KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs. - Test2 - elhamkhani - TriplyDB

KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs.

KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs.

http://www.wikidata.org/entity/Q34322749

about

Chromatin dynamics during cellular reprogramming KDM2B Recruitment of the Polycomb Group Complex, PRC1.1, Requires Cooperation between PCGF1 and BCORL1 The Triple-Code Model for Pancreatic Cancer: Cross Talk Among Genetics, Epigenetics, and Nuclear Structure Deregulation of F-box proteins and its consequence on cancer development, progression and metastasis.Mutations of Chromatin Structure Regulating Genes in Human Malignancies.Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo A developmental genetic analysis of the lysine demethylase KDM2 mutations in Drosophila melanogaster.Roles of F-box proteins in cancer Novel Scaffolds of Cell-Active Histone Demethylase Inhibitors Identified from High-Throughput Screening.Fbxl10 overexpression in murine hematopoietic stem cells induces leukemia involving metabolic activation and upregulation of Nsg2.NDY1/KDM2B functions as a master regulator of polycomb complexes and controls self-renewal of breast cancer stem cells.Increased mitochondrial function downstream from KDM5A histone demethylase rescues differentiation in pRB-deficient cells.Small molecule therapeutics targeting F-box proteins in cancer.Histone demethylase KDM2B regulates lineage commitment in normal and malignant hematopoiesis.Ubiquitination-mediated degradation of cell cycle-related proteins by F-box proteins Nitric oxide modifies global histone methylation by inhibiting Jumonji C domain-containing demethylases.Transcriptional control of autophagy-lysosome function drives pancreatic cancer metabolism KDM2A promotes lung tumorigenesis by epigenetically enhancing ERK1/2 signaling.Cytogenetic and molecular profile of endometrial stromal sarcoma.Tudor: a versatile family of histone methylation 'readers'.The roles of Jumonji-type oxygenases in human disease.Epigenetic pathway targets for the treatment of disease: accelerating progress in the development of pharmacological tools: IUPHAR Review 11.CDK5/FBW7-dependent ubiquitination and degradation of EZH2 inhibits pancreatic cancer cell migration and invasion.Inhibitors of Protein Methyltransferases and Demethylases.Recent advances in SCF ubiquitin ligase complex: Clinical implications Lysine-specific histone demethylases in normal and malignant hematopoiesis.Landscape of Genomic Alterations in Pituitary Adenomas.Epigenetic silencing of EYA2 in pancreatic adenocarcinomas promotes tumor growth.Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.KDM2B, an H3K36-specific demethylase, regulates apoptotic response of GBM cells to TRAIL.Lysine demethylase KDM4A associates with translation machinery and regulates protein synthesis.KDM2 Family Members are Regulated by HIF-1 in Hypoxia KDM2B/FBXL10 targets c-Fos for ubiquitylation and degradation in response to mitogenic stimulation F-box proteins in epigenetic regulation of cancer.STK38L kinase ablation promotes loss of cell viability in a subset of KRAS-dependent pancreatic cancer cell lines.FBXL10 contributes to the development of diffuse large B-cell lymphoma by epigenetically enhancing ERK1/2 signaling pathway.Targeting glioma stem-like cell survival and chemo-resistance through inhibition of lysine-specific histone demethylase KDM2B.KDM2B overexpression correlates with poor prognosis and regulates glioma cell growth.Screening of Conditionally Reprogrammed Patient-Derived Carcinoma Cells Identifies ERCC3-MYC Interactions as a Target in Pancreatic Cancer.Loss of KDM6A Activates Super-Enhancers to Induce Gender-Specific Squamous-like Pancreatic Cancer and Confers Sensitivity to BET Inhibitors.

P2860

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P2860

KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs.

http://www.wikidata.org/entity/Q34322749

description

2013 nî lūn-bûn

@nan

2013 թուականի Յունուարին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի հունվարին հրատարակված գիտական հոդված

@hy

2013年の論文

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2013年論文

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2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

@wuu

name

KDM2B promotes pancreatic canc ...... dent transcriptional programs.

@ast

KDM2B promotes pancreatic canc ...... dent transcriptional programs.

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KDM2B promotes pancreatic canc ...... dent transcriptional programs.

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type

label

KDM2B promotes pancreatic canc ...... dent transcriptional programs.

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KDM2B promotes pancreatic canc ...... dent transcriptional programs.

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KDM2B promotes pancreatic canc ...... dent transcriptional programs.

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prefLabel

KDM2B promotes pancreatic canc ...... dent transcriptional programs.

@ast

KDM2B promotes pancreatic canc ...... dent transcriptional programs.

@en

KDM2B promotes pancreatic canc ...... dent transcriptional programs.

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Journal of Clinical Investigation

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KDM2B promotes pancreatic canc ...... dent transcriptional programs.

@en

P2093

Alexandros Tzatsos

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Fei Lan

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Nabeel Bardeesy

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Patrick Trojer

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Peter J Park

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Polina Paskaleva

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Svetlana Stoykova

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Vikram Deshpande

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P2860

Polycomb group and SCF ubiquitin ligases are found in a novel BCOR complex that is recruited to BCL6 targets

Histone lysine demethylase JARID1a activates CLOCK-BMAL1 and influences the circadian clock

Covalent histone modifications--miswritten, misinterpreted and mis-erased in human cancers

Core signaling pathways in human pancreatic cancers revealed by global genomic analyses

Cooperative epigenetic modulation by cancer amplicon genes

Convergent structural alterations define SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeler as a central tumor suppressive complex in pancreatic cancer

EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells

The Trithorax group protein Lid is a trimethyl histone H3K4 demethylase required for dMyc-induced cell growth

Histone methylation by PRC2 is inhibited by active chromatin marks

Genome-wide analysis of the H3K4 histone demethylase RBP2 reveals a transcriptional program controlling differentiation

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727-739

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10.1172/JCI64535

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P433

2

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123

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Nabeel Bardeesy

Francesco Ferrari

Gianmarco Contino

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2013-01-16T00:00:00Z

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23321669

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3561797

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