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

DIS3 Dis3p

dis3, Rrp44, Dis3p
Encodes a subunit of the WAVE complex. The WAVE complex is required for activation of ARP2/3 complex which functions in actin microfilament nucleation and branching. Mutations cause defects in both the actin and microtubule cytoskeletons that result in aberrant epidermal cell expansion. itb1 mutants showed irregularities in trichome branch positioning and expansion. The SHD domain of this protein binds to BRK1 and overexpression of the SHD domain results in a dominant negative phenotype. (from NCBI)
Top mentioned proteins: CAN, exoribonuclease, caspase-3, KRAS, PIN
Papers on dis3
Mutational Spectrum, Copy Number Changes, and Outcome: Results of a Sequencing Study of Patients With Newly Diagnosed Myeloma.
Morgan et al., Newcastle upon Tyne, United Kingdom. In J Clin Oncol, Dec 2015
RESULTS: We identified 15 significantly mutated genes: IRF4, KRAS, NRAS, MAX, HIST1H1E, RB1, EGR1, TP53, TRAF3, FAM46C, DIS3, BRAF, LTB, CYLD, and FGFR3.
DIS3 shapes the RNA polymerase II transcriptome in humans by degrading a variety of unwanted transcripts.
Dziembowski et al., Warsaw, Poland. In Genome Res, Nov 2015
Human DIS3, the nuclear catalytic subunit of the exosome complex, contains exonucleolytic and endonucleolytic active domains.
Identification and characterization of cellular proteins interacting with Hepatitis E virus untranslated regions.
Arankalle et al., Pune, India. In Virus Res, Nov 2015
RNA pull-down and matrix-assisted laser desorption/ionization time-of-flight/time-of-flight (MALDI TOF/TOF) analysis revealed that DHX9, PTK-7, DIS3 and TCR E chain (CD3ɛ) of all the three cell lines interacted with HEV 3'UTR while RAD50 and TLE-4 interacted with HEV 5'UTR.
A compendium of DIS3 mutations and associated transcriptional signatures in plasma cell dyscrasias.
Neri et al., Milano, Italy. In Oncotarget, Oct 2015
DIS3 is a catalytic subunit of the human exosome complex, containing exonucleolytic (RNB) and endonucleolytic (PIN) domains, recently found mutated in multiple myeloma (MM), a clinically and genetically heterogeneous form of plasma cell (PC) dyscrasia.
An Interaction between RRP6 and SU(VAR)3-9 Targets RRP6 to Heterochromatin and Contributes to Heterochromatin Maintenance in Drosophila melanogaster.
Visa et al., Stockholm, Sweden. In Plos Genet, Sep 2015
Depletion of the exosome ribonucleases RRP6 and DIS3 stabilizes heterochromatic transcripts derived from transposons and repetitive sequences, and renders the heterochromatin less compact, as shown by micrococcal nuclease and proximity-ligation assays.
Distinct 18S rRNA precursors are targets of the exosome complex, the exoribonuclease RRP6L2 and the terminal nucleotidyltransferase TRL in Arabidopsis thaliana.
Lange et al., Strasbourg, France. In Plant J, Sep 2015
Our data show that, unlike in yeast and humans, an RRP6 homologue, the nucleolar exoribonuclease RRP6L2, and the exosome complex, together with RRP44, function in two distinct steps of pre-18S rRNA processing or degradation in Arabidopsis.
Longitudinal analysis of 25 sequential sample-pairs using a custom multiple myeloma mutation sequencing panel (M(3)P).
Braggio et al., Scottsdale, United States. In Ann Hematol, Jul 2015
Mutation analysis revealed KRAS as the most commonly mutated gene (36 % in each time point), followed by NRAS (20 and 16 %), TP53 (16 and 16 %), DIS3 (16 and 16 %), FAM46C (12 and 16 %), and SP140 (12 and 12 %).
The ribonuclease DIS3 promotes let-7 miRNA maturation by degrading the pluripotency factor LIN28B mRNA.
