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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 14 Mar 2013.

Ubiquitin specific peptidase 9, Y-linked

USP9Y, DFFRY, USP10
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)
Papers on USP9Y
Novel genes that mediate nuclear respiratory factor 1-regualted neurite outgrowth in neuroblastoma IMR-32 cells.
New
Huang et al., Tainan City, Taiwan. In Gene, 15 Mar 2013
Fifteen genes, MAPRE3, NPDC1, RAB3IP, TRAPPC3, SMAD5, PIP5K1A, USP10, SPRY4, GTF2F2, NR1D1, SUV39H2, SKA3, RHOA, RAPGEF6, and SMAP1 were selected for biological confirmation.
Stress granules inhibit apoptosis by reducing reactive oxygen species production.
New
Fujii et al., Niigata, Japan. In Mol Cell Biol, 28 Feb 2013
This antioxidant activity of SGs is controlled by two SG components, GTPase-activating protein SH3 domain binding protein 1 (G3BP1) and ubiquitin-specific protease 10 (USP10).
TP53 genomic status regulates sensitivity of gastric cancer cells to the histone methylation inhibitor 3-deazaneplanocin A (DZNep).
New
Tan et al., Singapore, Singapore. In Clin Cancer Res, Sep 2012
In TP53-WT lines, DZNep stabilized p53 by reducing ubiquitin conjugation through USP10 upregulation, resulting in activation of canonical p53 target genes.
Large scale phosphoproteome analysis of LNCaP human prostate cancer cells.
New
Sadar et al., Vancouver, Canada. In Mol Biosyst, Aug 2012
Phosphoproteins identified included transcription factors, co-regulators of the androgen receptor, and cancer-related proteins that include β-catenin, USP10, and histone deacetylase-2.
Screening for partial AZFa microdeletions in the Y chromosome of infertile men: is it of clinical relevance?
New
Botchan et al., Tel Aviv-Yafo, Israel. In Fertil Steril, Jul 2012
The DNA of 657 of them with undetected microdeletions was analyzed for partial AZFa deletion in the USP9Y and DDX3Y genes using sequence-tagged sites beyond EAA/EMQN recommendations.
Beclin1 controls the levels of p53 by regulating the deubiquitination activity of USP10 and USP13.
Impact
GeneRIF
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.
Review
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.
GeneRIF
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.
Impact
GeneRIF
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.
Impact
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.
GeneRIF
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.
Impact
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.
Review
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.
Tracking microdeletions of the AZF region in a patrilineal line of infertile men.
GeneRIF
Moura et al., Goiânia, Brazil. In Genet Mol Res, 2007
Study examined 26 family members of 13 patients with male infertility who showed deletions in the AZF region.
[Alteration of spermatogenesis and Y chromosome microdelations. Analysis of the DAZ gene family].
Review
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.
Impact
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.
Review
Impact
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.
Review
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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