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Catalog Number: (10330-818)
Supplier: Bioss
Description: Induces apoptosis in cooperation with SIAH1A. Acts as a mediator between p53/TP53 and BAX in a neuronal death pathway that is activated by DNA damage. Acts synergistically with TRAF2 and inhibits TNF induced apoptosis through activation of NF-kappa-B (By similarity). Possesses a tumor suppressing activity in glioma cells.


Catalog Number: (10230-072)
Supplier: Bioss
Description: Oligomeric Apaf-1 mediates the cytochrome c-dependent autocatalytic activation of pro-caspase-9 (Apaf-3), leading to the activation of caspase-3 and apoptosis. This activation requires ATP. Isoform 6 is less effective in inducing apoptosis.


Catalog Number: (89415-570)
Supplier: Prosci
Description: Ipaf 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 adaptor molecules and proteases including several members of the caspase family. Another family of proteins that functions as a critical regulator of apoptosis and NF kappa signaling pathways is the CED-4/Apaf-1 (apoptosis protein activating factor-1) protein family. Ipaf (ICE protease activating factor) is a CED-4/Apaf-1 family member that activates caspase-1/ICE and can induce apoptosis in human cells in a caspase-1 dependent manner. Ipaf and caspase-1 are thought to interact with each other through the association of the Ipaf amino-terminal CARD (caspase recruitment domain) and amino-terminal CARD of caspase-1.


Catalog Number: (75933-022)
Supplier: Rockland Immunochemical
Description: Apoptosis is an important process by which normal tissue homeostasis and function are maintained. One of the major signals that regulate this process is mediated by the activation of the Fas receptor by its ligand. This leads to the formation of a Fas-associated death domain (FADD)- containing death-inducing signaling complex and the activation of caspase-8, which in turn activates downstream effector caspases, such as caspase-3 and -7. Recent experiments have shown that overexpression of Toso, a novel regulator of Fas-induced apoptosis in lymphoid cells, in Jurkat cells as well as transgenic mice render these cells resistant to Fas-induced apoptosis but not to TRAIL-induced apoptosis. Furthermore, Toso was found to associate with FADD, suggesting that Toso functions by disrupting the formation of the death-inducing signaling complex.


Catalog Number: (10229-980)
Supplier: Bioss
Description: Involved in the activation cascade of caspases responsible for apoptosis execution. Binding of caspase-9 to Apaf-1 leads to activation of the protease which then cleaves and activates caspase-3. Promotes DNA damage-induced apoptosis in a ABL1/c-Abl-dependent manner. Proteolytically cleaves poly(ADP-ribose) polymerase (PARP). Isoform 2 lacks activity is an dominant-negative inhibitor of caspase-9.


Catalog Number: (77439-028)
Supplier: Bioss
Description: Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a '216-Asp-|-Gly-217' bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop-helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage.


Catalog Number: (10403-334)
Supplier: Bioss
Description: Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).


Catalog Number: (10321-370)
Supplier: Bioss
Description: Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).


Catalog Number: (75929-206)
Supplier: Rockland Immunochemical
Description: 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 adaptor molecules and proteases including several members of the caspase family. Another family of proteins that functions as a critical regulator of apoptosis and NFk signaling pathways is the CED-4/Apaf-1 (apoptosis protein activating factor-1) protein family. Ipaf (ICE protease activating factor) is a CED-4/Apaf-1 family member that activates caspase-1/ICE and can induce apoptosis in human cells in a caspase-1 dependent manner. Ipaf and caspase-1 are thought to interact with each other through the association of the Ipaf amino-terminal CARD (caspase recruitment domain) and amino-terminal CARD of caspase-1.


Catalog Number: (75930-858)
Supplier: Rockland Immunochemical
Description: Apoptosis is related to many diseases and development. Caspase-9 plays a central role in cell death induced by a variety of apoptosis activators. Cytochrome c, after released from mitochondria, binds to Apaf-1, which forms an apoptosome that in turn binds to and activate procaspase-9. Activated caspase-9 cleaves and activates the effector caspases (caspase-3, -6 and -7), which are responsible for the proteolytic cleavage of many key proteins in apoptosis. The tumor suppressor putative HLA-DR-associated proteins (PHAPs) were recently identified as important regulators of mitochondrion apoptosis. PHAP appears to facilitate apoptosome-medicated caspase-9 activation and to stimulate the mitochondrial apoptotic pathway. PHAP was also shown to oppose both Ras- and Myc-medicated cell transformation.


Catalog Number: (89361-126)
Supplier: Genetex
Description: Apoptosis is characterized by several morphological nuclear changes including chromatin condensation and nuclear fragmentation. These changes are triggered by the activation of members of caspase family, caspase activated DNase, and several novel proteins (1). A novel gene, the product of which causes chromatin condensation and DNA fragmentation, was recently identified, cloned, and designated apoptosis inducing factor (AIF) (2). Like the critical molecules, cytochrome c and caspase-9, in apoptosis, AIF localizes in mitochondria. AIF translocates to the nucleus when apoptosis is induced and induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. AIF induces chromatin condensation and large scale DNA fragmentation, which are the hallmarks of apoptosis, of the isolated nucleus and the nucleus in live cells by microinjection and apoptosis stimuli (2,3). AIF is highly conserved between human and mouse and widely expressed (2).


Catalog Number: (10321-366)
Supplier: Bioss
Description: Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).


Catalog Number: (10748-292)
Supplier: Prosci
Description: PHAP III Antibody: Apoptosis is related to many diseases and development. Caspase-9 plays a central role in cell death induced by a variety of apoptosis activators. Cytochrome c, after released from mitochondria, binds to Apaf-1, which forms an apoptosome that in turn binds to and activate procaspase-9. Activated caspase-9 cleaves and activates the effector caspases (caspase-3, -6 and -7), which are responsible for the proteolytic cleavage of many key proteins in apoptosis. The tumor suppressor putative HLA-DR-associated proteins (PHAPs) were recently identified as important regulators of mitochondrion apoptosis. PHAP appears to facilitate apoptosome-medicated caspase-9 activation and to stimulate the mitochondrial apoptotic pathway. PHAP was also shown to oppose both Ras- and Myc-medicated cell transformation.


Catalog Number: (10229-974)
Supplier: Bioss
Description: Involved in the activation cascade of caspases responsible for apoptosis execution. Binding of caspase-9 to Apaf-1 leads to activation of the protease which then cleaves and activates caspase-3. Promotes DNA damage-induced apoptosis in a ABL1/c-Abl-dependent manner. Proteolytically cleaves poly(ADP-ribose) polymerase (PARP). Isoform 2 lacks activity is an dominant-negative inhibitor of caspase-9.


Catalog Number: (10229-994)
Supplier: Bioss
Description: Involved in the activation cascade of caspases responsible for apoptosis execution. Binding of caspase-9 to Apaf-1 leads to activation of the protease which then cleaves and activates caspase-3. Promotes DNA damage-induced apoptosis in a ABL1/c-Abl-dependent manner. Proteolytically cleaves poly(ADP-ribose) polymerase (PARP). Isoform 2 lacks activity is an dominant-negative inhibitor of caspase-9.


Catalog Number: (76084-616)
Supplier: Bioss
Description: Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.


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