A polymorphic p53 response element in KIT ligand influences cancer risk and has undergone natural selection. - Wikidata - wikimedia - TriplyDB

A polymorphic p53 response element in KIT ligand influences cancer risk and has undergone natural selection.

A polymorphic p53 response element in KIT ligand influences cancer risk and has undergone natural selection.

http://www.wikidata.org/entity/Q34228309

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The search for cis-regulatory driver mutations in cancer genomes Evolutionary determinants of cancer The genomic landscape of testicular germ cell tumours: from susceptibility to treatment.Functional annotation of putative regulatory elements at cancer susceptibility Loci Integrative genomic analysis identifies that SERPINA6-rs1998056 regulated by FOXA/ERα is associated with female hepatocellular carcinoma.A functional p53 responsive polymorphism in KITLG, rs4590952, does not affect the risk of breast cancer.Skin as a living coloring book: how epithelial cells create patterns of pigmentation.OncoCis: annotation of cis-regulatory mutations in cancer.Linking polymorphic p53 response elements with gene expression in airway epithelial cells of smokers and cancer risk.Cell context dependent p53 genome-wide binding patterns and enrichment at repeats.The genetics of human migrations: Our ancestors migration out of Africa has left traces in our genomes that explain how they adapted to new environments Approaches for establishing the function of regulatory genetic variants involved in disease.Interactions of chromatin context, binding site sequence content, and sequence evolution in stress-induced p53 occupancy and transactivation.Identifying causal regulatory SNPs in ChIP-seq enhancers Systematical analyses of variants in CTCF-binding sites identified a novel lung cancer susceptibility locus among Chinese population TP53 engagement with the genome occurs in distinct local chromatin environments via pioneer factor activity Prediction of the damage-associated non-synonymous single nucleotide polymorphisms in the human MC1R gene Genome wide DNA methylation profiles provide clues to the origin and pathogenesis of germ cell tumors.Whole-genome cartography of p53 response elements ranked on transactivation potential.In-silico identification and functional validation of allele-dependent AR enhancers.Integrative genomic analysis reveals widespread enhancer regulation by p53 in response to DNA damage Comprehensive Expression Profiling and Functional Network Analysis of p53-Regulated MicroRNAs in HepG2 Cells Treated with Doxorubicin Np9, a cellular protein of retroviral ancestry restricted to human, chimpanzee and gorilla, binds and regulates ubiquitin ligase MDM2.Identification of four new susceptibility loci for testicular germ cell tumour.Distinct downstream targets manifest p53-dependent pathologies in mice.Epidemiology of Testicular Cancer in Oklahoma and the United States.Locus-specific databases in cancer: what future in a post-genomic era? The TP53 LSDB paradigm.Testicular cancer: biology and biomarkers.Sun-induced freckling: ephelides and solar lentigines.Cis-regulatory variation: significance in biomedicine and evolution.Examining the impact of gene variants on histone lysine methylation Common variants identified in genome-wide association studies of testicular germ cell tumour: an update, biological insights and clinical application.A Polymorphic Antioxidant Response Element Links NRF2/sMAF Binding to Enhanced MAPT Expression and Reduced Risk of Parkinsonian Disorders The importance of p53 pathway genetics in inherited and somatic cancer genomes.Genetic Modifiers of the p53 Pathway.Census and evaluation of p53 target genes.A coding single-nucleotide polymorphism in lysine demethylase KDM4A associates with increased sensitivity to mTOR inhibitors.The biology of germ cell tumors in disorders of sex development.Genetic changes associated with testicular cancer susceptibility.Identification of 19 new risk loci and potential regulatory mechanisms influencing susceptibility to testicular germ cell tumor.

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P2860

A polymorphic p53 response element in KIT ligand influences cancer risk and has undergone natural selection.

http://www.wikidata.org/entity/Q34228309

description

2013 nî lūn-bûn

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2013 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2013 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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A polymorphic p53 response ele ...... s undergone natural selection.

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J.CELL.2013.09.017

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A polymorphic p53 response ele ...... s undergone natural selection.

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Dan Su

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Douglas A Bell

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Elisabeth F P Peterse

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Emmanouela Repapi

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Natalia Sacilotto

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Neil F Box

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P2860

A map of recent positive selection in the human genome

An integrated map of genetic variation from 1,092 human genomes

Genome-wide analysis of transcription factor binding sites based on ChIP-Seq data

Common variation in KITLG and at 5q31.3 predisposes to testicular germ cell cancer.

Mapping short DNA sequencing reads and calling variants using mapping quality scores

Testicular cancer incidence trends in the USA (1975-2004): plateau or shifting racial paradigm?

Stem cell factor receptor/c-Kit: from basic science to clinical implications

DNA-binding specificities of human transcription factors

Variants near DMRT1, TERT and ATF7IP are associated with testicular germ cell cancer

A global map of p53 transcription-factor binding sites in the human genome

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410-422

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10.1016/J.CELL.2013.09.017

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Francesc Castro-giner

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