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RIPK3 Antibody
Purified Mouse Monoclonal Antibody (Mab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q9Y572 |
| Reactivity | Human |
| Predicted | Human |
| Host | Mouse |
| Clonality | monoclonal |
| Isotype | IgG1,κ |
| Clone/Animal Names | 2013CT892.86.49 |
| Calculated MW | 56887 Da |
| 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~~1:1000 |
| 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. |
| Storage | Maintain 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. |
| Precautions | RIPK3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| 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 |
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Provided below are standard protocols that you may find useful for product applications.
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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