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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.

DNA cross-link repair 1C

Artemis, a SCID, MART, phosphoribosylpyrophosphate synthetase, ARTS
This gene encodes a nuclear protein that is involved in V(D)J recombination and DNA repair. The protein has single-strand-specific 5'-3' exonuclease activity; it also exhibits endonuclease activity on 5' and 3' overhangs and hairpins when complexed with protein kinase, DNA-activated, catalytic polypeptide. Mutations in this gene cause Athabascan-type severe combined immunodeficiency (SCIDA). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MART-1, CAN, HAD, CD8, tyrosinase
Papers on Artemis
Co-existence of clonal expanded autologous and transplacental-acquired maternal T cells in recombination activating gene-deficient severe combined immunodeficiency.
New
Somech et al., Tel Aviv-Yafo, Israel. In Clin Exp Immunol, Jun 2014
We report a SCID patient with a novel mutation in the recombination activating gene (RAG)1 gene (4-BP DEL.1406 TTGC) who presented with immunodeficiency and OS.
Human melanoma metastases demonstrate nonstochastic site-specific antigen heterogeneity that correlates with T-cell infiltration.
New
Kammula et al., Doha, Qatar. In Clin Cancer Res, Jun 2014
To allow specific tumor cell profiling, we used established immunohistochemical methods to perform semiquantitative assessment for a panel of prototypic melanocyte differentiation antigens (MDA), including gp100, MART-1, and tyrosinase.
Structural insights into NHEJ: building up an integrated picture of the dynamic DSB repair super complex, one component and interaction at a time.
New
Tainer et al., Berkeley, United States. In Dna Repair (amst), May 2014
X-ray crystal structures, cryo-electron microscopy envelopes, and small angle X-ray scattering (SAXS) solution conformations and assemblies are defining most of the core protein components for NHEJ: Ku70/Ku80 heterodimer; the DNA dependent protein kinase catalytic subunit (DNA-PKcs); the structure-specific endonuclease Artemis along with polynucleotide kinase/phosphatase (PNKP), aprataxin and PNKP related protein (APLF); the scaffolding proteins XRCC4 and XLF (XRCC4-like factor); DNA polymerases, and DNA ligase IV (Lig IV).
Histone deacetylase inhibitor sensitizes apoptosis-resistant melanomas to cytotoxic human T lymphocytes through regulation of TRAIL/DR5 pathway.
New
Economou et al., Los Angeles, United States. In J Immunol, May 2014
To test these two hypotheses, we used an in vitro model of MART CTL-resistant melanoma sublines.
Safety, efficacy, and biomarkers of nivolumab with vaccine in ipilimumab-refractory or -naive melanoma.
New
Impact
Chen et al., Princeton, United States. In J Clin Oncol, Jan 2014
High pretreatment NY-ESO-1 and MART-1-specific CD8(+) T cells were associated with progression of disease.
The many faces of Artemis-deficient combined immunodeficiency - Two patients with DCLRE1C mutations and a systematic literature review of genotype-phenotype correlation.
Review
New
Jones et al., London, United Kingdom. In Clin Immunol, Dec 2013
We report 2 siblings with combined immunodeficiency (CID) and immunodysregulation caused by compound heterozygous Artemis mutations, including an exon 1-3 deletion generating a null allele, and a missense change (p.T71P).
Uterine tumors resembling ovarian sex cord tumors.
Review
New
Mohanty et al., Delhi, India. In Arch Pathol Lab Med, Dec 2013
Sex cord markers, such as inhibin, calretinin, CD99, WT1, and MART-1; epithelial markers, such as pancytokeratin and epithelial membrane antigen; smooth muscle markers, such as smooth muscle actin, desmin, and histone deacetylase 8; and miscellaneous markers, such as CD10, estrogen receptor, progesterone receptor, S100, and CD117, are often coexpressed.
Aberrant apoptotic machinery confers melanoma dual resistance to BRAF(V600E) inhibitor and immune effector cells: immunosensitization by a histone deacetylase inhibitor.
New
Economou et al., Los Angeles, United States. In Am J Clin Exp Immunol, Dec 2013
We generated melanoma sublines resistant to BRAFi vemurafenib and to CTL recognizing the MART-1 melanoma antigen.
Sept4/ARTS regulates stem cell apoptosis and skin regeneration.
