Noncanonical TGFβ Signaling Contributes to Aortic Aneurysm Progression in Marfan Syndrome Mice-Reference-Cited by-同舟云学术

Noncanonical TGFβ Signaling Contributes to Aortic Aneurysm Progression in Marfan Syndrome Mice

Published:2011-04-15 Issue:6027 Volume:332 Page:358-361
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Holm Tammy M.¹,Habashi Jennifer P.¹²,Doyle Jefferson J.¹,Bedja Djahida³,Chen YiChun¹,van Erp Christel¹,Lindsay Mark E.¹²,Kim David¹,Schoenhoff Florian¹,Cohn Ronald D.¹²,Loeys Bart L.⁴,Thomas Craig J.⁵,Patnaik Samarjit⁵,Marugan Juan J.⁵,Judge Daniel P.⁶,Dietz Harry C.¹²⁶

Affiliation:

1. Howard Hughes Medical Institute and Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

2. Division of Pediatric Cardiology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

3. Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

4. Centre for Medical Genetics, Ghent University, 9000 Ghent, Belgium.

5. National Institutes of Health Chemical Genomics Center, Rockville, MD 20850, USA.

6. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Abstract

Transforming growth factor–β promotes aortic aneurysm formation through activation of its “noncanonical” signaling pathway.

Funder

National Institutes of Health

National Human Genome Research Institute

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Link

http://www.sciencemag.org/content/332/6027/358.full.pdf

Reference27 articles.

1. Latent Transforming Growth Factor β-binding Protein 1 Interacts with Fibrillin and Is a Microfibril-associated Protein

2. TGF-β in the pathogenesis and prevention of disease: a matter of aneurysmic proportions

3. The Extracellular Matrix: Not Just Pretty Fibrils

4. New regulatory mechanisms of TGF-β receptor function

5. Smad-dependent and Smad-independent pathways in TGF-β family signalling

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