DNA demethylase activity maintains intestinal cells in an undifferentiated state following loss of APC. - Wikidata - wikimedia - TriplyDB

DNA demethylase activity maintains intestinal cells in an undifferentiated state following loss of APC.

DNA demethylase activity maintains intestinal cells in an undifferentiated state following loss of APC.

http://www.wikidata.org/entity/Q34147851

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Epigenetic modulators, modifiers and mediators in cancer aetiology and progression The roles of retinoic acid and retinoic acid receptors in inducing epigenetic changes Loss of Dnmt3b function upregulates the tumor modifier Ment and accelerates mouse lymphomagenesis Tissue-specific derepression of TCF/LEF controls the activity of the Wnt/β-catenin pathway.A metabolic switch controls intestinal differentiation downstream of Adenomatous polyposis coli (APC).DNA methylation in zebrafish.Changes in gene expression and cellular architecture in an ovarian cancer progression model.Uracil-DNA glycosylase is involved in DNA demethylation and required for embryonic development in the zebrafish embryo Dynamic Alu methylation during normal development, aging, and tumorigenesis.TAZ expression as a prognostic indicator in colorectal cancer.Somatic mutations, allele loss, and DNA methylation of the Cub and Sushi Multiple Domains 1 (CSMD1) gene reveals association with early age of diagnosis in colorectal cancer patients No evidence for AID/MBD4-coupled DNA demethylation in zebrafish embryos.Regulation and function of DNA methylation in plants and animals.Alcohol and aldehyde dehydrogenases: retinoid metabolic effects in mouse knockout models Modulation of Wnt/β-catenin signaling and proliferation by a ferrous iron chelator with therapeutic efficacy in genetically engineered mouse models of cancer.Histone deacetylase SIRT1 modulates and deacetylates DNA base excision repair enzyme thymine DNA glycosylase.Injury-dependent Müller glia and ganglion cell reprogramming during tissue regeneration requires Apobec2a and Apobec2b Wnts are dispensable for differentiation and self-renewal of adult murine hematopoietic stem cells.Directional DNA methylation changes and complex intermediate states accompany lineage specificity in the adult hematopoietic compartment.Pyrosequencing Analysis of APC Methylation Level in Human Prostate Tissues: A Molecular Marker for Prostate Cancer.Epigenetic regulation of colon cancer and intestinal stem cells Apc regulates the function of hematopoietic stem cells largely through β-catenin-dependent mechanisms.A comprehensive analysis of the effects of the deaminase AID on the transcriptome and methylome of activated B cells.TETonic shift: biological roles of TET proteins in DNA demethylation and transcription.Diagnosis, surveillance, and treatment strategies for familial adenomatous polyposis: rationale and update.Epigenetic reprogramming: is deamination key to active DNA demethylation?UHRF1 overexpression drives DNA hypomethylation and hepatocellular carcinoma The RON receptor tyrosine kinase promotes metastasis by triggering MBD4-dependent DNA methylation reprogramming.Zebrafish Discoveries in Cancer Epigenetics.β-catenin as a potential key target for tumor suppression.Epigenetics, development, and cancer: zebrafish make their mark..Demethylation and re-expression of epigenetically silenced tumor suppressor genes: sensitization of cancer cells by combination therapy.Genomic insights into WNT/β-catenin signaling.Tumor cell plasticity: the challenge to catch a moving target.AID and APOBEC deaminases: balancing DNA damage in epigenetics and immunity.Epigenetic Mechanisms as an Interface Between the Environment and Genome.α-Catenin interacts with APC to regulate β-catenin proteolysis and transcriptional repression of Wnt target genes.Inhibition of WNT signaling in the bone marrow niche prevents the development of MDS in the Apcdel/+ MDS mouse model.New sources of retinoic acid synthesis revealed by live imaging of an Aldh1a2-GFP reporter fusion protein throughout zebrafish development.Combined hypermethylation of APC and GSTP1 as a molecular marker for prostate cancer: quantitative pyrosequencing analysis.

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DNA demethylase activity maintains intestinal cells in an undifferentiated state following loss of APC.

http://www.wikidata.org/entity/Q34147851

description

2010 nî lūn-bûn

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2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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DNA demethylase activity maint ...... d state following loss of APC.

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DNA demethylase activity maint ...... d state following loss of APC.

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DNA demethylase activity maint ...... d state following loss of APC.

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DNA demethylase activity maint ...... d state following loss of APC.

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DNA demethylase activity maint ...... d state following loss of APC.

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DNA demethylase activity maint ...... d state following loss of APC.

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DNA demethylase activity maint ...... d state following loss of APC.

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Brad Sklow

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Bradley R Cairns

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David A Jones

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Fanuel T Hagos

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Kenneth F Grossmann

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Kunal Rai

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Lincoln D Nadauld

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Matthew Voas

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Rachel K Toth

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Randall Burt

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P2860

Histone demethylation mediated by the nuclear amine oxidase homolog LSD1

Reprogramming towards pluripotency requires AID-dependent DNA demethylation

Aldehyde dehydrogenase 1 is a marker for normal and malignant human colonic stem cells (SC) and tracks SC overpopulation during colon tumorigenesis

Regulated subset of G1 growth-control genes in response to derepression by the Wnt pathway

Coordinated histone modifications mediated by a CtBP co-repressor complex

The tumor suppressor adenomatous polyposis coli and caudal related homeodomain protein regulate expression of retinol dehydrogenase L

Activation-induced cytidine deaminase deaminates 5-methylcytosine in DNA and is expressed in pluripotent tissues: implications for epigenetic reprogramming

Deletion of the AU-rich RNA binding protein Apobec-1 reduces intestinal tumor burden in Apc(min) mice

Distribution, silencing potential and evolutionary impact of promoter DNA methylation in the human genome

Induction of tumors in mice by genomic hypomethylation

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