Phospho-RIP3 (Ser232) Antibody (YA9807)
(Synonyms: Receptor interacting protein 3; Receptor interacting serine threonine kinase 3; Receptor interacting serine/threonine protein kinase 3; Receptor-interacting protein 3; Receptor-interacting serine/threonine-protein kinase 3; RIP 3; RIP like protein kinase 3; RIP-3; RIP-like protein kinase 3; RIPK 3)
Based on 1 Customer Validation
Phospho-RIP3 (Ser232) Antibody (YA9807) is a Rabbit-derived and non-conjugated IgG Recombinant, Monoclonal antibody, targeting to Phospho-RIP3 (Ser232).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF
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Reactivity :
Mouse, Rat
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Formulation:
Supplied in TBS (pH7.4), 0.05% BSA, 40% Glycerol, 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
|---|---|---|
| Dilution Ratio | 1:1000 | 1:100 |
Product Details
Phospho-RIP3 (Ser232) Antibody (YA9807) is a Rabbit-derived and non-conjugated IgG Recombinant, Monoclonal antibody, targeting to Phospho-RIP3 (Ser232).
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Host Rabbit
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Species ReactivityMouse, Rat
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Calculated Molecular Weight Predicted band size: 53 kDa
Synthetic phospho-peptide corresponding to residues surrounding Ser232 of Human RIP3.
Endogenous
affinity purified
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in TBS (pH7.4), 0.05% BSA, 40% Glycerol, 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
RIP3 is a 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 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 (By similarity). In some cell types, also able to restrict viral replication by promoting cell death-independent responses. 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. 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 (By similarity). These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production (By similarity)[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17].
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Subcellular Localization
Cytoplasm, cytosol; Nucleus
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Expression
Tissue_Specificity: Expressed in embryo and in adult spleen, liver, testis, heart, brain and lung. -
Isoforms & Post-Translational Modification
Phospho-RIP3 has an amino acid length of 486, molecular weight is 53322 Da.
Autophosphorylated following interaction with ZBP1. Phosphorylation of Ser-204 plays a role in the necroptotic function of RIPK3 (By similarity). Autophosphorylates at Thr-231 and Ser-232 following activation by ZBP1: phosphorylation at these sites is a hallmark of necroptosis and is required for binding MLKL. -
Subunit
Interacts (via RIP homotypic interaction motif) with RIPK1 (via RIP homotypic interaction motif); this interaction induces RIPK1 phosphorylation and formation of a RIPK1-RIPK3 necrosis-inducing complex.
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SwissProt ID
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Synonyms
Receptor interacting protein 3; Receptor interacting serine threonine kinase 3; Receptor interacting serine/threonine protein kinase 3; Receptor-interacting protein 3; Receptor-interacting serine/threonine-protein kinase 3; RIP 3; RIP like protein kinase 3; RIP-3; RIP-like protein kinase 3; RIPK 3
Documentation
References
[1]. Nogusa S, et al. RIPK3 Activates Parallel Pathways of MLKL-Driven Necroptosis and FADD-Mediated Apoptosis to Protect against Influenza A Virus. Cell Host Microbe. 2016 Jul 13;20(1):13-24. [Content Brief]
[2]. Thapa RJ, et al. DAI Senses Influenza A Virus Genomic RNA and Activates RIPK3-Dependent Cell Death. Cell Host Microbe. 2016 Nov 9;20(5):674-681. [Content Brief]
[3]. Kuriakose T, et al. ZBP1/DAI is an innate sensor of influenza virus triggering the NLRP3 inflammasome and programmed cell death pathways. Sci Immunol. 2016 Aug 5;1(2):. [Content Brief]
[4]. Sridharan H, et al. Murine cytomegalovirus IE3-dependent transcription is required for DAI/ZBP1-mediated necroptosis. EMBO Rep. 2017 Aug;18(8):1429-1441. [Content Brief]
[5]. Zhang T, et al. Influenza Virus Z-RNAs Induce ZBP1-Mediated Necroptosis. Cell. 2020 Mar 19;180(6):1115-1129.e13. [Content Brief]
[6]. Jiao H, et al. Z-nucleic-acid sensing triggers ZBP1-dependent necroptosis and inflammation. Nature. 2020 Apr;580(7803):391-395. [Content Brief]
[7]. Rebsamen M, et al. DAI/ZBP1 recruits RIP1 and RIP3 through RIP homotypic interaction motifs to activate NF-kappaB. EMBO Rep. 2009 Aug;10(8):916-22. [Content Brief]
[8]. Upton JW, et al. DAI/ZBP1/DLM-1 complexes with RIP3 to mediate virus-induced programmed necrosis that is targeted by murine cytomegalovirus vIRA. Cell Host Microbe. 2012 Mar 15;11(3):290-7. [Content Brief]
[9]. Murphy JM, et al. The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism. Immunity. 2013 Sep 19;39(3):443-53. [Content Brief]
[10]. Kaiser WJ, et al. Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. J Biol Chem. 2013 Oct 25;288(43):31268-79. [Content Brief]
[11]. Xie T, et al. Structural insights into RIP3-mediated necroptotic signaling. Cell Rep. 2013 Oct 17;5(1):70-8. [Content Brief]
[12]. Newton K, et al. Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis. Science. 2014 Mar 21;343(6177):1357-60. [Content Brief]
[13]. Lin J, et al. RIPK1 counteracts ZBP1-mediated necroptosis to inhibit inflammation. Nature. 2016 Dec 1;540(7631):124-128. [Content Brief]
[14]. Newton K, et al. RIPK1 inhibits ZBP1-driven necroptosis during development. Nature. 2016 Dec 1;540(7631):129-133. [Content Brief]
[15]. Rickard JA, et al. RIPK1 regulates RIPK3-MLKL-driven systemic inflammation and emergency hematopoiesis. Cell. 2014 May 22;157(5):1175-88. [Content Brief]
[16]. Dillon CP, et al. RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3. Cell. 2014 May 22;157(5):1189-202. [Content Brief]
[17]. Daniels BP, et al. The Nucleotide Sensor ZBP1 and Kinase RIPK3 Induce the Enzyme IRG1 to Promote an Antiviral Metabolic State in Neurons. Immunity. 2019 Jan 15;50(1):64-76.e4. [Content Brief]
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