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Catalog Number: (10780-646)
Supplier: Peprotech
Description: Fas Ligand (FasL) is a member of the TNF superfamily that is expressed on the cell surface of activated T cells. Binding of FasL to Fas Receptor triggers apoptosis in Fas-bearing cells. FasL has the ability to kill T cells and activated B cells, which leads to down-regulation of the immune response. The mechanism of Fas-induced apoptosis involves recruitment of pro-caspase 8 through an adaptor molecule called FADD, followed by processing of the pro-enzyme into active forms. These active caspases then cleave various cellular substrates, leading to the eventual cell death. Both human and murine sFasL are fully active on human and murine cells. Recombinant Human sFas Ligand is a 17.9 kDa protein comprising the TNF-homologous region of FasL and contains an 8-residue N-terminal His-Tag.


Catalog Number: (10237-228)
Supplier: Bioss
Description: P19ARF Capable of inducing cell cycle arrest in G1 and G2 phases. Acts as a tumor suppressor. Binds to MDM2 and blocks its nucleocytoplasmic shuttling by sequestering it in the nucleolus. This inhibits the oncogenic action of MDM2 by blocking MDM2-induced degradation of p53 and enhancing p53-dependent transactivation and apoptosis. Also induces G2 arrest and apoptosis in a p53-independent manner by preventing the activation of cyclin B1/CDC2 complexes. Binds to BCL6 and down-regulates BCL6-induced transcriptional repression. Binds to E2F1 and MYC and blocks their transcriptional activator activity but has no effect on MYC transcriptional repression. Binds to TOP1/TOPOI and stimulates its activity. This complex binds to rRNA gene promoters and may play a role in rRNA transcription and/or maturation. Interacts with NPM1/B23 and promotes its polyubiquitination and degradation, thus inhibiting rRNA processing. Interacts with UBE2I/UBC9 and enhances sumoylation of a number of its binding partners including MDM2 and E2F1. Binds to HUWE1 and represses its ubiquitin ligase activity. May play a role in controlling cell proliferation and apoptosis during mammary gland development.


Catalog Number: (76483-770)
Supplier: AAT BIOQUEST INC
Description: Our Cell Meter™ assay kits are a set of tools for monitoring cellular functions.

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Catalog Number: (77436-868)
Supplier: Bioss
Description: The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is activated by various cell stimuli, and targets specific transcription factors, and thus mediates immediate-early gene expression in response to cell stimuli. The activation of this kinase by tumor-necrosis factor alpha (TNF-alpha) is found to be required for TNF-alpha induced apoptosis. This kinase is also involved in UV radiation induced apoptosis, which is thought to be related to cytochrom c-mediated cell death pathway. Studies of the mouse counterpart of this gene suggested that this kinase play a key role in T cell proliferation, apoptosis and differentiation. Five alternatively spliced transcript variants encoding distinct isoforms have been reported. [provided by RefSeq, Jun 2013].


Catalog Number: (10239-752)
Supplier: Bioss
Description: Tyrosine-protein kinase that acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. Required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. Plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. Promotes cell proliferation in keratinocytes and immature osteoblasts, but promotes apoptosis in differentiated osteoblasts. Phosphorylates PLCG1, FRS2 and PAK4. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal FGFR2 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1.


Catalog Number: (10408-320)
Supplier: Bioss
Description: Receptor for TNFRSF25 and TNFRSF6B. Mediates activation of NF-kappa-B. Inhibits vascular endothelial growth and angiogenesis (in vitro). Promotes activation of caspases and apoptosis.


Catalog Number: (10408-324)
Supplier: Bioss
Description: Receptor for TNFRSF25 and TNFRSF6B. Mediates activation of NF-kappa-B. Inhibits vascular endothelial growth and angiogenesis (in vitro). Promotes activation of caspases and apoptosis.


Catalog Number: (10299-930)
Supplier: Bioss
Description: This enzyme is necessary for target cell lysis in cell-mediated immune responses. It cleaves after Asp. Seems to be linked to an activation cascade of caspases (aspartate-specific cysteine proteases) responsible for apoptosis execution. Cleaves caspase-3, -7, -9 and 10 to give rise to active enzymes mediating apoptosis.


Catalog Number: (10362-724)
Supplier: Bioss
Description: Inhibits NF-kappa-B activation triggered by overexpression of RIPK1 and TRAF6 but not of RELA. Inhibits also tumor necrosis (TNF), IL-1 and TLR4-induced NF-kappa-B activation in a dose-dependent manner. Overexpression sensitizes cells to TNF-induced apoptosis. Could be involved in regulating NF-kappa-B activation and apoptosis. Is a potent inhibitory factor for osteoclast differentiation. Involved in protein degradation via the ubiquitin-proteasome system and plays a critical role in muscle atrophy. May act by anchoring ubiquitinylated proteins to the proteasome, playing a critical role in protein degradation.


Catalog Number: (10748-520)
Supplier: Prosci
Description: ASK1 Antibody: Mitogen-activated protein (MAP) kinase cascades are activated in response to various extracellular stimuli, including cytokines, growth factors and environmental stresses. A novel MAP kinase kinase kinase (MAPKKK) was recently identified and designated ASK1 (for apoptosis signal-regulating kinase 1) and MAPKKK5. ASK1 activated two different subgroups of MAPKK, MKK4 and MKK6, which in turn activated c-Jun N-terminal kinase (JNK) and p38 MAP kinase, respectively. ASK1/MAPKKK5 is activated by TNFR and Fas through the interaction with members of the TRAF family and Fas-associated protein Daxx. Overexpression of ASK1 induced apoptotic cell death, and a catalytically inactive form of ASK1 inhibited TNF-alpha -induced apoptosis. ASK1 is expressed in variety of tissues and cell lines.


