Specific activation of PLEKHG2-induced serum response element-dependent gene transcription by four-and-a-half LIM domains (FHL) 1, but not FHL2 or FHL3.

Autor:	Nishikawa M; a United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University , Yanagido, Gifu , Japan., Sato K; b Department of Molecular Pathobiochemistry, Gifu University Graduate School of Medicine , Yanagido, Gifu , Japan., Nakano S; c Department of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University , Yanagido, Gifu , Japan., Yamakawa H; d Kazusa DNA Research Institute, Kazusa-kamatari , Kisarazu, Chiba , Japan., Nagase T; d Kazusa DNA Research Institute, Kazusa-kamatari , Kisarazu, Chiba , Japan., Ueda H; a United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University , Yanagido, Gifu , Japan.; c Department of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University , Yanagido, Gifu , Japan.
Jazyk:	angličtina
Zdroj:	Small GTPases [Small GTPases] 2019 Sep; Vol. 10 (5), pp. 361-366. Date of Electronic Publication: 2017 Jun 19.
DOI:	10.1080/21541248.2017.1327838
Abstrakt:	PLEKHG2 is a Gβγ- and Gαs-dependent guanine nucleotide exchange factor for Rac1 and Cdc42 small GTPases and has been shown to mediate signaling pathways such as those for actin cytoskeletal reorganization and serum response element (SRE)-dependent gene transcription. We have shown that the four-and-a-half LIM domains (FHL) 1 acts as a positive regulator of PLEKHG2. Here, we evaluated the other FHL family members and found that the FHL1A specifically regulate the PLEKHG2 activity. Moreover, FHL1A further enhanced Gβγ- and PLEKHG2-induced SRE-dependent gene transcription, whereas FHL1A partially restored the attenuated PLEKHG2-induced SRE-dependent gene transcription by Gαs. Our results suggest that FHL1A specifically interacts with PLEKHG2 to regulate a function of PLEKHG2 that is modified by the interaction of Gβγ and Gαs.
Databáze:	MEDLINE
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