif-1. A novel Src homology 3 domain-containing protein that associates with Bax
DAP-kinase-mediated morphological changes are localization dependent and involve myosin-II phosphorylation
Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function
A novel caspase-2 complex containing TRAF2 and RIP1
[W206R]-procaspase 3: an inactivatable substrate for caspase 8
Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms
Identification of small-molecule inhibitors of interaction between the BH3 domain and Bcl-xL
Differential regulation of Bax and Bak by anti-apoptotic Bcl-2 family proteins Bcl-B and Mcl-1
Dismantling cell-cell contacts during apoptosis is coupled to a caspase-dependent proteolytic cleavage of beta-catenin
HtrA2 promotes cell death through its serine protease activity and its ability to antagonize inhibitor of apoptosis proteins
BAD/BCL-[X(L)] heterodimerization leads to bypass of G0/G1 arrest
Identification of Omi/HtrA2 as a mitochondrial apoptotic serine protease that disrupts inhibitor of apoptosis protein-caspase interaction
A single BIR domain of XIAP sufficient for inhibiting caspases
tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c
Study of DFF45 in its role of chaperone and inhibitor: two independent inhibitory domains of DFF40 nuclease activity
Identification of caspase 3-mediated cleavage and functional alteration of eukaryotic initiation factor 2alpha in apoptosis
The TNF receptor 1-associated protein TRADD signals cell death and NF-kappa B activation
Tumor necrosis factor-alpha-induced IKK phosphorylation of NF-kappaB p65 on serine 536 is mediated through the TRAF2, TRAF5, and TAK1 signaling pathway
Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins
The eIF4G homolog DAP5/p97 supports the translation of select mRNAs during endoplasmic reticulum stress
HeLa ZIP kinase induces diphosphorylation of myosin II regulatory light chain and reorganization of actin filaments in nonmuscle cells
Caspase-3-generated fragment of gelsolin: effector of morphological change in apoptosis
Caspase-2 induces apoptosis by releasing proapoptotic proteins from mitochondria
XIAP induces NF-kappaB activation via the BIR1/TAB1 interaction and BIR1 dimerization
Bim: a novel member of the Bcl-2 family that promotes apoptosis
Protein phosphatase 1alpha is a Ras-activated Bad phosphatase that regulates interleukin-2 deprivation-induced apoptosis
BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly
ZIP kinase is responsible for the phosphorylation of myosin II and necessary for cell motility in mammalian fibroblasts
Protein kinase C theta and epsilon promote T-cell survival by a rsk-dependent phosphorylation and inactivation of BAD
Suppression of survivin phosphorylation on Thr34 by flavopiridol enhances tumor cell apoptosis
An anti-apoptotic protein human survivin is a direct inhibitor of caspase-3 and -7
X-linked inhibitor of apoptosis protein (XIAP) inhibits caspase-3 and -7 in distinct modes
Caspase-3-induced gelsolin fragmentation contributes to actin cytoskeletal collapse, nucleolysis, and apoptosis of vascular smooth muscle cells exposed to proinflammatory cytokines
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death
NF-kappaB p105 is a target of IkappaB kinases and controls signal induction of Bcl-3-p50 complexes
CASH, a novel caspase homologue with death effector domains
Suppression of lipopolysaccharide-induced nuclear factor-kappaB activity by theaflavin-3,3'-digallate from black tea and other polyphenols through down-regulation of IkappaB kinase activity in macrophages
Regulation of apoptosis at cell division by p34cdc2 phosphorylation of survivin
The role of c-FLIP in modulation of CD95-induced apoptosis
IAP proteins: blocking the road to death's door
Bcl-XL protects BimEL-induced Bax conformational change and cytochrome C release independent of interacting with Bax or BimEL
Pro-caspase-3 is a major physiologic target of caspase-8
Unique and overlapping substrate specificities of caspase-8 and caspase-10
Inhibition of death receptor signals by cellular FLIP
A common binding site mediates heterodimerization and homodimerization of Bcl-2 family members
Disruption of the interaction of mammalian protein synthesis eukaryotic initiation factor 4B with the poly(A)-binding protein by caspase- and viral protease-mediated cleavages
The PIDDosome, a protein complex implicated in activation of caspase-2 in response to genotoxic stress
TNF-alpha induces two distinct caspase-8 activation pathways
Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
Mutagenesis of the BH3 domain of BAX identifies residues critical for dimerization and killing
Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death
The first alpha helix of Bax plays a necessary role in its ligand-induced activation by the BH3-only proteins Bid and PUMA
Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis
Activation of death-inducing signaling complex (DISC) by pro-apoptotic C-terminal fragment of RIP
Changes in integrity and association of eukaryotic protein synthesis initiation factors during apoptosis
Following a TRAIL: update on a ligand and its five receptors
Activation of the NF-kappaB pathway by caspase 8 and its homologs
Phosphatase-mediated crosstalk between MAPK signaling pathways in the regulation of cell survival
IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases
NMR structure and mutagenesis of the Fas (APO-1/CD95) death domain
Phosphatidylserine externalization during CD95-induced apoptosis of cells and cytoplasts requires ICE/CED-3 protease activity
Caspase-mediated cleavage of the stacking protein GRASP65 is required for Golgi fragmentation during apoptosis
c-IAP1 is cleaved by caspases to produce a proapoptotic C-terminal fragment
Mapping of the inducible IkappaB phosphorylation sites that signal its ubiquitination and degradation
Caspase-3-mediated cleavage of ROCK I induces MLC phosphorylation and apoptotic membrane blebbing
Activation of the apoptotic endonuclease DFF40 (caspase-activated DNase or nuclease). Oligomerization and direct interaction with histone H1
TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways
Molecular cloning and expression of a receptor for human tumor necrosis factor
Caspase-9, Bcl-XL, and Apaf-1 form a ternary complex
Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death
Exploiting the PI3K/AKT pathway for cancer drug discovery
Yama/CPP32 beta, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase
The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet
A novel form of DAP5 protein accumulates in apoptotic cells as a result of caspase cleavage and internal ribosome entry site-mediated translation
Conversion of Bcl-2 to a Bax-like death effector by caspases
Direct interaction between survivin and Smac/DIABLO is essential for the anti-apoptotic activity of survivin during taxol-induced apoptosis