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>   首页   >   产品   >   一抗   >   细胞生物学   >   RIPK3 Antibody   

RIPK3 Antibody

Purified Mouse Monoclonal Antibody (Mab)

     
  • 1 - RIPK3 Antibody AM8682b
    All lanes: Anti-RIPK3 Antibody at 1:2000 dilution Lane 1: HT-29 whole cell lysate Lane 2: K562 whole cell lysate Lysates/proteins at 20 µg per lane. Secondary: Goat Anti-Mouse IgG, (H+L), Peroxidase conjugated (ASP1613) at 1/8000 dilution. Observed band size: 46-62 KDa Blocking/Dilution buffer: 5% NFDM/TBST.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession Q9Y572
Reactivity Human
Predicted Human
Host Mouse
Clonality monoclonal
Isotype IgG1,κ
Clone Names 2013CT892.86.49
Calculated MW 56887 Da
Additional Information
Gene ID 11035
Other Names Receptor-interacting serine/threonine-protein kinase 3, 2.7.11.1, RIP-like protein kinase 3, Receptor-interacting protein 3, RIP-3, RIPK3, RIP3
Target/Specificity This RIPK3 antibody is generated from a mouse immunized with a recombinate protein from the human region of human RIPK3.
Dilution WB~~1:2000
E~~Use at an assay dependent concentration.
Format Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, followed by dialysis against PBS.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsRIPK3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name RIPK3 (HGNC:10021)
Function Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death (PubMed:19524512, PubMed:19524513, PubMed:22265413, PubMed:22265414, PubMed:22421439, PubMed:29883609, PubMed:32657447). Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1 (PubMed:19524512, PubMed:19524513, PubMed:22265413, PubMed:22265414, PubMed:22421439, PubMed:29883609, PubMed:32298652). Activated RIPK3 forms a necrosis- inducing complex and mediates phosphorylation of MLKL, promoting MLKL localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage (PubMed:19524512, PubMed:19524513, PubMed:22265413, PubMed:22265414, PubMed:22421439, PubMed:25316792, PubMed:29883609). In addition to TNF- induced necroptosis, necroptosis can also take place in the nucleus in response to orthomyxoviruses infection: following ZBP1 activation, which senses double-stranded Z-RNA structures, nuclear RIPK3 catalyzes phosphorylation and activation of MLKL, promoting disruption of the nuclear envelope and leakage of cellular DNA into the cytosol (By similarity). Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity (By similarity). Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation (PubMed:19524513). In some cell types, also able to restrict viral replication by promoting cell death- independent responses (By similarity). In response to Zika virus infection in neurons, promotes a cell death-independent pathway that restricts viral replication: together with ZBP1, promotes a death- independent transcriptional program that modifies the cellular metabolism via up-regulation expression of the enzyme ACOD1/IRG1 and production of the metabolite itaconate (By similarity). Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes (By similarity). RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL (PubMed:19498109). These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production (PubMed:19498109).
Cellular Location Cytoplasm, cytosol. Nucleus {ECO:0000250|UniProtKB:Q9QZL0}. Note=Mainly cytoplasmic Present in the nucleus in response to influenza A virus (IAV) infection. {ECO:0000250|UniProtKB:Q9QZL0}
Tissue Location Highly expressed in the pancreas. Detected at lower levels in heart, placenta, lung and kidney
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

Essential for necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members. Upon induction of necrosis, RIPK3 interacts with, and phosphorylates RIPK1 and MLKL to form a necrosis-inducing complex. RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL. These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production.

REFERENCES

Yu P.W.,et al.Curr. Biol. 9:539-542(1999).
Sun X.,et al.J. Biol. Chem. 274:16871-16875(1999).
Yang Y.,et al.Biochem. Biophys. Res. Commun. 332:181-187(2005).
Heilig R.,et al.Nature 421:601-607(2003).
Ota T.,et al.Nat. Genet. 36:40-45(2004).

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