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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Ubiquitin specific peptidase 42

USP42, ubiquitin specific peptidase-42
Top mentioned proteins: AML1, Ubiquitin, p22, Cryptic, CAN
Papers on USP42
Ubiquitin-specific peptidase 42 (USP42) functions to deubiquitylate histones and regulate transcriptional activity.
Vousden et al., Glasgow, United Kingdom. In J Biol Chem, 2015
Ubiquitin-specific peptidase 42 (USP42) is a deubiquitylating enzyme that can target p53 and contribute to the stabilization of p53 in response to stress.
Acute myeloid leukemia with t(7;21)(p22;q22) and 5q deletion: a case report and literature review.
Tirado et al., Los Angeles, United States. In Exp Hematol Oncol, 2013
The cryptic t(7;21)(p22;q22) rearrangement involving the USP42 gene appears to be a specific and recurrent cytogenetic abnormality.
5'RUNX1-3'USP42 chimeric gene in acute myeloid leukemia can occur through an insertion mechanism rather than translocation and may be mediated by genomic segmental duplications.
Albano et al., Bari, Italy. In Mol Cytogenet, 2013
RESULTS: We identified an adult AML case bearing a ins(21;7)(q22;p15p22) generating a 5'RUNX1-3'USP42 fusion gene on der(21) chromosome and causing USP42 gene over-expression.
Myeloid leukemia with t(7;21)(p22;q22) and 5q deletion.
Heim et al., Oslo, Norway. In Oncol Rep, 2013
The rare but recurrent RUNX1-USP42 fusion gene is the result of a t(7;21)(p22;q22) chromosomal translocation and has been described in 6 cases of acute myeloid leukemia (AML) and one case of refractory anemia with excess of blast.
A cytogenetic study of 397 consecutive acute myeloid leukemia cases identified three with a t(7;21) associated with 5q abnormalities and exhibiting similar clinical and biological features, suggesting a new, rare acute myeloid leukemia entity.
Mauvieux et al., Mulhouse, France. In Cancer Genet, 2012
Three cases of the recently described translocation, t(7;21)(p22;q22), were identified, which expressed RUNX1-USP42 (ubiquitin-specific protease 42) fusion transcripts, associated with 5q abnormalities and hyperploidy.
Regulation of p53 stability and function by the deubiquitinating enzyme USP42.
Vousden et al., Glasgow, United Kingdom. In Embo J, 2012
the function of USP42 is required to allow the rapid activation of p53-dependent transcription and a p53-dependent cell-cycle arrest in response to stress.
Microhomologies and topoisomerase II consensus sequences identified near the breakpoint junctions of the recurrent t(7;21)(p22;q22) translocation in acute myeloid leukemia.
Hébert et al., Montréal, Canada. In Genes Chromosomes Cancer, 2011
The t(7;21)(p22;q22) translocation, recently described in three cases of myeloid neoplasias, fuses the ubiquitin specific peptidase 42 gene, USP42, a member of the deubiquitinating enzyme family, to RUNX1.
Molecular characterisation of a recurrent, semi-cryptic RUNX1 translocation t(7;21) in myelodysplastic syndrome and acute myeloid leukaemia.
Tauro et al., Dundee, United Kingdom. In Br J Haematol, 2010
Reverse-transcription polymerase chain reaction (RT-PCR) and sequence analysis identified a fusion between RUNX1 and the gene encoding ubiquitin specific peptidase-42 (USP42), with splice-variants and variable break-points within RUNX1.
The expression of Usp42 during embryogenesis and spermatogenesis in mouse.
Baek et al., Seoul, South Korea. In Gene Expr Patterns, 2007
Northern blot analysis revealed that Usp42 is expressed mainly in brain, lung, thymus and testis, and at E10.5 the most during embryonic development.
A novel and cytogenetically cryptic t(7;21)(p22;q22) in acute myeloid leukemia results in fusion of RUNX1 with the ubiquitin-specific protease gene USP42.
Panagopoulos et al., Lund, Sweden. In Leukemia, 2006
FISH, 3'RACE, and RT-PCR revealed a fusion involving RUNX1 and the ubiquitin-specific protease (USP) gene USP42.
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