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anti-Mouse (Murine) COPS5 Antibodies:
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Fruit Fly (Drosophila melanogaster) Monoclonal COPS5 Primary Antibody for 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. in Oncogene 2002
Show all 8 Pubmed References
Human Monoclonal COPS5 Primary Antibody for IF, WB - ABIN968615
Chauchereau, Georgiakaki, Perrin-Wolff, Milgrom, Loosfelt: JAB1 interacts with both the progesterone receptor and SRC-1. in The Journal of biological chemistry 2000
Show all 6 Pubmed References
Human Monoclonal COPS5 Primary Antibody for IF, WB - ABIN968614
Claret, Hibi, Dhut, Toda, Karin: A new group of conserved coactivators that increase the specificity of AP-1 transcription factors. in Nature 1996
Show all 6 Pubmed References
Fruit Fly (Drosophila melanogaster) Monoclonal COPS5 Primary Antibody for IP, WB - ABIN152354
Doronkin, Djagaeva, Beckendorf: The COP9 signalosome promotes degradation of Cyclin E during early Drosophila oogenesis. in Developmental cell 2003
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COP9 (show COPS8 Antibodies) 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 Antibodies) and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 (show CCNB1 Antibodies) and Securin (show PTTG1 Antibodies) via APC (show APC Antibodies)/C.
COPS5 overexpression reduced spinophilin (show PPP1R9B Antibodies) 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 Antibodies) 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 Antibodies) activity.
Data indicate that in Cul4b (show CUL4B Antibodies)-deficient embryonic fibroblasts showed Jab1 accumulation.
CSN5 functions through CDK2 (show CDK2 Antibodies) to control premature senescence in a novel way, depending on cyclin E (show CCNE1 Antibodies) in the cytoplasm.
It was shown that disruption of CSN5 prevented the formation of tumors by p53 (show TP53 Antibodies)-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.
Furthermore, inhibition of COPS5 resulted in an elevation of Akt (show AKT1 Antibodies) expression and sensitized SOC (show UBXN11 Antibodies) cells to Akt (show AKT1 Antibodies) inhibitor MK2206. Suppression of COPS5 and Akt (show AKT1 Antibodies) offers a potential strategy for the treatment of SOC (show UBXN11 Antibodies).
The data identified CSN5 as a critical oncoprotein involved in migration and invasion of RCC (show XRCC1 Antibodies) cells, which could serve as a potential therapeutic target in RCC (show XRCC1 Antibodies) patients.
High JAB1 expression is associated with nasopharyngeal cancer.
oxLDL induces JAB1 expression and influences its cellular localization, whereby the p38 MAPK (show MAPK14 Antibodies) 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 Antibodies)/beta-catenin (show CTNNB1 Antibodies) 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 Antibodies) increases when Jab1 is overexpressed in SKBr3 breast cancer cells. PI3 kinase (show PIK3CA Antibodies) and AKT (show AKT1 Antibodies) were also activated by Jab1 overexpression.Copine3 and Jab1 binding regulates the ErbB2 (show ERBB2 Antibodies) signaling pathway.
The reverse correlation of Jab1 and Smad4 (show SMAD4 Antibodies) in PANC-1 cells may be involved in the Pathogenesis of prostate cancer. Jab1 can cause degradation of Smad4 (show SMAD4 Antibodies) via TGF-beta (show TGFB1 Antibodies) signal pathway.
Jab1/Csn5 expression with concurrent low p57 (show CDKN1C Antibodies) expression associated with poor overall survival in hepatocellular carcinoma
LPA (show APOA Antibodies) stimulated interaction of CSN5 with HIF1alpha (show HIF1A Antibodies) and MIF (show AMH Antibodies). Depletion of CSN5 mitigated the association between HIF1alpha (show HIF1A Antibodies) and MIF (show AMH Antibodies). We suggest HIF1alpha (show HIF1A Antibodies), MIF (show AMH Antibodies), and CSN5 form a ternary complex that is necessary to prevent degradation of HIF1alpha (show HIF1A Antibodies) under aerobic conditions
Integrin beta-1 (show ITGB1 Antibodies), transforming growth factorbeta1 and nuclear factorkappaB pathways are modified by CSN5 in hepatocllular carcinoma cells.
The work described here supports a previously unknown role for the CSN/COP9 (show COPS8 Antibodies) 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