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- W4289782005 abstract "Kynurenic acid (KynA) is tissue protective in cardiac, cerebral, renal, and retinal ischemia models, but the mechanism is unknown. KynA can bind to multiple receptors, including the aryl hydrocarbon receptor, the a7 nicotinic acetylcholine receptor (a7nAChR), multiple ionotropic glutamate receptors, and the orphan G protein-coupled receptor GPR35. Here, we show that GPR35 activation was necessary and sufficient for ischemic protection by KynA. When bound by KynA, GPR35 activated Gi- and G12/13-coupled signaling and trafficked to the outer mitochondria membrane, where it bound, apparantly indirectly, to ATP synthase inhibitory factor subunit 1 (ATPIF1). Activated GPR35, in an ATPIF1-dependent and pertussis toxin-sensitive manner, induced ATP synthase dimerization, which prevented ATP loss upon ischemia. These findings provide a rationale for the development of specific GPR35 agonists for the treatment of ischemic diseases." @default.
- W4289782005 created "2022-08-04" @default.
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- W4289782005 date "2022-08-05" @default.
- W4289782005 modified "2023-10-10" @default.
- W4289782005 title "Mitochondrial remodeling and ischemic protection by G protein–coupled receptor 35 agonists" @default.
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- W4289782005 doi "https://doi.org/10.1126/science.abm1638" @default.
- W4289782005 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35926043" @default.
- W4289782005 hasPublicationYear "2022" @default.
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