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p38α MAPK can positively or negatively regulate Rac‐1 activity depending on the presence of serum
Author(s) -
Zuluaga Susana,
Gutiérrez-Uzquiza Alvaro,
Bragado Paloma,
Álvarez-Barrientos Alberto,
Benito Manuel,
Nebreda Angel R.,
Porras Almudena
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.06.078
Subject(s) - serum response factor , chemistry , p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , gtp' , biology , signal transduction , biochemistry , transcription factor , gene , enzyme
The small GTP‐ase Rac‐1 can trigger p38 MAPK activation and, in turn, p38α can regulate signalling pathways that potentially impinge on Rac‐1 activity. We have investigated the cross‐talk between p38α and Rac‐1 and found that p38α regulates the association between Rac‐1 and caveolin‐1 in serum‐deprived cardiomyocytes. This interaction depends on cell attachment and correlates with higher levels of active Rac‐1. Actin organization might regulate the formation of Rac‐1–caveolin‐1 complexes. In contrast, the Rac‐1–caveolin‐1 interaction is almost undetectable in the presence of serum, where Rac‐1 activity is negatively regulated by p38α. Our results indicate that p38α can differentially contribute to Rac‐1 activation depending on the presence of serum.