Anti-RIPK3 Antibody
Rabbit polyclonal antibody to RIPK3
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB |
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Primary Accession | Q9Y572 |
Other Accession | Q9QZL0 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Calculated MW | 56887 Da |
Gene ID | 11035 |
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Other Names | RIP3; Receptor-interacting serine/threonine-protein kinase 3; RIP-like protein kinase 3; Receptor-interacting protein 3; RIP-3 |
Target/Specificity | Recognizes endogenous levels of RIPK3 protein. |
Dilution | WB~~WB (1/500 - 1/1000) |
Format | Liquid in 0.42% Potassium phosphate, 0.87% Sodium chloride, pH 7.3, 30% glycerol, and 0.09% (W/V) sodium azide. |
Storage | Store at -20 °C.Stable for 12 months from date of receipt |
Name | RIPK3 (HGNC:10021) |
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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
KLH-conjugated synthetic peptide encompassing a sequence within the center region of human RIPK3. The exact sequence is proprietary.
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