FEBS Lett 2008,
PMID: 18154735
Sebe, Attila; Masszi, András; Zulys, Matthew; Yeung, Tony; Speight, Pam; Rotstein, Ori D; Nakano, Hiroyasu; Mucsi, István; Szászi, Katalin; Kapus, András
We investigated the mechanism whereby cell contact injury stimulates the alpha-smooth muscle actin (SMA) promoter, a key process for epithelial-mesenchymal transition (EMT) during organ fibrosis. Contact disruption by low-Ca(2+) medium (LCM) activated Rac, PAK and p38 MAPK, and triggered the nuclear accumulation of myocardin-related transcription factor (MRTF), an inducer of the SMA promoter. Dominant negative (DN) Rac, DN-PAK, DN-p38, or the p38 inhibitor SB203580 suppressed the LCM-induced nuclear accumulation of MRTF and the activation of the SMA promoter. These studies define novel pathway(s) involving Rac, PAK, and p38 in the regulation of MRTF and the contact-dependent induction of EMT.
Document information provided by NCBI PubMed
Text Mining Data
transcription factor → PAK: "
Rac,
PAK and p38
regulate cell contact dependent nuclear translocation of myocardin related
transcription factor
"
transcription factor → p38: "
Rac, PAK and p38 regulate cell contact dependent nuclear translocation of myocardin related transcription factor
"
transcription factor → Rac: "
Rac , PAK and p38 regulate cell contact dependent nuclear translocation of myocardin related transcription factor
"
SMA ⊣ DN-PAK: "
Dominant negative ( DN ) Rac, DN-PAK , DN-p38, or the p38 inhibitor SB203580 suppressed the LCM induced nuclear accumulation of MRTF and the activation of the SMA promoter
"
SMA ⊣ DN-p38: "
Dominant negative ( DN ) Rac, DN-PAK, DN-p38 , or the p38 inhibitor SB203580 suppressed the LCM induced nuclear accumulation of MRTF and the activation of the SMA promoter
"
SMA ⊣ Rac: "
Dominant negative ( DN ) Rac , DN-PAK, DN-p38, or the p38 inhibitor SB203580 suppressed the LCM induced nuclear accumulation of MRTF and the activation of the SMA promoter
"
Manually curated Databases
No curated data.