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ASC/TMS1 Antibody

Rabbit Polyclonal Antibody

  • WB - ASC/TMS1 Antibody ABV10227
    Western blot analysis of ASC expression in HL60 cell lysate.
Product Information
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
Primary Accession Q9ULZ3
Other Accession AAH04470.1
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 21627 Da
Additional Information
Gene ID 29108
Application & Usage Western blotting (0.5-4 µg/ml). However, the optimal conditions should be determined individually. The affinity purified antibody detects the 25 kDa human and rat ASC/TMS1. HL60 cell lysate can be used as a positive control.
Other Names TMS1, hASC, PYCARD, CARD5, MGC10332
Target/Specificity ASC/TMS1
Antibody Form Liquid
Formulation 100 µg (0.5 mg/ml) affinity purified rabbit anti-ASC/TMS1 polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 30% glycerol, 0.5% BSA, 0.01% thimerosal.
Handling The antibody solution should be gently mixed before use.
Reconstitution & Storage -20 °C
Background Descriptions
PrecautionsASC/TMS1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Synonyms ASC, CARD5, TMS1
Function Functions as key mediator in apoptosis and inflammation. Promotes caspase-mediated apoptosis involving predominantly caspase-8 and also caspase-9 in a probable cell type-specific manner. Involved in activation of the mitochondrial apoptotic pathway, promotes caspase-8-dependent proteolytic maturation of BID independently of FADD in certain cell types and also mediates mitochondrial translocation of BAX and activates BAX-dependent apoptosis coupled to activation of caspase-9, -2 and -3. Involved in macrophage pyroptosis, a caspase-1-dependent inflammatory form of cell death and is the major constituent of the ASC pyroptosome which forms upon potassium depletion and rapidly recruits and activates caspase-1. In innate immune response believed to act as an integral adapter in the assembly of the inflammasome which activates caspase-1 leading to processing and secretion of proinflammatory cytokines. The function as activating adapter in different types of inflammasomes is mediated by the DAPIN and CARD domains and their homotypic interactions. Required for recruitment of caspase-1 to inflammasomes containing certain pattern recognition receptors, such as NLRP2, NLRP3, AIM2 and probably IFI16. In the NLRP1 and NLRC4 inflammasomes seems not be required but facilitates the processing of procaspase-1. In cooperation with NOD2 involved in an inflammasome activated by bacterial muramyl dipeptide leading to caspase-1 activation. May be involved in DDX58-triggered proinflammatory responses and inflammasome activation. Isoform 2 may have a regulating effect on the function as inflammasome adapter. Isoform 3 seems to inhibit inflammasome- mediated maturation of interleukin-1 beta. In collaboration with AIM2 which detects cytosolic double-stranded DNA may also be involved in a caspase-1-independent cell death that involves caspase-8. In adaptive immunity may be involved in maturation of dendritic cells to stimulate T-cell immunity and in cytoskeletal rearrangements coupled to chemotaxis and antigen uptake may be involved in post-transcriptional regulation of the guanine nucleotide exchange factor DOCK2; the latter function is proposed to involve the nuclear form. Also involved in transcriptional activation of cytokines and chemokines independent of the inflammasome; this function may involve AP-1, NF-kappa-B, MAPK and caspase-8 signaling pathways. For regulation of NF-kappa-B activating and inhibiting functions have been reported. Modulates NF-kappa-B induction at the level of the IKK complex by inhibiting kinase activity of CHUK and IKBK. Proposed to compete with RIPK2 for association with CASP1 thereby down-regulating CASP1-mediated RIPK2-dependent NF-kappa-B activation and activating interleukin-1 beta processing.
Cellular Location Cytoplasm. Endoplasmic reticulum. Mitochondrion. Nucleus. Note=Upstream of caspase activation, a redistribution from the cytoplasm to the aggregates occurs. These appear as hollow, perinuclear spherical, ball-like structures Upon NLRP3 inflammasome activation redistributes to the perinuclear space localizing to endoplasmic reticulum and mitochondria. Localized primarily to the nucleus in resting monocytes/macrophages and rapidly redistributed to the cytoplasm upon pathogen infection. Localized to large cytoplasmic aggregate appearing as a speck containing AIM2, PYCARD, CASP8 and bacterial DNA after infection with Francisella tularensis (By similarity)
Tissue Location Widely expressed at low levels. Detected in peripheral blood leukocytes, lung, small intestine, spleen, thymus, colon and at lower levels in placenta, liver and kidney Very low expression in skeletal muscle, heart and brain. Detected in the leukemia cell lines HL-60 and U-937, but not in Jurkat T- cell lymphoma and Daudi Burkitt's lymphoma. Detected in the melanoma cell line WM35, but not in WM793. Not detected in HeLa cervical carcinoma cells and MOLT-4 lymphocytic leukemia cells
Research Areas
Citations (0)

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ASC (also called TMS1) is a CARD domain containing protein. ASC induces apoptosis thro µgh activation of caspase-9 and inhibiting the survival of human breast cancer cells. Overexpression of ASC/TMS1 induced DNA fragmentation. ASC/TMS1 is expressed in a variety of human and mouse tissues.

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$ 245.00
Cat# ABV10227
(40 western blots)
Availability: 5-7days
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