J
Jun-ichi Hanai
Researcher at Beth Israel Deaconess Medical Center
Publications - 56
Citations - 10141
Jun-ichi Hanai is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: SMAD & Transactivation. The author has an hindex of 35, co-authored 56 publications receiving 9429 citations. Previous affiliations of Jun-ichi Hanai include Harvard University & Japan Society for the Promotion of Science.
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Journal ArticleDOI
Soluble endoglin contributes to the pathogenesis of preeclampsia.
Shivalingappa Venkatesha,Mourad Toporsian,Chun Lam,Jun-ichi Hanai,Tadanori Mammoto,Yeon Mee Kim,Yeon Mee Kim,Yuval Bdolah,Kee-Hak Lim,Hai Tao Yuan,Towia A. Libermann,Isaac E. Stillman,Drucilla J. Roberts,Patricia A. D'Amore,Franklin H. Epstein,Frank W. Sellke,Roberto Romero,Roberto Romero,Vikas P. Sukhatme,Michelle Letarte,S. Ananth Karumanchi +20 more
TL;DR: A novel placenta-derived soluble TGF-β coreceptor, endoglin (sEng), which is elevated in the sera of preeclamptic individuals, correlates with disease severity and falls after delivery, suggest that sEng may act in concert with sFlt1 to induce severe preeclampsia.
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BMP-7 counteracts TGF-β1–induced epithelial-to-mesenchymal transition and reverses chronic renal injury
Michael Zeisberg,Jun-ichi Hanai,Hikaru Sugimoto,Tadanori Mammoto,David M. Charytan,Frank Strutz,Raghu Kalluri +6 more
TL;DR: It is reported that BMP-7 reverses TGF-β1–induced epithelial-to-mesenchymal transition (EMT) by reinduction of E-cadherin, a key epithelial cell adhesion molecule, which provides evidence of cross talk between B MP-7 and TGF -β1 in the regulation of EMT in health and disease.
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TGF-beta receptor-mediated signalling through Smad2, Smad3 and Smad4.
Atsuhito Nakao,Takeshi Imamura,Takeshi Imamura,Serhiy Souchelnytskyi,Masahiro Kawabata,Akira Ishisaki,Eiichi Oeda,Kiyoshi Tamaki,Jun-ichi Hanai,Carl-Henrik Heldin,Kohei Miyazono,Peter ten Dijke +11 more
TL;DR: It is shown that Smad2 and Smad3 interacted with the kinase‐deficient TGF‐β type I receptor (TβR)‐I after it was phosphorylated by TβR‐II kinase, which suggests that T GF‐β induces heteromeric complexes of Smad 2, 3 and 4, and their concomitant translocation to the nucleus, which is required for efficient TGF-β signal transduction.
Journal ArticleDOI
Smad6 inhibits signalling by the TGF-Beta superfamily
Takeshi Imamura,Masao Takase,Ayako Nishihara,Eiichi Oeda,Jun-ichi Hanai,Masahiro Kawabata,Kohei Miyazono +6 more
TL;DR: The isolation of Smad6 in the mouse indicates that signals of the TGF-β superfamily are regulated both positively and negatively by members of the SMAD family.
Journal ArticleDOI
Interaction and Functional Cooperation of PEBP2/CBF with Smads SYNERGISTIC INDUCTION OF THE IMMUNOGLOBULIN GERMLINE Cα PROMOTER
Jun-ichi Hanai,Lin Feng Chen,Tomohiko Kanno,Naoko Ohtani-Fujita,Woo-Young Kim,Wei-hui Guo,Takeshi Imamura,Y Ishidou,Minoru Fukuchi,Meng Jiao Shi,Janet Stavnezer,Masahiro Kawabata,Kohei Miyazono,Yoshiaki Ito +13 more
TL;DR: It is shown that three mammalian α subunits of PEBP2/CBF form complexes with R-Smads that act in TGF-β/activin pathways as well as those acting in bone morphogenetic protein (BMP) pathways, and PEBP 2 may be a nuclear target of TGF -β/BMP signaling.