Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model. - Wikidata - awgldk - TriplyDB

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

http://www.wikidata.org/entity/Q35108003

about

The pathobiology of vascular malformations: insights from human and model organism genetics.Marfan Syndrome and Related Disorders: 25 Years of Gene Discovery.

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Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

http://www.wikidata.org/entity/Q35108003

description

2014 nî lūn-bûn

@nan

2014 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2014年の論文

@ja

2014年論文

@yue

2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@ast

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@en

type

label

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@ast

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@en

prefLabel

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@ast

Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@en

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JOURNAL.PONE.0089749

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Absence of cardiovascular manifestations in a haploinsufficient Tgfbr1 mouse model.

@en

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Bert Vandeghinste

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Bram Trachet

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

Christophe Casteleyn

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Filip De Vos

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Harry Dietz

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Jeroen Essers

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Julie De Backer

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Laurence Campens

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Marjolijn Renard

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

Patrick Segers

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P2860

Fibrillin, a new 350-kD glycoprotein, is a component of extracellular microfibrils

Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome

A syndrome of altered cardiovascular, craniofacial, neurocognitive and skeletal development caused by mutations in TGFBR1 or TGFBR2

Aneurysm syndromes caused by mutations in the TGF-beta receptor

Abnormal angiogenesis but intact hematopoietic potential in TGF-beta type I receptor-deficient mice

Cardiovascular malformations with normal smooth muscle differentiation in neural crest-specific type II TGFbeta receptor (Tgfbr2) mutant mice

Defective ALK5 signaling in the neural crest leads to increased postmigratory neural crest cell apoptosis and severe outflow tract defects

Double-outlet right ventricle and overriding tricuspid valve reflect disturbances of looping, myocardialization, endocardial cushion differentiation, and apoptosis in TGF-beta(2)-knockout mice

Dysregulation of TGF-beta activation contributes to pathogenesis in Marfan syndrome

Efficient and fast targeted production of murine models based on ENU mutagenesis.

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10.1371/JOURNAL.PONE.0089749

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2

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Bert Callewaert

Steven Staelens

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2014-02-24T00:00:00Z

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haploinsufficiency

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