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August 2022 GPR3 expression in retinal ganglion cells contributes to neuron survival and accelerates GPR3 is unique in its ability to constitutively activate the Gαs protein without a ligand, which elevates Our earlier reports suggested that GPR3 enhances both neurite outgrowth and neuronal survival. GPR3 was relatively highly expressed in retinal ganglion cells (RGCs). Evaluation of the effect of GPR3 on axonal regeneration using GPR3 knockout mice revealed that GPR3 in

Our previous work demonstrated that GPR3-mediated β-arrestin signaling modulates amyloid-β (Aβ) generation in vitro and that Gpr3 deficiency ameliorates Aβ pathology in vivo. However, Gpr3-deficient mice display several adverse phenotypes, including elevated anxiety-like behavior consequences of selective elimination of GPR3-mediated β-arrestin signaling in vivo. In contrast to Gpr3-deficient mice, G protein-biased GPR3 mice do not display elevated anxiety levels

roles of focal adhesion kinase (protein tyrosine kinase 2, PTK2), the shear-dependent collagen receptor GPR56 peptides that interfered with integrin αIIb binding (pCIB and pCIBm) or mimicked the activation of GPR56 integrin αIIbβ3, and CIB1 in collagen- and GPVI-dependent thrombus formation, which is modulated by GPR56

Curie PostDoc Fellowship in order to investigate and find better ligands for the orphan class A GPCRs , GPR3 , GPR6 , and GPR12 .

His research centers on the beta-2 adrenergic receptor and GPR65 , a proton-sensing receptor with promising He shares fascinating findings from his work on GPR65 , highlighting its unusual constitutive internalization Yamina underscores the therapeutic potential of GPR65, especially in the context of cancer immunotherapy

Find out in our latest episode featuring Ian Chronis, where we explore the surprising ways GPR65 signals