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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: (10466-526)
Supplier: Bioss
Description: Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].


Catalog Number: (10351-640)
Supplier: Bioss
Description: FADD (Fas Associated Death Domain) is an apoptosis adapter molecule enabling transduction of the apoptosis signal initiated via the FasL/Fas receptor interaction. The protein contains a C terminal death domain that interacts with the Fas receptor death domain. The N terminus contains a death effectors domain (DED) which recruits caspase to the death inducing signaling complex (DISC) and initiates the apoptotic caspase cascade. Recruitment of Caspase 8 to the Fas receptor results in oligomerization of the Caspase 8 protein, which in turn drives its autoactivation through self-cleavage. Activated Caspase 8 then activates other downstream caspases including Caspase 9, thereby commiting the cell to undergo apoptosis. FADD is implicated in non-apoptotic cellular pathways such as the regulation of cell cycle machinery in T lymphocytes. This is connected to the phosphorylation state of FADD and to the FasL/TRAIL induced transcriptional activation of cfos protooncogene. FADD also interacts with the hepatitis C virus core protein in the HEK 293 cell line.


Supplier: Adipogen
Description: The compound (Akt-I-1) inhibits only Akt1 (IC(50) 4.6 µM) and does not inhibit AKT2, or AKT3. The compound is a reversible inhibitor, and exhibits a linear mixed-type inhibition against ATP and peptide substrate. In addition to inhibiting kinase activity of AKT1 isoform, AKT-I-1 blocked the phosphorylation and activation of AKT1 by PDK1 (phosphoinositide-dependent kinase 1). The inhibitor was found to be cell-active and to block phosphorylation of Akt at Thr308 and Ser473, reduce the levels of active Akt in cells, block the phosphorylation of known Akt substrates and promote TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand)-induced apoptosis in LNCap prostate cancer cells.

Catalog Number: (76079-704)
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: (10798-484)
Supplier: Prosci
Description: Tumor necrosis factor receptor superfamily member 10B (TNFRSF10B) is also known as TNF-related apoptosis-inducing ligand receptor 2 (TRAILR2), Death receptor 5 (DR5), CD262, KILLER, is a member of the TNF-receptor superfamily, and contains an intracellular death domain. TNFRSF10B / DR-5 is widely expressed in adult and fetal tissues; very highly expressed in tumor cell lines. TRAILR2 / CD262 / DR5 is the receptor for the cytotoxic ligand TNFSF10/TRAIL. The adapter molecule FADD (a death domain containing adaptor protein) of TRAIL-R2 / TNFRSF10B recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. CD262 / DR5 Promotes the activation of NF-kappa-B. DR5 is essential for ER stress-induced apoptosis and is regulated by p53/TP53.


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: (10229-196)
Supplier: Bioss
Description: Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. Plays a role in apoptosis. Suppression of the anti-apoptotic members or activation of the pro-apoptotic members of the Bcl-2 family leads to altered mitochondrial membrane permeability resulting in release of cytochrome c into the cytosol. Binding of cytochrome c to Apaf-1 triggers the activation of caspase-9, which then accelerates apoptosis by activating other caspases.


Catalog Number: (10420-338)
Supplier: Bioss
Description: Serine/threonine-protein kinase that acts as a regulatory link between the membrane-associated Ras GTPases and the MAPK/ERK cascade, and this critical regulatory link functions as a switch determining cell fate decisions including proliferation, differentiation, apoptosis, survival and oncogenic transformation. RAF1 activation initiates a mitogen-activated protein kinase (MAPK) cascade that comprises a sequential phosphorylation of the dual-specific MAPK kinases (MAP2K1/MEK1 and MAP2K2/MEK2) and the extracellular signal-regulated kinases (MAPK3/ERK1 and MAPK1/ERK2). The phosphorylated form of RAF1 (on residues Ser-338 and Ser-339, by PAK1) phosphorylates BAD/Bcl2-antagonist of cell death at 'Ser-75'. Phosphorylates adenylyl cyclases: ADCY2, ADCY5 and ADCY6, resulting in their activation. Phosphorylates PPP1R12A resulting in inhibition of the phosphatase activity. Phosphorylates TNNT2/cardiac muscle troponin T. Can promote NF-kB activation and inhibit signal transducers involved in motility (ROCK2), apoptosis (MAP3K5/ASK1 and STK3/MST2), proliferation and angiogenesis (RB1). Can protect cells from apoptosis also by translocating to the mitochondria where it binds BCL2 and displaces BAD/Bcl2-antagonist of cell death. Regulates Rho signaling and migration, and is required for normal wound healing. Plays a role in the oncogenic transformation of epithelial cells via repression of the TJ protein, occludin (OCLN) by inducing the up-regulation of a transcriptional repressor SNAI2/SLUG, which induces down-regulation of OCLN. Restricts caspase activation in response to selected stimuli, notably Fas stimulation, pathogen-mediated macrophage apoptosis, and erythroid differentiation.


