Anti-RIPK3 antibody (468-518) {FITC} (STJ502809)

SKU:
STJ502809-100

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Host: Rabbit
Applications: ELISA/IP/WB
Reactivity: Bovine/Human/Monkey/Pig
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Rabbit polyclonal antibody anti-RIPK3 (468-518) is suitable for use in ELISA, Immunoprecipitation and Western Blot research applications.
Clonality: Polyclonal
Conjugation: FITC
Isotype: IgG
Purification: Affinity Purified
Concentration: 0.66-0.68 µg/µl
Dilution Range: WB: 1:500
DB: 1:10, 000
ELISA: 1:10, 000
IP: 1:200
Storage Instruction: Store at-20°C for long term storage. Avoid freeze-thaw cycles.
Gene Symbol: RIPK3
Gene ID: 11035
Uniprot ID: RIPK3_HUMAN
Immunogen Region: 468-518
Immunogen: Synthetic peptide taken within amino acid region 468-518 on human Receptor-interacting Serine/Threonine-protein kinase 3 protein.
Tissue Specificity Highly expressed in the pancreas. Detected at lower levels in heart, placenta, lung and kidney. Isoform 3: Expression is significantly increased in colon and lung cancers.
Post Translational Modifications (Microbial infection) Proteolytically cleaved by S.flexneri OspD3 within the RIP homotypic interaction motif (RHIM), leading to its degradation and inhibition of necroptosis. RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation. Autophosphorylated following interaction with ZBP1. Phosphorylation of Ser-199 plays a role in the necroptotic function of RIPK3. Autophosphorylates at Ser-227 following activation by ZBP1: phosphorylation at these sites is a hallmark of necroptosis and is required for binding MLKL. Phosphorylation at Thr-182 is important for its kinase activity, interaction with PELI1 and PELI1-mediated 'Lys-48'-linked polyubiquitination and for its ability to mediate TNF-induced necroptosis. Polyubiquitinated with 'Lys-48' and 'Lys-63'-linked chains by BIRC2/c-IAP1 and BIRC3/c-IAP2, leading to activation of NF-kappa-B. Polyubiquitinated with 'Lys-48'-linked chains by PELI1 leading to its subsequent proteasome-dependent degradation. Ubiquitinated by STUB1 leading to its subsequent proteasome-dependent degradation.
Function Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death. Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1. 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. 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. Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity. Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation. In some cell types, also able to restrict viral replication by promoting cell death-independent responses. 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. Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes. 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. (Microbial infection) In case of herpes simplex virus 1/HHV-1 infection, forms heteromeric amyloid structures with HHV-1 protein RIR1/ICP6 which may inhibit RIPK3-mediated necroptosis, thereby preventing host cell death pathway and allowing viral evasion.
Protein Name Receptor-Interacting Serine/Threonine-Protein Kinase 3
Rip-Like Protein Kinase 3
Receptor-Interacting Protein 3
Rip-3
Database Links Reactome: R-HSA-168927
Reactome: R-HSA-1810476
Reactome: R-HSA-2562578
Reactome: R-HSA-3295583
Reactome: R-HSA-5213460
Reactome: R-HSA-5675482
Reactome: R-HSA-9013957
Reactome: R-HSA-937041
Reactome: R-HSA-9686347
Reactome: R-HSA-9692913
Reactome: R-HSA-9692916
Cellular Localisation Cytoplasm
Cytosol
Nucleus
Mainly Cytoplasmic
Present In The Nucleus In Response To Influenza A Virus (Iav) Infection
Alternative Antibody Names Anti-Receptor-Interacting Serine/Threonine-Protein Kinase 3 antibody
Anti-Rip-Like Protein Kinase 3 antibody
Anti-Receptor-Interacting Protein 3 antibody
Anti-Rip-3 antibody
Anti-RIPK3 antibody
Anti-RIP3 antibody

Information sourced from Uniprot.org

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