GRIP1

Last update 08 May 2025

Basic Info

Synonyms

glutamate receptor interacting protein 1, Glutamate receptor-interacting protein 1, GRIP-1

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Introduction

May play a role as a localized scaffold for the assembly of a multiprotein signaling complex and as mediator of the trafficking of its binding partners at specific subcellular location in neurons (PubMed:10197531). Through complex formation with NSG1, GRIA2 and STX12 controls the intracellular fate of AMPAR and the endosomal sorting of the GRIA2 subunit toward recycling and membrane targeting (By similarity).

100 Clinical Results associated with GRIP1

100 Translational Medicine associated with GRIP1

0 Patents (Medical) associated with GRIP1

410

Literatures (Medical) associated with GRIP1

05 Feb 2025·NeuroReport

Artemisinin antagonizes cognitive disorder in hyperuricemia through glutamate receptor-interacting protein 1-suppressed pyroptosis

Article

Author: Chen, Yanfang ; Cao, Peng ; Wang, Huiqing ; Chen, Shuangxi

The prevalence of hyperuricemia (HUA) is climbing worldwide and persistent elevation of serum uric acid impairs cognitive function. This study aimed to explore the mechanisms of Artemisinin (Art) antagonizing cognitive disorder in HUA by suppressing pyroptosis. A mouse model of HUA was established by intraperitoneal injection of 300 mg/kg potassium oxonate (PO) in C57BL/6 mice for 14 days. The mice were simultaneously treated with Art, an agonist of pyroptosis Polyphyllin VI (PPVI), or glutamate receptor-interacting protein 1 (GRIP1) knockdown lentiviral plasmid. After treatment, serum uric acid, IL-6, and TNF-ɑ levels were examined, as well as hippocampal IL-1β and IL-18 levels, and the cognitive function of mice was assessed by the Morris water maze test. Pathological changes in the CA1 of the hippocampus were observed. Cleave-caspase-1, GSDMD-N, and GRIP1 protein level in the hippocampus was quantified by western blot. After PO induction, the escape latency and the time spent in the target quadrant increased in mice, cell arrangement in CA1 hippocampus was loose and disorganized, with obvious inflammatory infiltration and serious damage being observed, and the mouse hippocampus had elevated cleaved-caspase-1, GSDMD-N, IL-1β, and IL-18. Art treatment reduced pyroptosis in the hippocampus and improved cognitive disorder in HUA mice. Administration of PPVI aggravated cognitive disorder in Art-treated HUA mice, and Art improved cognitive dysfunction in HUA mice by inhibiting pyroptosis through upregulation of GRIP1. Art blunts pyroptosis in the hippocampus of HUA mice suffering from cognitive disorder by upregulating GRIP1.

01 Oct 2024·Cell Reports

WWC2 modulates GABAA-receptor-mediated synaptic transmission, revealing class-specific mechanisms of synapse regulation by WWC family proteins

Article

Author: Wilkerson, Julia R ; Volk, Lenora J ; Dunham, Thomas L ; Johnson, Richard C ; Huganir, Richard L

The WW and C2 domain-containing protein (WWC2) is implicated in several neurological disorders. Here, we demonstrate that WWC2 interacts with inhibitory, but not excitatory, postsynaptic scaffolds, consistent with prior proteomic identification of WWC2 as a putative component of the inhibitory postsynaptic density. Using mice lacking WWC2 expression in excitatory forebrain neurons, we show that WWC2 suppresses γ-aminobutyric acid type-A receptor (GABA_AR) incorporation into the plasma membrane and regulates HAP1 and GRIP1, which form a complex promoting GABA_AR recycling to the membrane. Inhibitory synaptic transmission is increased in CA1 pyramidal cells lacking WWC2. Furthermore, unlike the WWC2 homolog KIBRA (kidney/brain protein; WWC1), a key regulator of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) trafficking at excitatory synapses, the deletion of WWC2 does not affect synaptic AMPAR expression. In contrast, loss of KIBRA does not affect GABA_AR membrane expression. These data reveal synapse class-selective functions for WWC proteins as regulators of ionotropic neurotransmitter receptors and provide insight into mechanisms regulating GABA_AR membrane expression.

27 Aug 2024·Neurology

Genetic Associations With an Amyotrophic Lateral Sclerosis Reversal Phenotype

Article

Author: Bedlack, Richard S. ; Wu, Gang ; Crayle, Jesse I. ; Taylor, J. Paul ; Myers, Jason R. ; Benatar, Michael ; Wuu, Joanne ; Rampersaud, Evadnie

BACKGROUND AND OBJECTIVESThe term "ALS Reversal" describes patients who initially meet diagnostic criteria for amyotrophic lateral sclerosis (ALS) or had clinical features most consistent with progressive muscular atrophy (PMA) but subsequently demonstrated substantial and sustained clinical improvement. The objective of this genome-wide association study (GWAS) was to identify correlates of this unusual clinical phenotype.METHODSParticipants were recruited from a previously created database of individuals with the ALS Reversal phenotype. Whole-genome sequencing (WGS) data were compared with ethnicity-matched patients with typically progressive ALS enrolled through the CReATe Consortium's Phenotype-Genotype-Biomarker (PGB) study. These results were replicated using an independent ethnically matched WGS data set from Target ALS. Significant results were further explored with available databases of genetic regulatory markers and expression quantitative trait loci (eQTL) analysis.RESULTSWGS from 22 participants with documented ALS Reversals was compared with the PGB primary cohort (n = 103) and the Target ALS validation cohort (n = 140). Two genetic loci met predefined criteria for statistical significance (two-sided permutation p ≤ 0.01) and remained plausible after fine-mapping. The lead single nucleotide variant (SNV) from the first locus was rs4242007 (primary cohort GWAS OR = 12.0, 95% CI 4.1 to 34.6), which is in an IGFBP7 intron and is in near-perfect linkage disequilibrium with a SNV in the IGFBP7 promoter region. Both SNVs are associated with decreased frontal cortex IGFBP7 expression in eQTL data sets. Notably, 3 Reversals, but none of the typically progressive individuals (n = 243), were homozygous for rs4242007. The importance of the second locus, located near GRIP1, is uncertain given the absence of an associated effect on nearby gene transcription.DISCUSSIONWe found a significant association between the Reversal phenotype and an IGFBP7 noncoding SNV that is associated with IGFBP7 expression. This is biologically relevant as IGFBP7 is a reported inhibitor of the insulin growth factor-1 (IGF-1) receptor that activates the possibly neuroprotective IGF-1 signaling pathway. This finding is limited by small sample size but suggests that there may be merit in further exploration of IGF-1 pathway signaling as a therapeutic mechanism for ALS.TRIAL REGISTRATION INFORMATIONThis study was registered with ClinicalTrials.gov (NCT03464903) on March 14, 2018. The first participant was enrolled on June 22, 2018.

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GRIP1

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