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COP9 (show COPS8 Proteins) signalosome subunits 4 and 5 regulate multiple pleiotropic pathways in Drosophila melanogaster.
during oogenesis CSN5/JAB1, one subunit of the CSN, is required for meiotic progression and for establishment of both the AP and DV axes of the Drosophila oocyte
we link the CSN to the degradation of Cyclin E, which promotes the G1-S transition in the cell cycle and then is rapidly degraded by the ubiquitin-proteasome pathway
results presented here indicate that CSN5 is a negative regulator of Dorsal subcellular localization, and of hemocyte proliferation and differentiation
CSN3 (show CSN3 Proteins) and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 (show CCNB1 Proteins) and Securin (show PTTG1 Proteins) via APC (show APC Proteins)/C.
COPS5 overexpression reduced spinophilin (show PPP1R9B Proteins) in both the cortex (19%, p < 0.05) and the hippocampus (20%, p < 0.05), leading to significant deficits in learning and memory skills
Jab1 is an essential regulator of early embryonic limb development.
Lack of COPS5 in regenerating livers causes substantial replicative stress which triggers a cyclin-dependent kinase (show CDK1 Proteins) inhibitor(CDKN)2A genetic program leading to cell cycle arrest, polyploidy, and apoptosis.
Jab1 may transduce laminin211 signals to regulate Schwann cell number and differentiation during axonal sorting.
Study demonstrates that Jab1 represses chondrocyte hypertrophy in vivo, likely in part by downregulating BMP signaling and Runx2 (show RUNX2 Proteins) activity.
Data indicate that in Cul4b (show CUL4B Proteins)-deficient embryonic fibroblasts showed Jab1 accumulation.
CSN5 functions through CDK2 (show CDK2 Proteins) to control premature senescence in a novel way, depending on cyclin E (show CCNE1 Proteins) in the cytoplasm.
It was shown that disruption of CSN5 prevented the formation of tumors by p53 (show TP53 Proteins)-null cells that were transformed with an active form of Ras in subcutaneously injected mice. Depletion of CSN5 suppressed cell proliferation, and induced premature senescence.
These findings identify JAB1 as an important factor in checkpoint control during early B cell development, as well as in fate decisions in mature Ag-primed B cells.
The porcine JAB1 gene was cloned and characterized.
data suggests that Jab1-mediated phosphorylation of p53 (show TP53 Proteins) at Thr155 residue mediates nuclear export of p53 (show TP53 Proteins)
CSN5 is contributed to colorectal cancer development by actively driving aberrant WNT (show WNT2 Proteins) signaling through repression of the WNT (show WNT2 Proteins) antagonist DKK1 (show DKK1 Proteins).
The results of this study suggest that Jab1 promotes glioma cell proliferation and increased expression of Jab1 in glioma patients may amplify beta-catenin (show CTNNB1 Proteins) signaling to contribute to glioma cell proliferation.
Furthermore, inhibition of COPS5 resulted in an elevation of Akt (show AKT1 Proteins) expression and sensitized SOC (show UBXN11 Proteins) cells to Akt (show AKT1 Proteins) inhibitor MK2206. Suppression of COPS5 and Akt (show AKT1 Proteins) offers a potential strategy for the treatment of SOC (show UBXN11 Proteins).
The data identified CSN5 as a critical oncoprotein involved in migration and invasion of RCC (show XRCC1 Proteins) cells, which could serve as a potential therapeutic target in RCC (show XRCC1 Proteins) patients.
High JAB1 expression is associated with nasopharyngeal cancer.
oxLDL induces JAB1 expression and influences its cellular localization, whereby the p38 MAPK (show MAPK14 Proteins) signaling pathway is modified with consequences for inflammation of human MPhi in foam cells and atherosclerotic lesions.
We found that increased expression of JAB1 promoted odontogenic differentiation of DPSCs via Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling. The role of JAB1 in the odontogenic differentiation of DPSCs was further confirmed by knocking down JAB1. Our findings provide novel insights on odontogenic differentiation of DPSCs.
Copine3 binding to ErbB2 (show ERBB2 Proteins) increases when Jab1 is overexpressed in SKBr3 breast cancer cells. PI3 kinase (show PIK3CA Proteins) and AKT (show AKT1 Proteins) were also activated by Jab1 overexpression.Copine3 and Jab1 binding regulates the ErbB2 (show ERBB2 Proteins) signaling pathway.
The reverse correlation of Jab1 and Smad4 (show SMAD4 Proteins) in PANC-1 cells may be involved in the Pathogenesis of prostate cancer. Jab1 can cause degradation of Smad4 (show SMAD4 Proteins) via TGF-beta (show TGFB1 Proteins) signal pathway.
The work described here supports a previously unknown role for the CSN/COP9 (show COPS8 Proteins) signalosome in chromosome behavior during meiotic prophase I.
Data show that CSN-5 functions in muscle cells to regulate UNC-98 and -96, two M-line proteins.
KGB-1 and CSN-5 regulate GLH-1 levels, with GLH-1 targeted for proteosomal degradation by KGB-1 and stabilized by CSN-5.
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.
, COP9 complex subunit 5
, JUN activation domain-binding protein-1
, Jun activation domain binding protein
, drosophila COP9 signalosome homolog 5
, COP9 constitutive photomorphogenic homolog subunit 5 (Arabidopsis)
, COP9 signalosome complex subunit 5
, signalosome subunit 5
, COP9 signalosome subunit 5
, COP9 signalosome complex subunit 5-like
, COP9 complex S5
, Jun activation domain-binding protein 1
, Jun coactivator
, Kip1 C-terminus-interacting protein 2
, COP9 constitutive photomorphogenic-like subunit 5
, c-Jun activation domain binding protein-1
, 38 kDa Mov34 homolog
, COP9 constitutive photomorphogenic homolog subunit 5
, jun activation domain-binding protein 1
, COP9 (constitutive photomorphogenic) homolog, subunit 5