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RIPK3 / RIP3 Antibody (aa480-530)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P |
|---|---|
| Primary Accession | Q9Y572 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 57kDa |
| Dilution | IHC-P (10 µg/ml), WB (1-3 µg/ml), |
| 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 | A portion of amino acids 480-518 of human RIP3 |
| Reconstitution & Storage | Short term 4°C, long term aliquot and store at -20°C, avoid freeze thaw cycles. |
| Precautions | RIPK3 / RIP3 Antibody (aa480-530) 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 |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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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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