Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells. - Wikidata - awgldk - TriplyDB

Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells.

Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells.

http://www.wikidata.org/entity/Q33977987

about

Predicting targeted drug combinations based on Pareto optimal patterns of coexpression network connectivity Maximum growth and survival of estrogen receptor-alpha positive breast cancer cells requires the Sin3A transcriptional repressor.Progestin and antiprogestin responsiveness in breast cancer is driven by the PRA/PRB ratio via AIB1 or SMRT recruitment to the CCND1 and MYC promoters.Novel and emerging targeted-based cancer therapy agents and methods.Selective Inhibition of SIN3 Corepressor with Avermectins as a Novel Therapeutic Strategy in Triple-Negative Breast Cancer.Obesity Leads to Tissue, but not Serum Vitamin A Deficiency.Targeting the SIN3A-PF1 interaction inhibits epithelial to mesenchymal transition and maintenance of a stem cell phenotype in triple negative breast cancer.Blocking the PAH2 domain of Sin3A inhibits tumorigenesis and confers retinoid sensitivity in triple negative breast cancer SIN3A and SIN3B differentially regulate breast cancer metastasis.Retinoids regulate stem cell differentiation Epigenetics in C. elegans: facts and challenges.Targeting transcription factor corepressors in tumor cells.Metastasis suppression by BRMS1 associated with SIN3 chromatin remodeling complexes.E-cadherin plasticity in prostate cancer stem cell invasion Insights into the molecular mechanisms of action of bioportides: a strategy to target protein-protein interactions.Analysis of DNA methylation in single circulating tumor cells.Sin3a acts through a multi-gene module to regulate invasion in Drosophila and human tumors.Sulforaphane-Induced Cell Cycle Arrest and Senescence are accompanied by DNA Hypomethylation and Changes in microRNA Profile in Breast Cancer Cells.The potential of targeting Sin3B and its associated complexes for cancer therapy.Targeted interference of SIN3A-TGIF1 function by SID decoy treatment inhibits Wnt signaling and invasion in triple negative breast cancer cells.A novel somatic mutation of SIN3A detected in breast cancer by whole-exome sequencing enhances cell proliferation through ERα expression

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Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells.

http://www.wikidata.org/entity/Q33977987

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունիսին 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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name

Interference with Sin3 functio ...... iation in breast cancer cells.

@ast

Interference with Sin3 functio ...... iation in breast cancer cells.

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type

label

Interference with Sin3 functio ...... iation in breast cancer cells.

@ast

Interference with Sin3 functio ...... iation in breast cancer cells.

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prefLabel

Interference with Sin3 functio ...... iation in breast cancer cells.

@ast

Interference with Sin3 functio ...... iation in breast cancer cells.

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PNAS.1006737107

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Proceedings of the National Academy of Sciences of the United States of America

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Interference with Sin3 functio ...... iation in breast cancer cells.

@en

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Arthur Zelent

http://www.w3.org/2001/XMLSchema#string

Boris Leibovitch

http://www.w3.org/2001/XMLSchema#string

Eduardo F Farias

http://www.w3.org/2001/XMLSchema#string

Janice Murtagh

http://www.w3.org/2001/XMLSchema#string

Kevin Petrie

http://www.w3.org/2001/XMLSchema#string

Manuel Boix Chornet

http://www.w3.org/2001/XMLSchema#string

Tino Schenk

http://www.w3.org/2001/XMLSchema#string

P2860

Jagged1-mediated Notch activation induces epithelial-to-mesenchymal transition through Slug-induced repression of E-cadherin.

DNMT3L connects unmethylated lysine 4 of histone H3 to de novo methylation of DNA

Adhesion-independent mechanism for suppression of tumor cell invasion by E-cadherin.

Extension of the binding motif of the Sin3 interacting domain of the Mad family proteins

Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3

An amino-terminal domain of Mxi1 mediates anti-Myc oncogenic activity and interacts with a homolog of the yeast transcriptional repressor SIN3

Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer

The cancer epigenome--components and functional correlates

A role for mammalian Sin3 in permanent gene silencing

Morphogenesis and oncogenesis of MCF-10A mammary epithelial acini grown in three-dimensional basement membrane cultures

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11811-11816

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scholarly article

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10.1073/PNAS.1006737107

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26

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107

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44673022

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20547842

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2900697

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