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hRIP3 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q9Y572 |
| Other Accession | Q9Y572 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Clone Names | Ripk3 |
| Calculated MW | Predicted: 57kD Observed: 57 kD |
| Gene ID | 11035 |
|---|---|
| Alias Symbol | Ripk3 |
| Other Names | hRIP3 Antibody: Rip3, AW107945, 2610528K09Rik, RIP-like protein kinase 3, RIP-3 |
| Target/Specificity | Several isoforms of hRIP3 are known to exist. |
| Reconstitution & Storage | hRIP3 antibody can be stored at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | hRIP3 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
hRIP3 Antibody: Certain serine/threonine protein kinases, such as ASK1, RIP, DAP, and ZIP kinases, are mediators of apoptosis. Receptor interacting proteins including RIP and RIP2/RICK mediate apoptosis induced by TNFR1 and Fas, two prototype members in the death receptor family. A novel member in the RIP kinase family was recently identified and designated RIP3. RIP3 contains N-terminal kinase domain but, unlike RIP or RIP2, lacks the C-terminal death or CARD domain. RIP3 binds to RIP and TNFR1, mediates TNFR1 induced apoptosis, and attenuates RIP and TNFR1 induced NF-κB activation. Overexpression of RIP3 induces apoptosis and NF-κB activation. The messenger RNA of RIP3 is expressed in a subset of adult tissues.
References
Yu et al. Curr Biol. 1999;9(10):539-42. Sun et al. J Biol Chem. 1999;274(24):16871-5. Pazdernik et al. Mol Cell Bio. 1999; 19(10):6500-8 (WD0102)
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