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RIP3 Antibody
- SPECIFICATION
- CITATIONS: 2
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q9QZL0 |
| Other Accession | AAF03133, 6063101 |
| Reactivity | Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 57 kDa |
| Application Notes | RIP3 antibody can be used for detection of RIP3 by Western blot at 1 µg/mL. An approximately 57 kDa band can be detected. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 56532 |
|---|---|
| Other Names | RIP3 Antibody: Rip3, AW107945, 2610528K09Rik, Rip3, RIP-like protein kinase 3, RIP-3, receptor-interacting serine-threonine kinase 3 |
| Target/Specificity | Ripk3; |
| Reconstitution & Storage | Antibody can be stored at 4°C up to one year. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | RIP3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | Ripk3 {ECO:0000303|PubMed:27321907, ECO:0000312|MGI:MGI:2154952} |
|---|---|
| Function | Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death (PubMed:27321907, PubMed:27746097, PubMed:27917412, PubMed:28607035, PubMed:32200799, PubMed:32296175). Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1 (PubMed:19590578, PubMed:22423968, PubMed:24012422, PubMed:24019532, PubMed:24557836, PubMed:27746097, PubMed:27819681, PubMed:27819682, PubMed:24095729, PubMed:32200799, PubMed:27321907, PubMed:32296175). 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:24813849, PubMed:24813850, PubMed:27321907). 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 (PubMed:32200799, PubMed:32296175). Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity (PubMed:27321907). Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation (By similarity). In some cell types, also able to restrict viral replication by promoting cell death-independent responses (PubMed:30635240). In response to flavivirus 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 (PubMed:30635240). Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes (PubMed:30635240). RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL (By similarity). These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production (By similarity). |
| Cellular Location | Cytoplasm, cytosol. Nucleus. Note=Mainly cytoplasmic (PubMed:32200799, PubMed:32296175). Present in the nucleus in response to influenza A virus (IAV) infection (PubMed:32200799). |
| Tissue Location | Expressed in embryo and in adult spleen, liver, testis, heart, brain and lung. |
Provided below are standard protocols that you may find useful for product applications.
Background
RIP3 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 PW, Huang BC, Shen M, Quast J, Chan E, Xu X, Nolan GP, Payan DG, Luo Y. Identification of RIP3, a RIP-like kinase that activates apoptosis and NFκB. Curr Biol. 1999;9(10):539-42.
Sun X, Lee J, Navas T, Baldwin DT, Stewart TA, Dixit VM. RIP3, a novel apoptosis-inducing kinase. J Biol Chem. 1999;274(24):16871-5.
Pazdernik NJ, Donner DB, Goebl MG, Harrington MA. Mouse receptor interacting protein 3 does not contain a caspase-recruiting or a death domain but induces apoptosis and activates NF-κB. Mol Cell Bio. 1999; 19(10):6500-8 (WD0102)
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