Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis. - Wikidata - awgldk - TriplyDB

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

http://www.wikidata.org/entity/Q35210772

about

High-level inducible Smad4-reexpression in the cervical cancer cell line C4-II is associated with a gene expression profile that predicts a preferential role of Smad4 in extracellular matrix composition Pathways for aberrant angiogenesis in pancreatic cancer Genetic alterations in pancreatic carcinoma Influence of hypoxia and neoangiogenesis on the growth of pancreatic cancer Role of TGFβ in regulation of the tumor microenvironment and drug delivery (review)TGFβ Signaling in Tumor Initiation, Epithelial-to-Mesenchymal Transition, and Metastasis Targeted destruction of the orchestration of the pancreatic stroma and tumor cells in pancreatic cancer cases: molecular basis for therapeutic implications The myc-miR-17~92 axis blunts TGF{beta} signaling and production of multiple TGF{beta}-dependent antiangiogenic factors Smad4 dependency defines two classes of transforming growth factor {beta} (TGF-{beta}) target genes and distinguishes TGF-{beta}-induced epithelial-mesenchymal transition from its antiproliferative and migratory responses.Divergent mechanisms underlie Smad4-mediated positive regulation of the three genes encoding the basement membrane component laminin-332 (laminin-5).Secretion of MCP-1 and other paracrine factors in a novel tumor-bone coculture model.SMAD4 loss triggers the phenotypic changes of pancreatic ductal adenocarcinoma cells Pancreatic cancer: pathobiology, treatment options, and drug delivery.PRH/Hhex controls cell survival through coordinate transcriptional regulation of vascular endothelial growth factor signaling.Loss of smad4 in Sertoli and Leydig cells leads to testicular dysgenesis and hemorrhagic tumor formation in mice Biological approaches to therapy of pancreatic cancer.p53-responsive miR-194 inhibits thrombospondin-1 and promotes angiogenesis in colon cancers Effect of oridonin-mediated hallmark changes on inflammatory pathways in human pancreatic cancer (BxPC-3) cells.SEL1L a multifaceted protein playing a role in tumor progression.The molecular targets for the diagnosis and treatment of pancreatic cancer.Cooperative assembly of Co-Smad4 MH1 with R-Smad1/3 MH1 on DNA: a molecular dynamics simulation study Biology and management of pancreatic cancer.TGF-beta antagonists: why suppress a tumor suppressor?Expression of the type-1 repeats of thrombospondin-1 inhibits tumor growth through activation of transforming growth factor-beta.Genetics and prevention of pancreatic cancer.Pancreatic cancer stromal biology and therapy.Immunotherapy for pancreatic cancer - science driving clinical progress.miR-146a, an IL-1β responsive miRNA, induces vascular endothelial growth factor and chondrocyte apoptosis by targeting Smad4.Essential role of endothelial Smad4 in vascular remodeling and integrity.A deep boosting based approach for capturing the sequence binding preferences of RNA-binding proteins from high-throughput CLIP-seq data.Alteration of somatostatin receptor subtype 2 gene expression in pancreatic tumor angiogenesis Determination of TGFbeta1 protein level in human primary breast cancers and its relationship with survival.Hepatocyte growth factor/scatter factor mediates angiogenesis through positive VEGF and negative thrombospondin 1 regulation.Angiogenic gene signature in human pancreatic cancer correlates with TGF-beta and inflammatory transcriptomes.Targeting signal transduction in pancreatic cancer treatment.Thrombospondin-based antiangiogenic therapy.Genetic alterations in pancreatic cancer.Diffuse-type gastric carcinoma: progression, angiogenesis, and transforming growth factor beta signaling Current insights on the biology and clinical aspects of VEGF regulation.Thrombospondin and apoptosis: molecular mechanisms and use for design of complementation treatments.

P2860

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P2860

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

http://www.wikidata.org/entity/Q35210772

description

2000 nî lūn-bûn

@nan

2000 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2000年の論文

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2000年論文

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2000年論文

@zh-hant

2000年論文

@zh-hk

2000年論文

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2000年論文

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2000年论文

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name

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

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Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

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type

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Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

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Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

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prefLabel

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

@ast

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

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

P1476

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesis.

@en

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A Hintelmann

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

B Sipos

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C Eilert-Micus

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G Klöppel

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I Schwarte-Waldhoff

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J Lüttges

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N P Bouck

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O V Volpert

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S A Hahn

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S Klein-Scory

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P2860

TGF-beta signal transduction

Remarkable versatility of Smad proteins in the nucleus of transforming growth factor-beta activated cells

The Hallmarks of Cancer

TGF-beta signalling from cell membrane to nucleus through SMAD proteins

Characterization of functional domains within Smad4/DPC4

Mads and Smads in TGF beta signalling

Human Smad3 and Smad4 are sequence-specific transcription activators

Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma

Intestinal tumorigenesis in compound mutant mice of both Dpc4 (Smad4) and Apc genes

Smad2 and Smad3 positively and negatively regulate TGF beta-dependent transcription through the forkhead DNA-binding protein FAST2

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