BMPR-II deficiency elicits pro-proliferative and anti-apoptotic responses through the activation of TGFβ-TAK1-MAPK pathways in PAH-Reference-Cited by-同舟云学术

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BMPR-II deficiency elicits pro-proliferative and anti-apoptotic responses through the activation of TGFβ-TAK1-MAPK pathways in PAH

Published:2012-03-02 Issue:11 Volume:21 Page:2548-2558
ISSN:0964-6906
Container-title:Human Molecular Genetics
language:en
Short-container-title:

Author:

Nasim Md Talat,Ogo Takeshi,Chowdhury Hasnin M.,Zhao Lan,Chen Chien-nien,Rhodes Christopher,Trembath Richard C.

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology,General Medicine

Reference33 articles.

1. Heterozygous germline mutations in BMPR2, encoding a TGF-beta receptor, cause familial primary pulmonary hypertension. The International PPH Consortium;Nat. Genet.,2000

2. Immunolocalisation of BMPR-II and TGF-ss type I and II receptors in primary plexogenic pulmonary hypertension;J. Heart Lung Transplant,2001

3. Bone morphogenetic protein signalling in heritable versus idiopathic pulmonary hypertension;Eur. Respir. J.,2009

4. Bone morphogenetic protein-7 (osteogenic protein-1) inhibits smooth muscle cell proliferation and stimulates the expression of markers that are characteristic of SMC phenotype in vitro;J. Cell Physiol.,2000

5. Inhibition of rat vascular smooth muscle proliferation in vitro and in vivo by bone morphogenetic protein-2;J. Clin. Invest.,1997

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