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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 10 Nov 2014.

Ubiquitin specific peptidase 9, Y-linked

This gene is a member of the peptidase C19 family. It encodes a protein that is similar to ubiquitin-specific proteases, which cleave the ubiquitin moiety from ubiquitin-fused precursors and ubiquitinylated proteins. [provided by RefSeq, Mar 2009] (from NCBI)
Top mentioned proteins: Ubiquitin, MEN, HAD, DAZ, p53
Papers on USP9Y
Copy number differences of Y chromosomal genes between superior and inferior quality semen producing crossbred (Bos taurus × Bos indicus) bulls.
De et al., Karnāl, India. In Anim Biotechnol, 31 Dec 2014
In this study, copy numbers of three Y chromosomal genes TSPY, DDX3Y, and USP9Y in genomic DNA were estimated and compared in two groups of crossbred (Bos taurus × Bos indicus) bulls of ten each, superior and inferior quality semen producing bulls, which were classified based on their seminal quality parameters.
Transcription-mediated chimeric RNAs in prostate cancer: time to revisit old hypothesis?
Lu et al., Hangzhou, China. In Omics, 31 Oct 2014
We attempted to confirm one of the fusion genes, USP9Y-TTTY15, by reverse transcription PCR, but detected the presence of the USP9Y-TTTY15 fusion transcript in cancer samples, nonmalignant prostate tissues, and normal tissues from other organs, demonstrating that it is a transcription-induced chimeric RNA, which is commonly produced in normal tissues.
MicroRNA-191 promotes pancreatic cancer progression by targeting USP10.
Gao et al., Shanghai, China. In Tumour Biol, Sep 2014
Collectively, these data suggest that miR-191 could promote pancreatic cancer progression through targeting USP10, implicating a novel mechanism for the tumorigenesis.
Resveratrol induces apoptosis by directly targeting Ras-GTPase-activating protein SH3 domain-binding protein 1.
Dong et al., Austin, United States. In Oncogene, Aug 2014
We also found that G3BP1 negatively regulates p53 expression by interacting with ubiquitin-specific protease 10 (USP10), a deubiquitinating enzyme of p53.
Deubiquitination and stabilization of T-bet by USP10.
Shi et al., Shanghai, China. In Biochem Biophys Res Commun, Aug 2014
Here we identified USP10, a carboxyl-terminal ubiquitin-processing protease, could interact with T-bet in the nucleus.
Beclin1 controls the levels of p53 by regulating the deubiquitination activity of USP10 and USP13.
Yuan et al., Shanghai, China. In Cell, 2011
USP10 mediates the deubiquitination of p53, regulating deubiquitination activity of USP10 and USP13 by Beclin1 provides a mechanism for Beclin1 to control the levels of p53.
Interplay between p53-family, their regulators, and PARPs in DNA repair.
Emami, Saint-Pierre-des-Corps, France. In Clin Res Hepatol Gastroenterol, 2011
We highlight the recent progress in the analysis of protein signals to p53, including PARPs, and ubiquitination cascade proteins MDM2, CRM1, USP10 and 14-3-3σ.
The deubiquitinating enzyme USP10 regulates the endocytic recycling of CFTR in airway epithelial cells.
Stanton et al., United States. In Channels (austin), 2010
a novel function for USP10 in facilitating the deubiquitination of CFTR in early endosomes, thereby enhancing the endocytic recycling and cell surface expression of CFTR.
USP10 regulates p53 localization and stability by deubiquitinating p53.
Lou et al., Rochester, United States. In Cell, 2010
Findings reveal USP10 to be a novel regulator of p53, providing an alternative mechanism of p53 inhibition in cancers with wild-type p53.
USP10: friend and foe.
Shiloh et al., Leiden, Netherlands. In Cell, 2010
In this issue, Yuan et al. (2010) identify the deubiquitinating protease USP10 as a new regulator of p53 in the DNA damage response and tumor development.
The deubiquitinating enzyme USP10 regulates the post-endocytic sorting of cystic fibrosis transmembrane conductance regulator in airway epithelial cells.
Stanton et al., United States. In J Biol Chem, 2009
USP10 has a role in facilitating the deubiquitination of CFTR in early endosomes and thereby enhancing the endocytic recycling of CFTR
Spermatogenesis in a man with complete deletion of USP9Y.
Piomboni et al., Siena, Italy. In N Engl J Med, 2009
Deletions in the azoospermia factor region AZFa on the human Y chromosome and, more specifically, in the region that encompasses the ubiquitin-specific peptidase 9, Y-linked gene USP9Y have been implicated in infertility associated with oligospermia and azoospermia.
An evolutionary perspective on Y-chromosomal variation and male infertility.
Tyler-Smith, Sanger, United States. In Int J Androl, 2008
Comparison with the chimpanzee Y chromosome indicates that USP9Y is dispensable in apes, but that multiple copies of TSPY1 may have an important role.
AZF gene expression analysis in peripheral leukocytes and testicular cells from idiopathic infertility.
Wu et al., Nanjing, China. In Arch Androl, 2007
Frequency of AZF microdeletions in peripheral leukocytes and testicular cells in Chinese men with idiopathic infertility.
[Alteration of spermatogenesis and Y chromosome microdelations. Analysis of the DAZ gene family].
Tessari et al., Padova, Italy. In Minerva Endocrinol, 2002
The genes responsible for the testicular phenotype observed in these subjects are DBY and USP9Y for AZFa, RBMY1 for AZFb, and DAZ for AZFc.
A Y-encoded subunit of the translation initiation factor Eif2 is essential for mouse spermatogenesis.
Burgoyne et al., London, United Kingdom. In Nat Genet, 2001
4,5), Smcy, Uty, Usp9y (also known as Dffry), Eif2s3y (also known as Eif-2gammay) and Dby10; all have closely similar X-encoded homologs.
Y chromosome microdeletions and alterations of spermatogenesis.
Ferlin et al., Padova, Italy. In Endocr Rev, 2001
Deletions in these regions remove one or more of the candidate genes (DAZ, RBMY, USP9Y, and DBY) and cause severe testiculopathy leading to male infertility.
Role of the AZFa candidate genes in male infertility.
Ferlin et al., Padova, Italy. In J Endocrinol Invest, 2000
It contains three genes, USP9Y, DBY and UTY, but only the former two can be at present considered candidate genes for the infertile phenotype associated with deletion of this interval.
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