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G-Protein-Coupled Lysophosphatidic Acid Receptors and Their Regulation of AKT Signaling
Univ Punjab, Inst Biochem & Biotechnol, Lahore 54590, Pakistan..
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
2016 (engelsk)Inngår i: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 17, nr 2Artikkel, forskningsoversikt (Fagfellevurdert) Published
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Abstract [en]

A hallmark of G-protein-coupled receptors (GPCRs) is their ability to recognize and respond to chemically diverse ligands. Lysophospholipids constitute a relatively recent addition to these ligands and carry out their biological functions by activating G-proteins coupled to a large family of cell-surface receptors. This review aims to highlight salient features of cell signaling by one class of these receptors, known as lysophosphatidic acid (LPA) receptors, in the context of phosphatidylinositol 3-kinase (PI3K)-AKT pathway activation. LPA moieties efficiently activate AKT phosphorylation and activation in a multitude of cell types. The interplay between LPA, its receptors, the associated Gi/o subunits, PI3K and AKT contributes to the regulation of cell survival, migration, proliferation and confers chemotherapy-resistance in certain cancers. However, detailed information on the regulation of PI3K-AKT signals induced by LPA receptors is missing from the literature. Here, some urgent issues for investigation are highlighted.

sted, utgiver, år, opplag, sider
2016. Vol. 17, nr 2
Emneord [en]
G-protein coupled receptors (GPCR), lysophosphatidic acid (LPA), PI3K, AKT
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URN: urn:nbn:se:uu:diva-298961DOI: 10.3390/ijms17020215ISI: 000371830800097OAI: oai:DiVA.org:uu-298961DiVA, id: diva2:948668
Forskningsfinansiär
Swedish Cancer SocietyTilgjengelig fra: 2016-07-13 Laget: 2016-07-12 Sist oppdatert: 2022-02-10bibliografisk kontrollert

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