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Eukaryotic translation initiation factor 3, subunit A

p185, CUL7
The protein encoded by this gene is a component of an E3 ubiquitin-protein ligase complex. The encoded protein interacts with TP53, CUL9, and FBXW8 proteins. Defects in this gene are a cause of 3M syndrome type 1 (3M1). Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Dec 2009] (from NCBI)
Top mentioned proteins: erbB-2, CAN, HAD, ACID, p53
Papers on p185
Trastuzumab Inhibits Growth of HER2-Negative Gastric Cancer Cells Through Gastrin-Initialized CCKBR Signaling.
Fu et al., China. In Dig Dis Sci, Dec 2015
BACKGROUND: Administration of trastuzumab, a fully humanized monoclonal antibody targeted to the human epidermal growth factor receptor 2 (HER2, p185), has improved outcomes for patients with HER2-positive gastric cancer (GC), but some relevant issues remain to be investigated and will emerge with new anti-GC drugs.
Changes in facial appearance from neonate to adult in 3-M syndrome patient with novel CUL7 gene mutations.
Tsukahara et al., In J Pediatr Endocrinol Metab, Nov 2015
Three genes, cullin 7 (CUL7), coiled-coil domain containing 8, and obscurin-like 1 are genetic candidates of 3-M syndrome.
The role of cullin proteins in gastric cancer.
Yao et al., Hohhot, China. In Tumour Biol, Nov 2015
There are seven cullin proteins that have been identified in eukaryotes: CUL1, CUL2, CUL3, CUL4A, CUL4B, CUL5, and CUL7/p53-associated parkin-like cytoplasmic protein.
Neuregulin 1 as an endogenous regulator of nicotinic acetylcholine receptors in adult major pelvic ganglion neurons.
Jeong et al., Wŏnju, South Korea. In Biochem Biophys Res Commun, Sep 2015
The biological activity of the released sNRG1 was detected by tyrosine phosphorylation (p185) of the ErbB2 receptors in MPG neurons.
Excess of rare, inherited truncating mutations in autism.
Eichler et al., Seattle, United States. In Nat Genet, Jun 2015
This analysis identifies a second class of candidate genes (for example, RIMS1, CUL7 and LZTR1) where transmitted mutations may create a sensitized background but are unlikely to be completely penetrant.
3-M syndrome: a novel CUL7 mutation associated with respiratory distress and a good response to GH therapy.
Fatih et al., Abu Dhabi, United Arab Emirates. In Endocrinol Diabetes Metab Case Rep, 2014
UNLABELLED: 3-M syndrome is a rare autosomal recessive disorder caused by mutations in the CUL7, OBSL1 and CCDC8 genes.
Regulation of insulin receptor substrate-1 by mTORC2 (mammalian target of rapamycin complex 2).
Jacinto et al., United States. In Biochem Soc Trans, 2013
Defective IRS-1 degradation was due to attenuated expression of the CUL7 (Cullin 7) ubiquitin ligase substrate-targeting sub-unit Fbw8.
Exploring the spectrum of 3-M syndrome, a primordial short stature disorder of disrupted ubiquitination.
Black et al., Manchester, United Kingdom. In Clin Endocrinol (oxf), 2012
To date, mutations in three genes CUL7, OBSL1 and CCDC8 have been shown to cause 3-M.
Regulation of hepatitis C virus translation initiation by iron: role of eIF3 and La protein.
Li et al., Hangzhou, China. In Virus Res, 2012
Iron promotes the translation initiation of hepatitis C virus by stimulating the expression of eIF3A and La proteins.
Characterization of the Cullin7 E3 ubiquitin ligase--heterodimerization of cullin substrate receptors as a novel mechanism to regulate cullin E3 ligase activity.
Hagen et al., Singapore, Singapore. In Cell Signal, 2012
binding of Cul1-Rbx1 to Cul7-Rbx1 is mediated via heterodimerization of Fbxw8 with other F-box proteins which function to recruit substrates into the E3 ligase complex
A minor isoform of the human RNA polymerase II subunit hRPB11 (POLR2J) interacts with several components of the translation initiation factor eIF3.
Shpakovski et al., Moscow, Russia. In Biochemistry (mosc), 2011
POLR2J interacts with three different subunits of eIF3, eIF3a, eIF3i, and eIF3m.
Exome sequencing identifies CCDC8 mutations in 3-M syndrome, suggesting that CCDC8 contributes in a pathway with CUL7 and OBSL1 to control human growth.
Black et al., Manchester, United Kingdom. In Am J Hum Genet, 2011
We propose that CUL7, OBSL1, and CCDC8 are members of a pathway controlling mammalian growth.
The genetics of 3-M syndrome: unravelling a potential new regulatory growth pathway.
Clayton et al., Manchester, United Kingdom. In Horm Res Paediatr, 2010
discussion of roles of CUL7, OBSL1 (obscurin-like 1), and CCDC8 (coiled-coil domain containing protein 8) in growth and development using findings from patients with Miller-McKusick-Malvaux syndrome and Silver-Russell syndrome [REVIEW]
The cullin protein family.
Pan et al., München, Germany. In Genome Biol, 2010
The mammalian cullin protein family comprises eight members (CUL1 to CUL7 and PARC), which are characterized by a cullin homology domain.
Identification of mutations in CUL7 in 3-M syndrome.
Cormier-Daire et al., Paris, France. In Nat Genet, 2005
25 distinct mutations in the gene cullin 7 mappped to chromosome 6 were identified in 29 families with 3-M syndrome.
Copy number of chromosome 17 but not HER2 amplification predicts clinical outcome of patients with pancreatic ductal adenocarcinoma.
Hosch et al., Hamburg, Germany. In J Clin Oncol, 2005
In contrast, no prognostic influence on patient outcome was found for the amplification of the HER2 oncogene or p185(HER2) overexpression.
Design of multivalent complexes using the barnase*barstar module.
Plückthun et al., Moscow, Russia. In Nat Biotechnol, 2003
Using fusions with anti-p185(HER2-ECD) 4D5 scFv, we show that the anticipated gain in avidity from monomer to dimer to trimer is obtained and that favorable tumor targeting properties are achieved.
The Prognostic Significance of the Overexpression of HER-2/ neu in Korean Gastric Carcinomas and the In Vitro Effects of Anti-HER-2/neu Antibody on Cell Growth in the Gastric Carcinoma Cell Lines.
Lee et al., In Cancer Res Treat, 2003
PURPOSE: The HER2 gene encodes a 185-kd transmembrane glycoprotein receptor (p185(HER2)) that has partial homology with the epidermal growth factor receptor (EGFR) and shares intrinsic tyrosine kinase activity.
c-erbB-2 is of independent prognostic relevance in gastric cancer and is associated with the expression of tumor-associated protease systems.
Heiss et al., München, Germany. In J Clin Oncol, 2000
PURPOSE: The c-erbB-2 gene (encoding the protein p185) is overexpressed in diverse human cancers and has been implicated to be of prognostic value in gastric cancer.
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