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anti-Mouse (Murine) COPS5 Anticorps:
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Fruit Fly (Drosophila melanogaster) Monoclonal COPS5 Primary Antibody pour ICC, IF - ABIN267291
Gemmill, Bemis, Lee, Sozen, Baron, Zeng, Erickson, Hooper, Drabkin: The TRC8 hereditary kidney cancer gene suppresses growth and functions with VHL in a common pathway. dans Oncogene 2002
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Human Monoclonal COPS5 Primary Antibody pour IF, WB - ABIN968615
Chauchereau, Georgiakaki, Perrin-Wolff, Milgrom, Loosfelt: JAB1 interacts with both the progesterone receptor and SRC-1. dans The Journal of biological chemistry 2000
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Human Monoclonal COPS5 Primary Antibody pour IF, WB - ABIN968614
Claret, Hibi, Dhut, Toda, Karin: A new group of conserved coactivators that increase the specificity of AP-1 transcription factors. dans Nature 1996
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Fruit Fly (Drosophila melanogaster) Monoclonal COPS5 Primary Antibody pour IP, WB - ABIN152354
Doronkin, Djagaeva, Beckendorf: The COP9 signalosome promotes degradation of Cyclin E during early Drosophila oogenesis. dans Developmental cell 2003
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COP9 (Montrer COPS8 Anticorps) 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 (Montrer CSN3 Anticorps) and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 (Montrer CCNB1 Anticorps) and Securin (Montrer PTTG1 Anticorps) via APC (Montrer APC Anticorps)/C.
COPS5 overexpression reduced spinophilin (Montrer PPP1R9B Anticorps) 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 (Montrer CDK1 Anticorps) 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 (Montrer RUNX2 Anticorps) activity.
Data indicate that in Cul4b (Montrer CUL4B Anticorps)-deficient embryonic fibroblasts showed Jab1 accumulation.
CSN5 functions through CDK2 (Montrer CDK2 Anticorps) to control premature senescence in a novel way, depending on cyclin E (Montrer CCNE1 Anticorps) in the cytoplasm.
It was shown that disruption of CSN5 prevented the formation of tumors by p53 (Montrer TP53 Anticorps)-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.
The authors find that UCHL3 (Montrer Uchl3 Anticorps) regulates COPS5-dependent deneddylation of Cullin1, which is an essential component of SCF (Montrer KITLG Anticorps)(beta-TrCP (Montrer BTRC Anticorps)) complex and associated with SCF (Montrer KITLG Anticorps)(beta-TrCP (Montrer BTRC Anticorps)) activities. The authors further demonstrate that UCHL3 (Montrer Uchl3 Anticorps) upregulates the levels of SCF (Montrer KITLG Anticorps)(beta-TrCP (Montrer BTRC Anticorps)) substrates including IFN-I receptor IFNAR1 (Montrer IFNAR1 Anticorps), which enhances IFN-I mediated signaling pathway and antiviral activity.
Collectively, our findings suggest that JAB1 activates the neuronal differentiation ability of CPNE1 (Montrer CPNE1 Anticorps) through the binding of C2A domain in CPNE1 (Montrer CPNE1 Anticorps) with MPN (Montrer PRSS27 Anticorps) domain in JAB1.
data suggests that Jab1-mediated phosphorylation of p53 (Montrer TP53 Anticorps) at Thr155 residue mediates nuclear export of p53 (Montrer TP53 Anticorps)
CSN5 is contributed to colorectal cancer development by actively driving aberrant WNT (Montrer WNT2 Anticorps) signaling through repression of the WNT (Montrer WNT2 Anticorps) antagonist DKK1 (Montrer DKK1 Anticorps).
The results of this study suggest that Jab1 promotes glioma cell proliferation and increased expression of Jab1 in glioma patients may amplify beta-catenin (Montrer CTNNB1 Anticorps) signaling to contribute to glioma cell proliferation.
Furthermore, inhibition of COPS5 resulted in an elevation of Akt (Montrer AKT1 Anticorps) expression and sensitized SOC (Montrer UBXN11 Anticorps) cells to Akt (Montrer AKT1 Anticorps) inhibitor MK2206. Suppression of COPS5 and Akt (Montrer AKT1 Anticorps) offers a potential strategy for the treatment of SOC (Montrer UBXN11 Anticorps).
The data identified CSN5 as a critical oncoprotein involved in migration and invasion of RCC (Montrer XRCC1 Anticorps) cells, which could serve as a potential therapeutic target in RCC (Montrer XRCC1 Anticorps) patients.
High JAB1 expression is associated with nasopharyngeal cancer.
oxLDL induces JAB1 expression and influences its cellular localization, whereby the p38 MAPK (Montrer MAPK14 Anticorps) 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 (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) 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.
The work described here supports a previously unknown role for the CSN/COP9 (Montrer COPS8 Anticorps) 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