J
Jianfeng Wu
Researcher at University of California, San Francisco
Publications - 11
Citations - 3329
Jianfeng Wu is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Integrin & Vitronectin. The author has an hindex of 9, co-authored 10 publications receiving 3158 citations.
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Journal ArticleDOI
The integrin alpha v beta 6 binds and activates latent TGF beta 1: a mechanism for regulating pulmonary inflammation and fibrosis.
John S. Munger,Xiaozhu Huang,Hisaaki Kawakatsu,Mark J. D. Griffiths,Stephen L. Dalton,Jianfeng Wu,Jean-Francois Pittet,Naftali Kaminski,Chrystelle Garat,Michael A. Matthay,Daniel B. Rifkin,Dean Sheppard +11 more
TL;DR: In this article, Latency-Aged Peptide (LAP) was shown to be a ligand for the integrin alpha v beta 6 and that alpha-v beta 6-expressing cells induce spatially restricted activation of TGF beta 1.
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Inactivation of the integrin beta 6 subunit gene reveals a role of epithelial integrins in regulating inflammation in the lung and skin.
Xiaozhu Huang,Jianfeng Wu,Darrell L. Cass,David J. Erle,David B. Corry,Stephen G. Young,Robert V. Farese,Dean Sheppard +7 more
TL;DR: Results suggest that the epithelial integrin alpha v beta 6 participates in the modulation of epithelial inflammation, and genetic or acquired alterations in this integrin could contribute to the development of inflammatory diseases of epithel organs, such as the lungs and skin.
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Fatal Bilateral Chylothorax in Mice Lacking the Integrin α9β1
TL;DR: The results suggest that the α9 integrin is required for the normal development of the lymphatic system, including the thoracic duct, and that α9 deficiency could be one cause of congenital chylothorax.
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Normal Development, Wound Healing, and Adenovirus Susceptibility in β5-Deficient Mice
TL;DR: The data suggest that αvβ5 is not essential for normal development, reproduction, adenovirus infection, or the healing of cutaneous wounds.
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The integrin alphavbeta6 is critical for keratinocyte migration on both its known ligand, fibronectin, and on vitronectin
TL;DR: Alphav beta6-mediated migration on both ligands was dramatically augmented by treatment with phorbol myrisate acetate (PMA) or with hepatocyte growth factor, and augmentation of migration by either stimulus could be abolished by the PKC inhibitor GF109203X, suggesting a critical role for PKC in enhancement of alphavbeta6- mediated cell migration.