Catalog Number: (10749-610)
Supplier: Prosci
Description: cIAP Antibody: Apoptosis, or programmed cell death, is related to many diseases, such as cancer. Apoptosis is triggered by a variety of stimuli including members in the TNF family and can be prevented by the inhibitor of apoptosis (IAP) proteins. IAP proteins form a conserved gene family that binds to and inhibits cell death proteases. The two isoforms of c-IAP (c-IAP1 and c-IAP2) are structurally related to XIAP, containing 3 baculoviral IAP repeat (BIR) motifs that are essential and sufficient for the binding and inhibition of caspases-3, -7. The c-IAPs can associate with the death receptor TNF-R2, and mediate the ubiquitinization of TRAF2 following the binding of TNF-alpha by its receptor. Omi, a negative regulator of c-IAP, inhibits its activity by catalytically cleaving c-IAP. Another negative regulator, Smac/DIABLO, acts by enhancing the auto-ubiquitization activity of c-IAP.


Catalog Number: (89415-268)
Supplier: Prosci
Description: ICAD Antibody: Apoptosis is related to many diseases and induced by a family of cell death receptors and their ligands. Cell death signals are transduced by death domain containing adapter molecules and members of the caspase family of proteases. These death signals finally cause the degradation of chromosomal DNA by activated DNase. A human DNA fragmentation factor (DFF) was identified recently which is cleaved by caspase-3 during apoptosis. Mouse homologue of human DFF was identified as a DNase inhibitor designated ICAD, for inhibitor of caspase-activated DNase. Upon cleavage of DFF/ICAD, a caspase activated deoxyribonuclease (CAD) is released and activated and eventually causes the degradation of DNA in the nuclei. Therefore, the cleavage of CAD inhibitor molecule DFF/ICAD, which causes DNase activation and DNA degradation, is the hallmark of apoptotic cell death.


Catalog Number: (10299-950)
Supplier: Bioss
Description: This enzyme is necessary for target cell lysis in cell-mediated immune responses. It cleaves after Asp. Seems to be linked to an activation cascade of caspases (aspartate-specific cysteine proteases) responsible for apoptosis execution. Cleaves caspase-3, -7, -9 and 10 to give rise to active enzymes mediating apoptosis.


Catalog Number: (89415-972)
Supplier: Prosci
Description: ASK1 Antibody: Mitogen-activated protein (MAP) kinase cascades are activated in response to various extracellular stimuli, including cytokines, growth factors and environmental stresses. A novel MAP kinase kinase kinase (MAPKKK) was recently identified and designated ASK1 (for apoptosis signal-regulating kinase 1) and MAPKKK5. ASK1 activated two different subgroups of MAPKK, MKK4 and MKK6, which in turn activated c-Jun N-terminal kinase (JNK) and p38 MAP kinase, respectively. ASK1/MAPKKK5 is activated by TNFR and Fas through the interaction with members of the TRAF family and Fas-associated protein Daxx. Overexpression of ASK1 induced apoptotic cell death, and a catalytically inactive form of ASK1 inhibited TNF-alpha -induced apoptosis. ASK1 is expressed in variety of tissues and cell lines.


Catalog Number: (10466-444)
Supplier: Bioss
Description: TID1 is a human homolog of the Drosophila tumor suppressor lethal tumerous imaginal discs and encodes two mitochondrial matrix localized splice variants of human Tid1 designated hTid1S and hTid1L. These proteins are the conserved members of the DnaJ family of proteins which act as cochaperons for mitochondrial Hsp70. They contain a conserved tetrahedrical J domain which binds to Hsp70 chaperones and activates their ATPase activity. Expression of hTid1L increases apoptosis induced by DNA damaging agents as mitomycin C and TNF alpha. A J domain mutant of hTid1L can dominantly suppress apoptosis and in sharp contrast the J domain mutant of hTid1S increases apoptosis. Expression of hTid1S and hTid1L affects cytochrome c release from the mitochondria and caspase 3 activation, while activation of caspase 8 is unaffected. It is strongly suggested that these two splice variants exert their anti and pro apoptotic effects through discrete substrates and activities. Hence the relative abundance of these proteins or their substrates may allow the mitochondria to dampen or enhance the apoptotic signals.


Catalog Number: (10466-450)
Supplier: Bioss
Description: TID1 is a human homolog of the Drosophila tumor suppressor lethal tumerous imaginal discs and encodes two mitochondrial matrix localized splice variants of human Tid1 designated hTid1S and hTid1L. These proteins are the conserved members of the DnaJ family of proteins which act as cochaperons for mitochondrial Hsp70. They contain a conserved tetrahedrical J domain which binds to Hsp70 chaperones and activates their ATPase activity. Expression of hTid1L increases apoptosis induced by DNA damaging agents as mitomycin C and TNF alpha. A J domain mutant of hTid1L can dominantly suppress apoptosis and in sharp contrast the J domain mutant of hTid1S increases apoptosis. Expression of hTid1S and hTid1L affects cytochrome c release from the mitochondria and caspase 3 activation, while activation of caspase 8 is unaffected. It is strongly suggested that these two splice variants exert their anti and pro apoptotic effects through discrete substrates and activities. Hence the relative abundance of these proteins or their substrates may allow the mitochondria to dampen or enhance the apoptotic signals.


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