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COP9 constitutive photomorphogenic homolog subunit 5

Jab1, CSN5, Jun activation domain-binding protein 1
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: AP-1, Ubiquitin, p27, Cullin, CAN
Papers using Jab1 antibodies
Phosphorylation by Akt1 promotes cytoplasmic localization of Skp2 and impairs APCCdh1-mediated Skp2 destruction
Kyprianou Natasha, In PLoS ONE, 2008
... PA); Fbx7, Fbx31, Novus Biologicals; Flag, Nedd8 and Sirt1, Cell Signaling; hemagglutinin (HA), Sp1 and Csn5, Santa Cruz Biotechnology.
Papers on Jab1
Role of p97/Valosin-containing protein (VCP) and Jab1/CSN5 in testicular ischaemia-reperfusion injury.
Delibasi et al., Ankara, Turkey. In J Mol Histol, Feb 2016
Furthermore, Jab1/CSN5 expression was gradually upregulated and p97/VCP expression was downregulated in IR injury according to western blotting and immunohistochemistry.
JAB1 is Involved in Neuropathic Pain by Regulating JNK and NF-κB Activation After Chronic Constriction Injury.
Xu et al., Nantong, China. In Neurochem Res, Jan 2016
Jun activation domain-binding protein (JAB1) is a multifunctional protein that participates in several signaling pathways, controlling cell proliferation and apoptosis.
CSNAP Is a Stoichiometric Subunit of the COP9 Signalosome.
Sharon et al., Israel. In Cell Rep, Nov 2015
We show that CSNAP binds CSN3, CSN5, and CSN6, and its incorporation into the CSN complex is mediated through the C-terminal region involving conserved aromatic residues.
RECK impedes DNA repair by inhibiting the erbB/JAB1/Rad51 signaling axis and enhances chemosensitivity of breast cancer cells.
Hung et al., Kao-hsiung, Taiwan. In Am J Cancer Res, 2014
RECK inhibited the erbB signaling and attenuated the expression of the downstream molecules Jun activation domain-binding protein 1 (JAB1) and the DNA repair protein RAD51 to impede DNA repair and to increase drug sensitivity.
HIF1α-Induced by Lysophosphatidic Acid Is Stabilized via Interaction with MIF and CSN5.
Yun et al., Atlanta, United States. In Plos One, 2014
It has been shown previously that CSN9 signalosome subunit 5 (CSN5) interacts with HIF1α to stabilize HIF1α under aerobic conditions.
Crystal structure of the human COP9 signalosome.
Thomä et al., Basel, Switzerland. In Nature, 2014
NEDD8 cleavage by CSN is catalysed by CSN5, a Zn(2+)-dependent isopeptidase that is inactive in isolation.
Plant COP9 signalosome subunit 5, CSN5.
Wei et al., Chongqing, China. In Plant Sci, 2014
This highly conserved gene has been a subject of intense research in part because human Csn5 (Jab1) has been tightly linked to cancer.
Emerging roles of Jab1/CSN5 in DNA damage response, DNA repair, and cancer.
Claret et al., Houston, United States. In Cancer Biol Ther, 2014
Jab1/CSN5 is a multifunctional protein that plays an important role in integrin signaling, cell proliferation, apoptosis, and the regulation of genomic instability and DNA repair.
Structure and function of MPN (Mpr1/Pad1 N-terminal) domain-containing proteins.
Echalier et al., Montpellier, France. In Curr Protein Pept Sci, 2013
In eukaryotes, MPN domain-containing proteins are commonly found in association with other molecules in large protein complexes, where examples comprise; the 26S proteasome and the COP9 (Constitutive photomorphogenesis 9) signalosome complexes, including the MPN subunits, POH1 and Mov34, CSN5 and CSN6, respectively.
[MIF in head and neck cancer: a new therapeutic target ?].
Saussez et al., In Rev Laryngol Otol Rhinol (bord), 2012
MIF binding to its receptor is responsible for the activation of several signaling pathways (ERK1/2 - MAPK, JAB1 - CSN5, PI3K - Akt), the inhibition of p53 and the stimulation of angiogenic factors including VEGF and IL-8.
Endothelin receptor signaling: new insight into its regulatory mechanisms.
Miwa et al., Japan. In J Pharmacol Sci, 2012
The ETR signaling is also regulated by GIPs such as Jun activation domain-binding protein 1.
Jab1 interacts with brain-specific kinase 2 (BRSK2) and promotes its degradation in the ubiquitin-proteasome pathway.
Yu et al., Shanghai, China. In Biochem Biophys Res Commun, 2012
these findings provide a novel regulatory mechanism of BRSK2 through direct interaction with Jab1.
Role of CSN5/JAB1 in Wnt/β-catenin activation in colorectal cancer cells.
Bernhagen et al., Aachen, Germany. In Febs Lett, 2012
role of CSN in the pathogenesis of CRC via regulation of the Wnt/beta-catenin pathway
Altered expression of COP9 signalosome proteins in preeclampsia.
Cimsir et al., Tokat, Turkey. In Gynecol Endocrinol, 2012
An increased level of CSN1 and CSN5 as an important part of the ubiquitin proteasome system (UPS) might be associated with the pathophysiology of preeclampsia.
Jab1/CSN5 negatively regulates p27 and plays a role in the pathogenesis of nasopharyngeal carcinoma.
Yang et al., Guangzhou, China. In Cancer Res, 2012
Jab1/CSN5 negatively regulates p27 and plays a role in the pathogenesis of nasopharyngeal carcinoma.
JAB1 is essential for B cell development and germinal center formation and inversely regulates Fas ligand and Bcl6 expression.
Gessner et al., Erlangen, Germany. In J Immunol, 2012
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 molecular basis of CRL4DDB2/CSA ubiquitin ligase architecture, targeting, and activation.
Thomä et al., Basel, Switzerland. In Cell, 2011
Instead, the COP9 signalosome (CSN) mediates the CRL4(DDB2) inhibition in a CSN5 independent, nonenzymatic, fashion.
In the pursuit of complexity: systems medicine in cancer biology.
Miller et al., Singapore, Singapore. In Cancer Cell, 2006
The amplification of two genes, MYC and CSN5, appeared to be correlated with the wound response cassette.
Genetic regulators of large-scale transcriptional signatures in cancer.
Chang et al., Stanford, United States. In Nat Genet, 2006
Using this method we show that the wound response signature, a poor-prognosis expression pattern of 512 genes in breast cancer, is induced by coordinate amplifications of MYC and CSN5 (also known as JAB1 or COPS5).
CSN facilitates Cullin-RING ubiquitin ligase function by counteracting autocatalytic adapter instability.
Wolf et al., Boston, United States. In Nat Cell Biol, 2005
The dispensable csn5 genes become essential for viability when adapter recruitment to Cul1p is compromised.
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