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Rabbit Anti-PYCARD Polyclonal Antibody#abs135824

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Description

Catalog-specification	Delivery time	USD price
abs135824-100ug	1-2 Weeks	301.0
abs135824-50ug	1-2 Weeks	201.0

Overview
catalog	abs135824
Description	TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD) is a pro-apoptotic protein comprising a pyrin domain (PYD) at the N-terminus and a caspase recruitment domain (CARD) at the C-terminus. It is also known as CARD5 or PYCARD, and has a molecular weight of 22 kDa. In breast cancer cells, TMS1 was first discovered to be silenced due to methylation (2), and it is also silenced in other types of cancers such as ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). The expression of TMS1 can be stimulated by pro-apoptotic and inflammatory factors (9). When apoptosis occurs, TMS1 is translocated from the cytosol to the mitochondria where it interacts with mitochondrial Bax to promote the release of cytochrome c and subsequent apoptosis (10). Moreover, TMS1 acts as a crucial component of inflammatory signaling by binding to and activating caspase-1 in response to pro-inflammatory signals (11).
Other names	The Apoptosis-associated speck-like protein containing a CARD, also known as ASC, is a protein in humans encoded by the PYCARD gene. It is involved in the process of programmed cell death, or apoptosis, and is responsible for recruiting the proteins necessary for the activation of caspases, which execute apoptosis. In addition to its role in apoptosis, ASC has been shown to be involved in multiple other cellular processes and pathways, including inflammation and immune response regulation. It contains both a PYD domain and a CARD domain, which are crucial for its function. In some studies, ASC has been implicated in various diseases, including cancer, neurodegenerative disorders, and inflammatory diseases. The protein is also referred to as TMS1 or Target of Methylation Induced Silencing 1.
Source	Rabbit
Specificity	Endogenous levels of total PYCARD can be accurately detected by using the PYCARD Antibody. This antibody is specifically designed to detect the total amount of PYCARD present naturally in a sample. With this antibody, you can be assured of reliable and accurate results in your experiments. Whether you are examining PYCARD expression or studying its biological functions, the PYCARD Antibody is an invaluable tool for your research. Don't settle for less, get the best antibody for PYCARD detection - the PYCARD Antibody.
Species Reactivity	Human;Mouse;Rat
Predictive reaction species	Sheep;Bovine;
Antigen	PYCARD
Application	For Western Blotting, the recommended dilution range is between 1:500 to 1:2000. When it comes to Immunohistochemistry, the ideal dilution factor falls between 1:50 to 1:200. For Immunofluorescence or Immunocytochemistry, you can use a dilution range of 1:100 to 1:500. Finally, for ELISA that involves peptide analysis, a dilution factor of 1:20000 to 1:40000 is generally recommended. To paraphrase the information provided above, the dilution range recommended for Western Blotting ranges from 1:500 to 1:2000, while the ideal dilution for Immunohistochemistry ranges from 1:50 to 1:200. For Immunofluorescence or Immunocytochemistry, a dilution range of 1:100 to 1:500 is advised. For ELISA using peptide analysis, the recommended dilution range is 1:20000 to 1:40000.
Immunogen	A synthesized peptide derived from human PYCARD.
MW	25kDa
Properties
Concentration	1mg/ml
purification	The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin .
Clonality	Polyclonal Antibody
Stability & Storage	Store at -20 °C for one year. Avoid repeated freeze/thaw cycles
Storage buffer	Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt.
Target
Background	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 pyrin 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. Modulates host resistance to DNA virus infection, probably by inducing the cleavage of and inactivating MB21D1 in presence of cytoplasmic double-stranded DNA (PubMed:28314590).
Tissue specificity	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.
Posttranslational modification	Phosphorylated.
Celluar localization	Cytosol;Endoplasmic reticulum;Extracellular region or secreted;Lysosome;Mitochondrion;Nucleus;
UniPort	Q9ULZ3