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AGAP2: ModulatingTGFβ1-Signaling inthe Regulation ofLiver Fibrosis Amaia Navarro‐CorcueraEduardo AnsorenaCristina Montiel‐Duarte2020 год

AGAP2: Modulating TGFβ1-Signaling in the Regulation of Liver Fibrosis
review

Полный текстСтраница публикацииПубликация в OpenAlex
Аннотация: 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-β1) 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-β1 in the liver. The present review is focused on the interrelated molecular effects between AGAP2 and TGFβ1 expression, presenting AGAP2 as a new player in the signaling of this pro-fibrotic cytokine, thereby contributing to the progression of hepatic fibrosis.
Год издания: 2020
Авторы: Amaia Navarro‐Corcuera, Eduardo Ansorena, Cristina Montiel‐Duarte, María J. Iraburu
Издательство: Multidisciplinary Digital Publishing Institute
Источник: International Journal of Molecular Sciences
Ключевые слова: Liver physiology and pathology, Protein Kinase Regulation and GTPase Signaling, TGF-β signaling in diseases
Другие ссылки: International Journal of Molecular Sciences (PDF)
International Journal of Molecular Sciences (HTML)
DOAJ (DOAJ: Directory of Open Access Journals) (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
Nottingham Trent University's Institutional Repository (Nottingham Trent Repository) (HTML)
PubMed (HTML)