Tonon et al., Milano, Italy. In Nucleic Acids Res, Jun 2015
Recent sequencing efforts have identified the ribonuclease DIS3 as one of the most frequently mutated genes in this disease.
Advances in the pathogenesis and diagnosis of multiple myeloma.
Bergsagel et al., Scottsdale, United States. In Int J Lab Hematol, May 2015
Mutations that result in constitutive activation of the NFkB pathway and that inactivate TP53, CDKN2C, KDM6A, FAM46C, and DIS3 are also recurrent.
The 3' to 5' Exoribonuclease DIS3: From Structure and Mechanisms to Biological Functions and Role in Human Disease.
Newbury et al., Brighton, United Kingdom. In Biomolecules, 2014
DIS3 is a conserved exoribonuclease and catalytic subunit of the exosome, a protein complex involved in the 3' to 5' degradation and processing of both nuclear and cytoplasmic RNA species.
The exosome controls alternative splicing by mediating the gene expression and assembly of the spliceosome complex.
Guo et al., Guangzhou, China. In Sci Rep, 2014
In Neurospora, the silencing of rrp44, which encodes the catalytic subunit of the exosome, changed the expression of a set of spliceosomal snRNA, snRNP genes and SR protein related genes.
Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy.
Golub et al., Cambridge, United States. In Cancer Cell, 2014
We observed frequent mutations in KRAS (particularly in previously treated patients), NRAS, BRAF, FAM46C, TP53, and DIS3 (particularly in nonhyperdiploid MM).
Elastic coupling between RNA degradation and unwinding by an exoribonuclease.
Ha et al., Urbana, United States. In Science, 2012
instead of unwinding RNA in single base pair steps, Rrp44 accumulates the energy released by multiple single nucleotide step hydrolysis reactions until about four base pairs are unwound in a burst
Germline mutations in DIS3L2 cause the Perlman syndrome of overgrowth and Wilms tumor susceptibility.
Maher et al., Birmingham, United Kingdom. In Nat Genet, 2012
We mapped a previously unknown susceptibility locus to 2q37.1 and identified germline mutations in DIS3L2, a homolog of the Schizosaccharomyces pombe dis3 gene, in individuals with Perlman syndrome.
Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing.
DiPersio et al., Saint Louis, United States. In Nature, 2012
In addition to discovering novel, recurrently mutated genes (for example, WAC, SMC3, DIS3, DDX41 and DAXX) in AML, we also found two major clonal evolution patterns during AML relapse: (1) the founding clone in the primary tumour gained mutations and evolved into the relapse clone, or (2) a subclone of the founding clone survived initial therapy, gained additional mutations and expanded at relapse.
Pronounced and extensive microtubule defects in a Saccharomyces cerevisiae DIS3 mutant.
Andrulis et al., Cleveland, United States. In Yeast, 2011
DIS3 mutant showed extensive microtubule defects.
Drosophila melanogaster Dis3 N-terminal domains are required for ribonuclease activities, nuclear localization and exosome interactions.
Andrulis et al., Cleveland, United States. In Nucleic Acids Res, 2010
the dDis3 N-terminus is sufficient for endoribonuclease activity in vitro and that proper N-terminal domain structure is critical for activity of the full-length polypeptide.
The human core exosome interacts with differentially localized processive RNases: hDIS3 and hDIS3L.
Jensen et al., Warsaw, Poland. In Embo J, 2010
Data show that hDIS3 and hDIS3L are active exonucleases, but only hDIS3 has retained endonucleolytic activity, and suggest that three different ribonucleases can serve as catalytic subunits for the exosome in human cells.
Genome-wide analysis reveals distinct substrate specificities of Rrp6, Dis3, and core exosome subunits.
Andrulis et al., Cleveland, United States. In Rna, 2010
Genome-wide analysis reveals distinct substrate specificities of Dis3, and core exosome subunits
The exosome regulates circadian gene expression in a posttranscriptional negative feedback loop.
Liu et al., Dallas, United States. In Cell, 2009
Silencing of RRP44, the catalytic subunit of the exosome, elevates frq RNA levels and impairs clock function.
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