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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
Genetic deletion of Csn5 in Apoe (show APOE Proteins)(-/-) mice markedly exacerbated atherosclerotic lesion formation.
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.
BCL-G interacts with JAB1 in swine, revealing a molecular model for apoptosis
The porcine JAB1 gene was cloned and characterized.
verexpression of COPS5, through its isopeptidase activity, leads to ubiquitination and proteasome-mediated degradation of NCoR (show NCOR1 Proteins), a key corepressor for ERalpha (show ESR1 Proteins) and tamoxifen-mediated suppression of ERalpha (show ESR1 Proteins) target genes.
These findings provide novel insights into molecular mechanism of let-7d and Jab1 in tumor development and progression of breast cancer, and thus let-7d/Jab1 are novel potential therapeutic targets for breast cancer patients.
We identified a novel Jab1-Trx (show VAC14 Proteins) axis that is a key cellular process in the pathobiologic characteristics of acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)-M5). Targeting the ROS (show ROS1 Proteins)/Jab1/Trx (show VAC14 Proteins) pathway could be beneficial in the treatment of AML (show RUNX1 Proteins)-M5
These data identified CSN5 as a critical oncoprotein involved in progression of hepatocellular carcinoma (HCC (show FAM126A Proteins)) cells, which could serve as a potential therapeutic target in HCC (show FAM126A Proteins) patients.
The authors find that UCHL3 (show Uchl3 Proteins) regulates COPS5-dependent deneddylation of Cullin1, which is an essential component of SCF (show KITLG Proteins)(beta-TrCP (show BTRC Proteins)) complex and associated with SCF (show KITLG Proteins)(beta-TrCP (show BTRC Proteins)) activities. The authors further demonstrate that UCHL3 (show Uchl3 Proteins) upregulates the levels of SCF (show KITLG Proteins)(beta-TrCP (show BTRC Proteins)) substrates including IFN-I receptor IFNAR1 (show IFNAR1 Proteins), which enhances IFN-I mediated signaling pathway and antiviral activity.
Collectively, our findings suggest that JAB1 activates the neuronal differentiation ability of CPNE1 (show CPNE1 Proteins) through the binding of C2A domain in CPNE1 (show CPNE1 Proteins) with MPN (show PRSS27 Proteins) domain in JAB1.
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 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