COP9 constitutive photomorphogenic homolog subunit 5

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COP9 signalosome subunit 5
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols COPS5 ; CSN5; JAB1; MOV-34; SGN5
External IDs OMIM604850 MGI1349415 HomoloGene55992 GeneCards: COPS5 Gene
RNA expression pattern
PBB GE COPS5 201652 at tn.png
PBB GE COPS5 gnf1h08492 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 10987 26754
Ensembl ENSG00000121022 ENSMUSG00000025917
UniProt Q92905 O35864
RefSeq (mRNA) NM_006837 NM_001277101
RefSeq (protein) NP_006828 NP_001264030
Location (UCSC) Chr 8:
67.96 – 68 Mb
Chr 1:
10.02 – 10.04 Mb
PubMed search [1] [2]

COP9 constitutive photomorphogenic homolog subunit 5 (Arabidopsis), also known as COPS5 or Csn5, is a gene conserved from humans to Saccharomyces cerevisiae.[1]

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 a coactivator that increases the specificity of JUN/AP1 transcription factors.[1]

Interactions[edit]

COP9 constitutive photomorphogenic homolog subunit 5 has been shown to interact with Macrophage migration inhibitory factor,[2] GFER,[3] BCL3,[4] Ubiquitin carboxy-terminal hydrolase L1,[5] S100A7[6] and C-jun.[7]

See also[edit]

References[edit]

  1. ^ a b "Entrez Gene: COPS5 COP9 constitutive photomorphogenic homolog subunit 5 (Arabidopsis)". 
  2. ^ Kleemann, R; Hausser A, Geiger G, Mischke R, Burger-Kentischer A, Flieger O, Johannes F J, Roger T, Calandra T, Kapurniotu A, Grell M, Finkelmeier D, Brunner H, Bernhagen J (November 2000). "Intracellular action of the cytokine MIF to modulate AP-1 activity and the cell cycle through Jab1". Nature (ENGLAND) 408 (6809): 211–6. doi:10.1038/35041591. ISSN 0028-0836. PMID 11089976. 
  3. ^ Lu, Chengrong; Li Yong, Zhao Yanlin, Xing Guichin, Tang Fei, Wang Qingming, Sun Yuhui, Wei Handong, Yang Xiaoming, Wu Chutse, Chen Jianguo, Guan Kun-Liang, Zhang Chenggang, Chen Huipeng, He Fuchu (January 2002). "Intracrine hepatopoietin potentiates AP-1 activity through JAB1 independent of MAPK pathway". FASEB J. (United States) 16 (1): 90–2. doi:10.1096/fj.01-0506fje. PMID 11709497. 
  4. ^ Dechend, R; Hirano F; Lehmann K; Heissmeyer V; Ansieau S; Wulczyn F G; Scheidereit C; Leutz A (June 1999). "The Bcl-3 oncoprotein acts as a bridging factor between NF-kappaB/Rel and nuclear co-regulators". Oncogene (ENGLAND) 18 (22): 3316–23. doi:10.1038/sj.onc.1202717. ISSN 0950-9232. PMID 10362352. 
  5. ^ Caballero, Otávia L; Resto Vicente; Patturajan Meera; Meerzaman Daoud; Guo Ming Zhou; Engles James; Yochem Robert; Ratovitski Edward; Sidransky David; Jen Jin (May 2002). "Interaction and colocalization of PGP9.5 with JAB1 and p27(Kip1)". Oncogene (England) 21 (19): 3003–10. doi:10.1038/sj.onc.1205390. ISSN 0950-9232. PMID 12082530. 
  6. ^ Emberley, Ethan D; Niu Yulian; Leygue Etienne; Tomes Ladislav; Gietz R Daniel; Murphy Leigh C; Watson Peter H (April 2003). "Psoriasin interacts with Jab1 and influences breast cancer progression". Cancer Res. (United States) 63 (8): 1954–61. ISSN 0008-5472. PMID 12702588. 
  7. ^ Claret, F X; Hibi M; Dhut S; Toda T; Karin M (October 1996). "A new group of conserved coactivators that increase the specificity of AP-1 transcription factors". Nature (ENGLAND) 383 (6599): 453–7. doi:10.1038/383453a0. ISSN 0028-0836. PMID 8837781. 

Further reading[edit]