COPS5 (8q13.1)
- Also known as
- CSN5; JAB1; SGN5; MOV-34
- Summary
- The protein encoded by this gene is one of the eight subunits of COP9 signalosome, a highly conserved protein complex that functions as an important regulator in multiple signaling pathways. The structure and function of COP9 signalosome is similar to that of the 19S regulatory particle of 26S proteasome. COP9 signalosome has been shown to interact with SCF-type E3 ubiquitin ligases and act as a positive regulator of E3 ubiquitin ligases. This protein is reported to be involved in the degradation of cyclin-dependent kinase inhibitor CDKN1B/p27Kip1. It is also known to be an coactivator that increases the specificity of JUN/AP1 transcription factors. [provided by RefSeq, Jul 2008]
- Expression
- Ubiquitous expression in testis (RPKM 37.3), heart (RPKM 32.6) and 25 other tissues See more
- CSN5/JAB1 suppresses the WNT inhibitor DKK1 in colorectal cancer cells. Jumpertz S, et al. Cell Signal, 2017 Jun. PMID 28229932
- Oxidized LDL-induced JAB1 influences NF-κB independent inflammatory signaling in human macrophages during foam cell formation. Schwarz A, et al. J Biomed Sci, 2017 Feb 7. PMID 28173800, Free PMC Article
- Jab1 promotes glioma cell proliferation by regulating Siah1/β-catenin pathway. Zhu Y, et al. J Neurooncol, 2017 Jan. PMID 27640199
- JAB1 accelerates odontogenic differentiation of dental pulp stem cells. Lian M, et al. J Mol Histol, 2016 Jun. PMID 26989054
- Suppression of CSN5 promotes the apoptosis of gastric cancer cells through regulating p53-related apoptotic pathways. Sang MM, et al. Bioorg Med Chem Lett, 2015 Aug 1. PMID 26048783
GeneRIFs: Gene References Into FunctionsWhat's a GeneRIF?
- We identified a novel Jab1-Trx axis that is a key cellular process in the pathobiologic characteristics of acute myeloid leukemia (AML-M5). Targeting the ROS/Jab1/Trx pathway could be beneficial in the treatment of AML-M5
- These data identified CSN5 as a critical oncoprotein involved in progression of hepatocellular carcinoma (HCC) cells, which could serve as a potential therapeutic target in HCC patients.
- The authors find that UCHL3 regulates COPS5-dependent deneddylation of Cullin1, which is an essential component of SCF(beta-TrCP) complex and associated with SCF(beta-TrCP) activities. The authors further demonstrate that UCHL3 upregulates the levels of SCF(beta-TrCP) substrates including IFN-I receptor IFNAR1, which enhances IFN-I mediated signaling pathway and antiviral activity.
- Collectively, our findings suggest that JAB1 activates the neuronal differentiation ability of CPNE1 through the binding of C2A domain in CPNE1 with MPN domain in JAB1.
- data suggests that Jab1-mediated phosphorylation of p53 at Thr155 residue mediates nuclear export of p53
- CSN5 is contributed to colorectal cancer development by actively driving aberrant WNT signaling through repression of the WNT antagonist DKK1.
- The results of this study suggest that Jab1 promotes glioma cell proliferation and increased expression of Jab1 in glioma patients may amplify beta-catenin signaling to contribute to glioma cell proliferation.
- Furthermore, inhibition of COPS5 resulted in an elevation of Akt expression and sensitized SOC cells to Akt inhibitor MK2206. Suppression of COPS5 and Akt offers a potential strategy for the treatment of SOC.
- The data identified CSN5 as a critical oncoprotein involved in migration and invasion of RCC cells, which could serve as a potential therapeutic target in RCC patients.
- High JAB1 expression is associated with nasopharyngeal cancer.
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