|Other Names||Receptor-interacting serine/threonine-protein kinase 3, RIP-like protein kinase 3, Receptor-interacting protein 3, RIP-3, RIPK3, RIP3|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7819b was selected from the C-term region of human RIPK3 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Essential for necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members. Upon induction of necrosis, RIPK3 interacts with, and phosphorylates RIPK1 and MLKL to form a necrosis-inducing complex. 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.|
|Cellular Location||Cytoplasm, cytosol. Cell membrane Mitochondrion|
|Tissue Location||Highly expressed in the pancreas. Detected at lower levels in heart, placenta, lung and kidney. Isoform 3 is significantly increased in colon and lung cancers|
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Provided below are standard protocols that you may find useful for product applications.
RIPK3 is a member of the receptor-interacting protein (RIP) family of serine/threonine protein kinases, and contains a C-terminal domain unique from other RIP family members. The encoded protein is predominantly localized to the cytoplasm, and can undergo nucleocytoplasmic shuttling dependent on novel nuclear localization and export signals. It is a component of the tumor necrosis factor (TNF) receptor-I signaling complex, and can induce apoptosis and weakly activate the NF-kappaB transcription factor.
Yu, P.W., et al., Curr. Biol. 9(10):539-542 (1999).Sun, X., et al., J. Biol. Chem. 274(24):16871-16875 (1999).
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