|Other Accession||Q9JMA1, Q0IIF7, NP_005142.1|
|Other Names||Ubiquitin carboxyl-terminal hydrolase 14, Deubiquitinating enzyme 14, Ubiquitin thioesterase 14, Ubiquitin-specific-processing protease 14, USP14, TGT|
|Target/Specificity||The synthetic peptide sequence is selected from aa 370-383 of HUMAN USP14|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI 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||Proteasome-associated deubiquitinase which releases ubiquitin from the proteasome targeted ubiquitinated proteins. Ensures the regeneration of ubiquitin at the proteasome. Is a reversibly associated subunit of the proteasome and a large fraction of proteasome-free protein exists within the cell. Required for the degradation of the chemokine receptor CXCR4 which is critical for CXCL12-induced cell chemotaxis. Serves also as a physiological inhibitor of endoplasmic reticulum-associated degradation (ERAD) under the non-stressed condition by inhibiting the degradation of unfolded endoplasmic reticulum proteins via interaction with ERN1. Indispensable for synaptic development and function at neuromuscular junctions (NMJs).|
|Cellular Location||Cytoplasm. Cell membrane; Peripheral membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
This gene encodes a member of the ubiquitin-specific processing (UBP) family of proteases that is a deubiquitinating enzyme (DUB) with His and Cys domains. This protein is located in the cytoplasm and cleaves the ubiquitin moiety from ubiquitin-fused precursors and ubiquitinylated proteins. Mice with a mutation that results in reduced expression of the ortholog of this protein are retarded for growth, develop severe tremors by 2 to 3 weeks of age followed by hindlimb paralysis and death by 6 to 10 weeks of age. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
Davila, S., et al. Genes Immun. 11(3):232-238(2010)
Chen, P.C., et al. J. Neurosci. 29(35):10909-10919(2009)
Mines, M.A., et al. J. Biol. Chem. 284(9):5742-5752(2009)
Nagai, A., et al. Biochem. Biophys. Res. Commun. 379(4):995-1000(2009)
Koulich, E., et al. Mol. Biol. Cell 19(3):1072-1082(2008)
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