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Biochemical Analysis of the Polycystin-1 Complexity Generated by Proteolytic Cleavage at the G Protein-Coupled Receptor Proteolysis Site
Published in Jinghua Hu, Yong Yu, Polycystic Kidney Disease, 2019
Rebecca Walker, Hangxue Xu, Qiong Huang, Feng Qian
PC1deN: GPS cleavage also gives rise to a distinct pool of PC1NTF. This fragment, termed PC1deN, is derived from dissociation of the two halves of PC1cFL. PC1deN is a major endogenous PC1 form in many tissues, is predominantly Endo-H resistant and is associated with the plasma membrane of renal epithelial cells.9 In analogous models of adhesion GPCRs, detachment of the N-terminal fragment has been suggested to represent an activation mechanism. Indeed, constitutive activation of an aGPCR (GPR56) has been achieved by deletion of the N-terminal sequence, mimicking cleavage.67 The function of this form of PC1 currently remains unclear.
Cytotoxic T Lymphocytes Expressing GPR56 are Up-regulated in the Peripheral Blood of Patients with Active Rheumatoid Arthritis and Reflect Disease Progression
Published in Immunological Investigations, 2022
Xingyue Zeng, Mohan Zheng, Tianci Liu, Ayibaota Bahabayi, Shi Song, Xiayidan Alimu, Rui Kang, Songsong Lu, Ying Song, Chen Liu
As a cytotoxic particle, GZMB induces the apoptotic pathway of downstream cells by co-secreting with perforin, and stimulates CTL proliferation and activity by cleaving its self-proteins (Darrah et al. 2017; Kumar et al. 2015; Niland et al. 2010; Trapani and Smyth 2002). Granzymes and perforin were reported to be co-expressed with GPR56 in T and NK cells (Peng et al. 2011; Tian et al. 2017). In CTL cell-related studies, GPR56 has received more and more attention. As a member of the G protein-coupled receptor superfamily, GPR56 is expressed on cytotoxic cells, and GPR56 expression continues to increase as cytotoxicity matures (Peng et al. 2011). However, there is currently no study of the clinical significance of GPR56 in autoimmune diseases. Therefore, the relevant role of GPR56 in GZMB+ CTL cells of patients with rheumatoid arthritis deserves further study and exploration.
Unravelling the genetic architecture of autosomal recessive epilepsy in the genomic era
Published in Journal of Neurogenetics, 2018
Jeffrey D. Calhoun, Gemma L. Carvill
Polymicrogyria (PMG) is a focal brain malformation characterized by abnormal folds, or gyri (Stutterd & Leventerer, 2014). Specifically, PMG is a condition in which an excess of gyri are present and these gyri are smaller than gyri present in healthy persons. Variants in GPR56 were reported in 12 AR pedigrees presenting with bilateral frontoparietal PMG (BFPP) (Piao et al., 2004). BFPP patients display a complex phenotype including seizures, ID, gait abnormalities and language impairment, consistent with functional defects in the frontal lobe (Chang et al., 2003; Piao et al., 2002). GPR56 encodes a member of the adhesion-GPCR family that link cell–cell adhesion to intracellular signaling and act to regulate neuronal development (Sigoillot, Monk, Piao, Selimi, & Harty, 2016). Gpr56 knockout mouse studies revealed that loss of Gpr56 expression results in defects in the pial basement membrane followed by neuronal ectopia (Li et al., 2008). Biochemical characterization has revealed multiple molecular mechanisms for GPR56-related BFPP, including reduced cell surface expression and altered localization to lipid rafts (Chiang et al., 2011). Other genes including OCLN and FIG4 have been implicated in AR neurodevelopmental disorders with PMG and epilepsy (Baulac et al., 2014; O'Driscoll et al., 2010).
The essential role of G protein-coupled receptor (GPCR) signaling in regulating T cell immunity
Published in Immunopharmacology and Immunotoxicology, 2018
Adhesion GPCRs are one of the five subgroups of GPCRs, which possesses a GPCR proteolysis site (GPS) and an exceptionally long extracellular N-terminal region. GPR56 is a member of the adhesion GPCRs, which is expressed in restricted cells like NK and cytotoxic T lymphocytes. Ke et al. reported that the expression of GPR56 is significantly increased in virus-specific CD8 + T cells during human CMV infection. Besides, GPR56 has also been shown to be associated with the T cell migration52. GPR56 may become a novel marker of human cytotoxic T lymphocytes and affect the migration of these cells.