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anti-Mouse (Murine) 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
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
Show all 4 Pubmed References
COP9 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(-/-) mice markedly exacerbated atherosclerotic lesion formation.
CSN3 and CSN5 are involved in oocyte meiosis by regulating degradation of Cyclin B1 and Securin via APC/C.
COPS5 overexpression reduced spinophilin 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 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 activity.
Data indicate that in Cul4b-deficient embryonic fibroblasts showed Jab1 accumulation.
CSN5 functions through CDK2 to control premature senescence in a novel way, depending on cyclin E in the cytoplasm.
It was shown that disruption of CSN5 prevented the formation of tumors by p53-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.
Growth factor erv1-like (Gfer) inhibits the COP9 signalosome subunit jun activation-domain binding protein 1 (Jab1)-mediated degradation of the cyclin-dependent kinase inhibitor p27(kip1) to restrict proliferation of hematopoietic stem cells.
the COP9 signalosome subunit 5 (CSN5) is required for activation of proinflammatory kinases p38 and Erk and for down-regulation of the expression of genes regulated by nuclear factor E2-related factor 2
Jab1 is essential for efficient DNA repair and mechanistically link Jab1 to the maintenance of genome integrity and to cell survival.
CSN5/Jab1 controls different events of the cell cycle
Kip1 inhibits Jab1 mediated c-Jun dependent transcription
the analysis of JAB1/CSN5 expression pattern in the mouse embryo
Jab1 controls cell cycle progression and cell survival by regulating multiple cell cycle signaling pathways
The small Jab1-containing subcomplex may be a novel mediator of anchorage and cell-cell contact-dependent signal transduction
the interaction between Brn-2 and Jab1 may provide some insights into the understanding of neuronal development and neurodegenerative diseases
jab1 is more critical for vestibular macular hair cell development before 30 hours
BCL-G interacts with JAB1 in swine, revealing a molecular model for apoptosis
The porcine JAB1 gene was cloned and characterized.
A positive correlation was found between the expression of LASP1 and COPS5 while a negative correlation existed between 14-3-3sigma and COPS5/LASP1 in most CRC samples.
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, a key corepressor for ERalpha and tamoxifen-mediated suppression of ERalpha 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 axis that is a key cellular process in the pathobiologic characteristics of acute myeloid leukemia (AML-M5). Targeting the ROS/Jab1/Trx pathway could be beneficial in the treatment of AML-M5
These data identified CSN5 as a critical oncoprotein involved in progression of hepatocellular carcinoma (HCC) cells, which could serve as a potential therapeutic target in HCC patients.
The authors find that UCHL3 regulates COPS5-dependent deneddylation of Cullin1, which is an essential component of SCF(beta-TrCP) complex and associated with SCF(beta-TrCP) activities. The authors further demonstrate that UCHL3 upregulates the levels of SCF(beta-TrCP) substrates including IFN-I receptor IFNAR1, which enhances IFN-I mediated signaling pathway and antiviral activity.
Collectively, our findings suggest that JAB1 activates the neuronal differentiation ability of CPNE1 through the binding of C2A domain in CPNE1 with MPN domain in JAB1.
data suggests that Jab1-mediated phosphorylation of p53 at Thr155 residue mediates nuclear export of p53
CSN5 is contributed to colorectal cancer development by actively driving aberrant WNT signaling through repression of the WNT antagonist DKK1.
The results of this study suggest that Jab1 promotes glioma cell proliferation and increased expression of Jab1 in glioma patients may amplify beta-catenin signaling to contribute to glioma cell proliferation.
Furthermore, inhibition of COPS5 resulted in an elevation of Akt expression and sensitized SOC cells to Akt inhibitor MK2206. Suppression of COPS5 and Akt offers a potential strategy for the treatment of SOC.
The data identified CSN5 as a critical oncoprotein involved in migration and invasion of RCC cells, which could serve as a potential therapeutic target in RCC patients.
High JAB1 expression is associated with nasopharyngeal cancer.
oxLDL induces JAB1 expression and influences its cellular localization, whereby the p38 MAPK 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/beta-catenin 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 increases when Jab1 is overexpressed in SKBr3 breast cancer cells. PI3 kinase and AKT were also activated by Jab1 overexpression.Copine3 and Jab1 binding regulates the ErbB2 signaling pathway.
The reverse correlation of Jab1 and Smad4 in PANC-1 cells may be involved in the Pathogenesis of prostate cancer. Jab1 can cause degradation of Smad4 via TGF-beta signal pathway.
Jab1/Csn5 expression with concurrent low p57 expression associated with poor overall survival in hepatocellular carcinoma
LPA stimulated interaction of CSN5 with HIF1alpha and MIF. Depletion of CSN5 mitigated the association between HIF1alpha and MIF. We suggest HIF1alpha, MIF, and CSN5 form a ternary complex that is necessary to prevent degradation of HIF1alpha under aerobic conditions
The work described here supports a previously unknown role for the CSN/COP9 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