Disease-associated GPR56 Mutations Cause Bilateral Frontoparietal Polymicrogyria via Multiple Mechanisms

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Bilateral frontoparietal polymicrogyria (BFPP) syndrome secondary to a 16q12.1-q21 chromosome deletion involving GPR56 gene

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Site-specific N-glycosylation regulates the GPS auto-proteolysis of CD97

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GPR56 as a novel marker identifying the CD56dull CD16+ NK cell subset both in blood stream and in inflamed peripheral tissues

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Functional Cross-interaction of the Fragments Produced by the Cleavage of Distinct Adhesion G-protein-coupled Receptors

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GPR56-Regulated Granule Cell Adhesion Is Essential for Rostral Cerebellar Development

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Orphan G Protein-coupled Receptor GPR56 Regulates Neural Progenitor Cell Migration via a Gα12/13 and Rho Pathway

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GPR56 Regulates Pial Basement Membrane Integrity and Cortical Lamination

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Biochemical characterization of genetic mutations of GPR56 in patients with bilateral frontoparietal polymicrogyria (BFPP)

(2007) Ning Ke et al.   BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS