AGAP2: modulating TGF beta 1-Signaling in the regulation of liver fibrosis
Keywords: 
AGAP2
Arf GAP
TGF beta 1
Liver fibrosis
Receptor recycling
Issue Date: 
2020
ISSN: 
1422-0067
Note: 
This article is an open accessarticle distributed under the terms and conditions of the Creative Commons Attribution
Citation: 
Navarro-Corcuera, A. (Amaia); Ansorena-Artieda, E. (Eduardo); Montiel-Duarte, C. (Cristina); et al. "AGAP2: modulating TGF beta 1-Signaling in the regulation of liver fibrosis". International Journal of Molecular Sciences. 21 (4), 2020, 1400
Abstract
AGAP2 (Arf GAP with GTP-binding protein-like domain, Ankyrin repeat and PH domain 2) isoform 2 is a protein that belongs to the Arf GAP (GTPase activating protein) protein family. These proteins act as GTPase switches for Arfs, which are Ras superfamily members, being therefore involved in signaling regulation. Arf GAP proteins have been shown to participate in several cellular functions including membrane trafficking and actin cytoskeleton remodeling. AGAP2 is a multi-tasking Arf GAP that also presents GTPase activity and is involved in several signaling pathways related with apoptosis, cell survival, migration, and receptor trafficking. The increase of AGAP2 levels is associated with pathologies as cancer and fibrosis. Transforming growth factor beta-1 (TGF-beta 1) is the most potent pro-fibrotic cytokine identified to date, currently accepted as the principal mediator of the fibrotic response in liver, lung, and kidney. Recent literature has described that the expression of AGAP2 modulates some of the pro-fibrotic effects described for TGF-beta 1 in the liver. The present review is focused on the interrelated molecular effects between AGAP2 and TGF beta 1 expression, presenting AGAP2 as a new player in the signaling of this pro-fibrotic cytokine, thereby contributing to the progression of hepatic fibrosis.

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