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Endoglin Modulation of TGF-ß1-Induced Collagen Synthesis is Dependent on ERK1/2 MAPK Activation
Author(s) -
Alicia RodríguezBarbero,
Juana Obreo,
Patricia Álvarez-Muñoz,
Atanasio Pandiella,
Carmelo Bernabéu,
José M. LópezNovoa
Publication year - 2006
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000095181
Subject(s) - endoglin , extracellular matrix , transforming growth factor , mapk/erk pathway , transfection , chemistry , microbiology and biotechnology , myocyte , transforming growth factor beta , type i collagen , western blot , p38 mitogen activated protein kinases , extracellular , signal transduction , biology , endocrinology , biochemistry , gene , stem cell , cd34
Transforming growth factor-beta1 (TGF-beta1) plays a pivotal role in the extracellular matrix accumulation observed in fibrotic diseases. Endoglin is an important component of the TGF-beta receptor complex highly expressed in tissues undergoing fibrotic processes. Endoglin expression regulates the effect of TGF-beta on extracellular matrix synthesis. The purpose of our study has been to understand the molecular mechanism by which endoglin exerts its effects on fibrosis and the possible role of MAP kinases in these effects.

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