New
Impact
Steller et al., New York City, United States. In Science, Aug 2013
We found that mice deficient for the proapoptotic Sept4/ARTS gene have elevated numbers of hair follicle stem cells (HFSCs) that are protected against apoptosis.
Regeneration of human tumor antigen-specific T cells from iPSCs derived from mature CD8(+) T cells.
New
Impact
Kawamoto et al., Yokohama, Japan. In Cell Stem Cell, Feb 2013
In this study, we established iPSCs from mature cytotoxic T cells specific for the melanoma epitope MART-1.
Hearing loss and PRPS1 mutations: Wide spectrum of phenotypes and potential therapy.
Review
Yan et al., Miami, United States. In Int J Audiol, 2013
Gain of function mutations in PRPS1 cause a superactivity of the PRS-I protein whereas the loss-of-function mutations result in X-linked nonsyndromic sensorineural deafness type 2 (DFN2), or in syndromic deafness including Arts syndrome and X-linked Charcot-Marie-Tooth disease-5 (CMTX5).
True arrestins and arrestin-fold proteins: a structure-based appraisal.
Review
Klein et al., Grenoble, France. In Prog Mol Biol Transl Sci, 2012
Based on the recent literature, true arrestins (visual and β-arrestins), ARRDCs, and yeast ARTS are the closest from a functional point of view.
Potent 19-norvitamin D analogs for prostate and liver cancer therapy.
Review
Chen et al., Tokyo, Japan. In Future Med Chem, 2012
Among them, 2α- and 2β-(3-hydroxypropyl)-1α,25-dihydroxy-19-norvitamin D(3) (MART-10 and -11, respectively) and 14-epi-2α- and 14-epi-2β-(3-hydroxypropyl)-1α,25-dihydroxy-19-norvitamin D(3) (14-epi-MART-10 and 14-epi-MART-11, respectively) were found to be the most promising.
Artemis C-terminal region facilitates V(D)J recombination through its interactions with DNA Ligase IV and DNA-PKcs.
GeneRIF
Cortes et al., New York City, United States. In J Exp Med, 2012
Point mutations in Artemis that disrupt its interaction with Ligase IV or DNA-PKcs reduce V(D)J recombination.
Similar temporal and spatial recruitment of native 19S and 20S proteasome subunits to transcriptionally active chromatin.
GeneRIF
Tansey et al., Nashville, United States. In Proc Natl Acad Sci U S A, 2012
Data show that proteasome subunits Rpt1, Rpt4, Rpn8, Rpn12, Pre6, and Pre10 are recruited to GAL10 rapidly upon galactose induction.
Phosphoribosylpyrophosphate synthetase superactivity and recurrent infections is caused by a p.Val142Leu mutation in PRS-I.
GeneRIF
de Brouwer et al., Cleveland, United States. In Am J Med Genet A, 2012
missense mutations in PRPS1 can cause a continuous spectrum of features ranging from progressive non-syndromic postlingual hearing impairment to uric acid overproduction, and recurrent infections depending on the functional sites that are affected
Artemis interacts with the Cul4A-DDB1DDB2 ubiquitin E3 ligase and regulates degradation of the CDK inhibitor p27.
GeneRIF
Legerski et al., Houston, United States. In Cell Cycle, 2012
Regulation of p27 by Artemis and DDB2 is important for cell cycle progression in normally proliferating cells.
Molecular analysis of X-linked inborn errors of purine metabolism: HPRT1 and PRPS1 mutations.
GeneRIF
Fujimori et al., Japan. In Nucleosides Nucleotides Nucleic Acids, 2011
Three HPRT1 mutations in Lesch-Nyhan families were identified but no mutation was identified in any patient in the analysis of PRPS1.
H2AX prevents CtIP-mediated DNA end resection and aberrant repair in G1-phase lymphocytes.
Impact
Sleckman et al., United States. In Nature, 2011
Although there are several cellular nucleases that could perform this function, only the Artemis nuclease is able to do so efficiently.
Antigen processing by nardilysin and thimet oligopeptidase generates cytotoxic T cell epitopes.
Impact
Melief et al., Leiden, Netherlands. In Nat Immunol, 2011
Nardilysin and TOP were required, either together or alone, for the generation of a tumor-specific CTL epitope from PRAME, an immunodominant CTL epitope from Epstein-Barr virus protein EBNA3C, and a clinically important epitope from the melanoma protein MART-1.
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