Catalog Number: (10420-376)
Supplier: Bioss
Description: Serine/threonine-protein kinase that acts as a regulatory link between the membrane-associated Ras GTPases and the MAPK/ERK cascade, and this critical regulatory link functions as a switch determining cell fate decisions including proliferation, differentiation, apoptosis, survival and oncogenic transformation. RAF1 activation initiates a mitogen-activated protein kinase (MAPK) cascade that comprises a sequential phosphorylation of the dual-specific MAPK kinases (MAP2K1/MEK1 and MAP2K2/MEK2) and the extracellular signal-regulated kinases (MAPK3/ERK1 and MAPK1/ERK2). The phosphorylated form of RAF1 (on residues Ser-338 and Ser-339, by PAK1) phosphorylates BAD/Bcl2-antagonist of cell death at 'Ser-75'. Phosphorylates adenylyl cyclases: ADCY2, ADCY5 and ADCY6, resulting in their activation. Phosphorylates PPP1R12A resulting in inhibition of the phosphatase activity. Phosphorylates TNNT2/cardiac muscle troponin T. Can promote NF-kB activation and inhibit signal transducers involved in motility (ROCK2), apoptosis (MAP3K5/ASK1 and STK3/MST2), proliferation and angiogenesis (RB1). Can protect cells from apoptosis also by translocating to the mitochondria where it binds BCL2 and displaces BAD/Bcl2-antagonist of cell death. Regulates Rho signaling and migration, and is required for normal wound healing. Plays a role in the oncogenic transformation of epithelial cells via repression of the TJ protein, occludin (OCLN) by inducing the up-regulation of a transcriptional repressor SNAI2/SLUG, which induces down-regulation of OCLN. Restricts caspase activation in response to selected stimuli, notably Fas stimulation, pathogen-mediated macrophage apoptosis, and erythroid differentiation.


Catalog Number: (10328-320)
Supplier: Bioss
Description: Cleaves P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. Can also hydrolyze P(1)-P(4)-bis(5'-adenosyl) tetraphosphate (Ap4A), but has extremely low activity with ATP. Modulates transcriptional activation by CTNNB1 and thereby contributes to regulate the expression of genes essential for cell proliferation and survival, such as CCND1 and BIRC5. Plays a role in the induction of apoptosis via SRC and AKT1 signaling pathways. Inhibits MDM2-mediated proteasomal degradation of p53/TP53 and thereby plays a role in p53/TP53-mediated apoptosis. Induction of apoptosis depends on the ability of FHIT to bind P(1)-P(3)-bis(5'-adenosyl) triphosphate or related compounds, but does not require its catalytic activity, it may in part come from the mitochondrial form, which sensitizes the low-affinity Ca(2+) transporters, enhancing mitochondrial calcium uptake. Functions as tumor suppressor.


Catalog Number: (10353-186)
Supplier: Bioss
Description: Cleaves P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. Can also hydrolyze P(1)-P(4)-bis(5'-adenosyl) tetraphosphate (Ap4A), but has extremely low activity with ATP. Modulates transcriptional activation by CTNNB1 and thereby contributes to regulate the expression of genes essential for cell proliferation and survival, such as CCND1 and BIRC5. Plays a role in the induction of apoptosis via SRC and AKT1 signaling pathways. Inhibits MDM2-mediated proteasomal degradation of p53/TP53 and thereby plays a role in p53/TP53-mediated apoptosis. Induction of apoptosis depends on the ability of FHIT to bind P(1)-P(3)-bis(5'-adenosyl) triphosphate or related compounds, but does not require its catalytic activity, it may in part come from the mitochondrial form, which sensitizes the low-affinity Ca(2+) transporters, enhancing mitochondrial calcium uptake. Functions as tumor suppressor.


Catalog Number: (76483-774)
Supplier: AAT BIOQUEST INC
Description: Our Cell Meter™ assay kits are a set of tools for monitoring cellular functions.

Small Business Enterprise Minority or Woman-Owned Business Enterprise


Catalog Number: (75792-938)
Supplier: Prosci
Description: Caspase-11 not only activates caspase-1, that is required for the maturation of proinflammatory cytokines such as interleukin-1 (IL-1) and interleukin-18 (IL-18), but also activates caspase-3, leading to cellular apoptosis under pathological conditions. In most cells, caspase-11 is only expressed upon induction with pro-inflammatory stimuli. Caspase-11 is an essential mediator of endotoxic shock and caspase-11-deficient mice are resistant to endotoxic shock. LPS-induced caspase-11 regulates lymphocyte apoptosis by activating both caspase-3 and caspase-7.


Catalog Number: (89154-392)
Supplier: Enzo Life Sciences
Description: Caspase-11 not only activates caspase-1, that is required for the maturation of proinflammatory cytokines such as interleukin-1 (IL-1) and interleukin-18 (IL-18), but also activates caspase-3, leading to cellular apoptosis under pathological conditions. In most cells, caspase-11 is only expressed upon induction with pro-inflammatory stimuli. Caspase-11 is an essential mediator of endotoxic shock and caspase-11-deficient mice are resistant to endotoxic shock. LPS-induced caspase-11 regulates lymphocyte apoptosis by activating both caspase-3 and caspase-7. Human caspase-4, thought to be the homolog of mouse caspase-11, may be an effective therapeutic target for treatment of septic shock.


Catalog Number: (89161-416)
Supplier: Enzo Life Sciences
Description: Ingenol is a diterpenoid related to phorbol. Activates protein kinase C (PKC) and competes with [3H]phorbol dibutyrate for binding to PKCα (Ki for binding=240 nM). Induces apoptosis. Anticancer agent. Shows potent antileukemic activity in the P388 mouse assay.


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