ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth. - Test2 - elhamkhani - TriplyDB

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

http://www.wikidata.org/entity/Q34096297

about

A Survey of Strategies to Modulate the Bone Morphogenetic Protein Signaling Pathway: Current and Future Perspectives Targeting BMP signalling in cardiovascular disease and anaemia BMPs and their clinical potentials Specificity and Structure of a High Affinity Activin Receptor-like Kinase 1 (ALK1) Signaling Complex Activin receptor-like kinases: a diverse family playing an important role in cancer Enhanced responses to angiogenic cues underlie the pathogenesis of hereditary hemorrhagic telangiectasia 2 TMPRSS2:ERG gene fusion variants induce TGF-β signaling and epithelial to mesenchymal transition in human prostate cancer cells Bone morphogenetic protein 2 signaling negatively modulates lymphatic development in vertebrate embryos.ALK1 signaling inhibits angiogenesis by cooperating with the Notch pathway.Molecular pathways: can activin-like kinase pathway inhibition enhance the limited efficacy of VEGF inhibitors?Structural and functional insights into endoglin ligand recognition and binding.Activin receptor inhibitors--dalantercept.Bone Morphogenetic Protein (BMP) signaling in development and human diseases Endoglin requirement for BMP9 signaling in endothelial cells reveals new mechanism of action for selective anti-endoglin antibodies.Prodomains of transforming growth factor beta (TGFbeta) superfamily members specify different functions: extracellular matrix interactions and growth factor bioavailability.Endoplasmic reticulum (ER) stress inducible factor cysteine-rich with EGF-like domains 2 (Creld2) is an important mediator of BMP9-regulated osteogenic differentiation of mesenchymal stem cells ALK1 as an emerging target for antiangiogenic therapy of cancer Soluble endoglin specifically binds bone morphogenetic proteins 9 and 10 via its orphan domain, inhibits blood vessel formation, and suppresses tumor growth The soluble form of BMPRIB is a novel therapeutic candidate for treating bone related disorders.The Prodomain-Containing BMP9 Produced from a Stable Line Effectively Regulates the Differentiation of Mesenchymal Stem Cells.Rapid Activation of Bone Morphogenic Protein 9 by Receptor-mediated Displacement of Pro-domains.Deficiency for endoglin in tumor vasculature weakens the endothelial barrier to metastatic dissemination BMP9-regulated angiogenic signaling plays an important role in the osteogenic differentiation of mesenchymal progenitor cells.Transforming Growth Factor-β Family Ligands Can Function as Antagonists by Competing for Type II Receptor Binding.Context-dependent signaling defines roles of BMP9 and BMP10 in embryonic and postnatal development.Role of TGF-β and the tumor microenvironment during mammary tumorigenesis Circulating Bmp10 acts through endothelial Alk1 to mediate flow-dependent arterial quiescence Specific cancer rates may differ in patients with hereditary haemorrhagic telangiectasia compared to controls.Inhibition of ALK1 signaling with dalantercept combined with VEGFR TKI leads to tumor stasis in renal cell carcinoma.BMP signaling in vascular development and disease.Liposomes targeting tumour stromal cells.Novel targets for VEGF-independent anti-angiogenic drugs.Advances in targeted therapeutic agents.Activin receptor-like kinase 1 as a target for anti-angiogenesis therapy.TGF-β & BMP receptors endoglin and ALK1: overview of their functional role and status as antiangiogenic targets.Application of small organic molecules reveals cooperative TGFβ and BMP regulation of mesothelial cell behaviors.Sorafenib-based combined molecule targeting in treatment of hepatocellular carcinoma.Production, Isolation, and Structural Analysis of Ligands and Receptors of the TGF-β Superfamily.Moving beyond vascular endothelial growth factor-targeted therapy in renal cell cancer: latest evidence and therapeutic implications.Tumor angiogenesis and vascular normalization: alternative therapeutic targets.

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P2860

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

http://www.wikidata.org/entity/Q34096297

description

2010 nî lūn-bûn

@nan

2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@ast

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@en

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@nl

type

label

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@ast

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@en

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@nl

prefLabel

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@ast

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@en

ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@nl

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1535-7163.MCT-09-0650

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Molecular Cancer Therapeutics

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ALK1-Fc inhibits multiple mediators of angiogenesis and suppresses tumor growth.

@en

P2093

Aaron W Mulivor

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

Asya V Grinberg

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

Dianne Mitchell

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

Eileen G Pobre

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

Jasbir Seehra

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Jeffrey A Ucran

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Kathryn W Underwood

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Nicolas Solban

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

R Scott Pearsall

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

Ravindra Kumar

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379-388

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scholarly article

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10.1158/1535-7163.MCT-09-0650

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2

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9

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2010-02-02T00:00:00Z

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20124460

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