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anti-Mouse (Murine) COPS5 Antikörper:
anti-Human COPS5 Antikörper:
anti-Rat (Rattus) COPS5 Antikörper:
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Fruit Fly (Drosophila melanogaster) Monoclonal COPS5 Primary Antibody für 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 für 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 für 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
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Fruit Fly (Drosophila melanogaster) Monoclonal COPS5 Primary Antibody für 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 (zeige COPS8 Antikörper) 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 (zeige CSN3 Antikörper) and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 (zeige CCNB1 Antikörper) and Securin (zeige PTTG1 Antikörper) via APC (zeige APC Antikörper)/C.
COPS5 overexpression reduced spinophilin (zeige PPP1R9B Antikörper) 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 (zeige CDK1 Antikörper) 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 (zeige RUNX2 Antikörper) activity.
Data indicate that in Cul4b (zeige CUL4B Antikörper)-deficient embryonic fibroblasts showed Jab1 accumulation.
CSN5 functions through CDK2 (zeige CDK2 Antikörper) to control premature senescence in a novel way, depending on cyclin E (zeige CCNE1 Antikörper) in the cytoplasm.
It was shown that disruption of CSN5 prevented the formation of tumors by p53 (zeige TP53 Antikörper)-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 (zeige AKT1 Antikörper) expression and sensitized SOC (zeige UBXN11 Antikörper) cells to Akt (zeige AKT1 Antikörper) inhibitor MK2206. Suppression of COPS5 and Akt (zeige AKT1 Antikörper) offers a potential strategy for the treatment of SOC (zeige UBXN11 Antikörper).
The data identified CSN5 as a critical oncoprotein involved in migration and invasion of RCC (zeige XRCC1 Antikörper) cells, which could serve as a potential therapeutic target in RCC (zeige XRCC1 Antikörper) patients.
High JAB1 expression is associated with nasopharyngeal cancer.
oxLDL induces JAB1 expression and influences its cellular localization, whereby the p38 MAPK (zeige MAPK14 Antikörper) 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 (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) 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 (zeige ERBB2 Antikörper) increases when Jab1 is overexpressed in SKBr3 breast cancer cells. PI3 kinase (zeige PIK3CA Antikörper) and AKT (zeige AKT1 Antikörper) were also activated by Jab1 overexpression.Copine3 and Jab1 binding regulates the ErbB2 (zeige ERBB2 Antikörper) signaling pathway.
The reverse correlation of Jab1 and Smad4 (zeige SMAD4 Antikörper) in PANC-1 cells may be involved in the Pathogenesis of prostate cancer. Jab1 can cause degradation of Smad4 (zeige SMAD4 Antikörper) via TGF-beta (zeige TGFB1 Antikörper) signal pathway.
Jab1/Csn5 expression with concurrent low p57 (zeige CDKN1C Antikörper) expression associated with poor overall survival in hepatocellular carcinoma
LPA (zeige APOA Antikörper) stimulated interaction of CSN5 with HIF1alpha (zeige HIF1A Antikörper) and MIF (zeige AMH Antikörper). Depletion of CSN5 mitigated the association between HIF1alpha (zeige HIF1A Antikörper) and MIF (zeige AMH Antikörper). We suggest HIF1alpha (zeige HIF1A Antikörper), MIF (zeige AMH Antikörper), and CSN5 form a ternary complex that is necessary to prevent degradation of HIF1alpha (zeige HIF1A Antikörper) under aerobic conditions
Integrin beta-1 (zeige ITGB1 Antikörper), 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 (zeige COPS8 Antikörper) 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