Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/49603
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Título : L- and S-endoglin differentially modulate TGFbeta1 signaling mediated by ALK1 and ALK5 in L6E9 myoblasts
Autor : Velasco, Soraya, Alvarez-Muñoz, Patricia, Pericacho, Miguel, ten Dijke, Peter, Bernabéu Quirante, Carmelo, Lopez-Novoa, José Miguel, Rodriguez-Barbero, Alicia
Palabras clave : TGFβ
L-endoglin
S-endoglin ALK1
ALK5
Id1
PAI1
Smads
Collagen I
Proliferation
Fecha de publicación : 15-Mar-2008
Editor: Company of Biologists
Resumen: TGFβ regulates cellular processes by binding to type I and type II TGFβ receptors (TβRI and TβRII, respectively). In addition to these signaling receptors, endoglin is an accessory TGFβ receptor that regulates TGFβ signaling. Although there are two different alternatively spliced isoforms of endoglin, L-endoglin (L, long) and S-endoglin (S, short), little is known about the effects of S-endoglin isoform on TGFβ signaling. Here, we have analyzed the TGFβ1 signaling pathways and the effects of L- and S-endoglin in endoglin-deficient L6E9 cells. We found that TGFβ activates two distinct TβRI-Smad signaling pathways: ALK1-Smad1-Id1 and ALK5-Smad2-PAI1, in these cells. Interestingly, L-endoglin enhanced the ALK1-Id1 pathway, while S-endoglin promoted the ALK5-PAI1 route. These effects on signaling are supported by biological effects on TGFβ1-induced collagen I expression and inhibition of cell proliferation. Thus, while L-endoglin decreased TGFβ1-induced collagen I and CTGF expression and increased TGFβ1-induced proliferation, S-endoglin strongly increased TGFβ1-induced collagen I and CTGF expression, and reduced TGFβ1-induced cell proliferation
Descripción : 7 páginas, 7 figuras -- PAGS nros. 913-919
Versión del editor: http://dx.doi.org/ 10.1242/​jcs.023283
URI : http://hdl.handle.net/10261/49603
ISSN: 0021-9533
DOI: 10.1242/​jcs.023283
Citación : Journal of Cell Science 121: 913-919 (2008)
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