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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
Show all 8 Pubmed References
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
Genetic deletion of Csn5 in Apoe (Montrer APOE Anticorps)(-/-) mice markedly exacerbated atherosclerotic lesion formation.
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.
BCL-G interacts with JAB1 in swine, revealing a molecular model for apoptosis
The porcine JAB1 gene was cloned and characterized.
CSN5 directly bound survivin and decreased its ubiquitination to enhance the protein stability of survivin.
verexpression of COPS5, through its isopeptidase activity, leads to ubiquitination and proteasome-mediated degradation of NCoR (Montrer NCOR1 Anticorps), a key corepressor for ERalpha (Montrer ESR1 Anticorps) and tamoxifen-mediated suppression of ERalpha (Montrer ESR1 Anticorps) 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 (Montrer VAC14 Anticorps) axis that is a key cellular process in the pathobiologic characteristics of acute myeloid leukemia (Montrer BCL11A Anticorps) (AML (Montrer RUNX1 Anticorps)-M5). Targeting the ROS (Montrer ROS1 Anticorps)/Jab1/Trx (Montrer VAC14 Anticorps) pathway could be beneficial in the treatment of AML (Montrer RUNX1 Anticorps)-M5
These data identified CSN5 as a critical oncoprotein involved in progression of hepatocellular carcinoma (HCC (Montrer FAM126A Anticorps)) cells, which could serve as a potential therapeutic target in HCC (Montrer FAM126A Anticorps) patients.
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.
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