Ask about this productRelated genes to: GRM7 Blocking Peptide
- Gene:
- GRM7 NIH gene
- Name:
- glutamate metabotropic receptor 7
- Previous symbol:
- -
- Synonyms:
- GLUR7, GPRC1G, mGlu7, MGLUR7, PPP1R87
- Chromosome:
- 3p26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-11
- Date modifiied:
- 2016-10-05
Related products to: GRM7 Blocking Peptide
Related articles to: GRM7 Blocking Peptide
- Metabotropic glutamate receptors (mGluRs) are best known for modulating synaptic transmission, yet accumulating evidence shows that they are also widely expressed in peripheral tissues, including the testis. Methodologically, this work integrates a narrative synthesis of the literature with an in-silico bioinformatic analysis of bulk (GTEx) and single-cell (HPA, CellxGene) RNA-seq datasets, aiming to clarify how mGluRs contribute to testicular physiology. After outlining the striking structural and metabolic parallels between brain and testis-tight barrier systems, selenium-dependent redox control, and exceptionally complex alternative splicing-we confirm that several mGluR subtypes are expressed in Sertoli, Leydig, and germ cells. GRM7 and GRM8 emerge as the dominant transcripts during the late stages of spermatogenesis, and their co-expression networks are strongly linked to axoneme assembly, cilium-driven motility, mitogen-activated protein kinase (MAPK) signaling, and spermatid differentiation. These results point to a role for mGluR-dependent, cyclic adenosine monophosphate (cAMP)-sensitive pathways in fine-tuning sperm maturation and motility. We further discuss how mGluR activity interfaces with the hypothalamic- pituitary-gonadal (HPG) axis and local estrogen signaling, highlighting implications for male infertility, novel contraceptive strategies, and the safe therapeutic targeting of mGluRs in neuropsychiatry. Overall, the data reinforce the concept of a brain-testis continuum, in which glutamatergic signaling is pivotal not only to neuronal plasticity but also to spermatogenesis, steroidogenesis, and sperm function. - Source: PubMed
Publication date: 2026/05/13
Barlattani TommasoCaridi MatteoPellicelli ValeriaCamussi DilettaAlborghetti MarikaDi Menna LuisaPacitti FrancescaNicoletti Ferdinando - Autism Spectrum Disorder (ASD) is a genetically heterogeneous neurodevelopmental condition involving multiple genes. This study aimed to comprehensively review the genetic landscape of ASD in the Iranian population, identifying gene variants associated with increased risk, to facilitate improved diagnosis and targeted interventions. A systematic review and meta-analysis were conducted on genetic association studies of ASD in Iran up to August 2025. Comprehensive searches were performed in PubMed, Scopus, Web of Science, and Persian databases using relevant keywords. Quality assessment was performed using the Joanna Briggs Institute critical appraisal tools. Meta-analyses were carried out using Review Manager software, assessing heterogeneity and publication bias. Protein-protein interaction networks were constructed via STRING and analyzed with Cytoscape to identify key hub genes and enriched neurodevelopmental pathways. In this study, genes RORA, MTRR, MTR, Reelin, VDR, VMAT1, ACE I/D, MOCOS, HOTAIR, ANRIL, RIT2, MMP-9, GRM7, FOXP3, and GRIN2B showed significant associations with the occurrence of autism. Findings reinforce associations between multiple gene polymorphisms, especially RORA rs4774388 and MOCOS rs594445, with the risk of ASD. This systematic review and meta-analysis emphasize the multifactorial genetic contributions to ASD in the Iranian population, highlighting key risk loci and neurodevelopmental pathways. The findings underscore the importance of integrating genetic, epigenetic, and environmental factors for understanding ASD etiology and developing population-tailored diagnostic and therapeutic strategies. Future studies employing larger cohorts and multi-omics approaches are warranted to further elucidate the complex genetic architecture of ASD in diverse ethnic groups. - Source: PubMed
Barfeh DelaramShahesmaeilinejad ArmitaEslami Shahrbabaki MahinKaramooz AnahitaShekari FatemehZare Arashlouei Azam - Intellectual disability with mild dysmorphic features may be attributed to perinatal complications such as neonatal hypoxia. However, chromosomal abnormalities may underlie these phenotypes. We report a case with rare copy number variants that are likely to have neurodevelopmental relevance. - Source: PubMed
Publication date: 2026/02/19
Rangel-Méndez Jorge ARubi-Castellanos RodrigoContreras-Capetillo SilvinaGonzález-Herrera LizbethPinto-Escalante Doris - Scoliosis is the most common developmental spinal deformity, but its genetic underpinnings remain only partially understood. To identify scoliosis-related loci, we utilized dual energy X-ray absorptiometry (DXA) scans from 57,588 individuals in the UK Biobank (UKB), and quantified spinal curvature using deep learning-based vertebral segmentation and landmarking to measure cumulative horizontal displacement. On a subset of 150 individuals, our automated image-derived curvature measurements showed a correlation of 0.83 with clinical Cobb angle assessments, supporting their validity as a proxy for scoliosis severity. To connect spinal curvature to genetics, we conducted a genome-wide association study (GWAS). Our quantitative imaging phenotype identified 2 novel loci associated with scoliosis in a European population. These loci are in SEM1/SHFM1 and on an lncRNA on chr 3 located between EDEM1 and GRM7. Genetic correlation analysis revealed significant overlap between our image-based GWAS and ICD-10-based GWAS in the UKB and the Biobank of Japan. We show that our quantitative GWAS identifies more genome-wide significant loci than a case-control scoliosis dataset with ten times the sample size. Our results illustrate the potential of quantitative imaging phenotypes to uncover genetic associations that are challenging to capture with medical records alone and identify new loci for functional follow-up. - Source: PubMed
Publication date: 2026/03/26
Zeosky MichaelKun EucharistReddy SiddharthPandey DevanshXu LiaoyiWang Joyce YLi ChenfeiGray Ryan SWise Carol AOtomo NaoNarasimhan Vagheesh M - Mild traumatic brain injury (mTBI) disproportionately affects children and adolescents and has been associated with poorer neurocognitive performance, but the biological mechanisms driving symptom variability and severity remain understudied. In accordance with the omnigenic disease model, we integrated gene-by-mTBI interaction genome-wide association studies on neurocognition from the Adolescent Brain Cognitive Development (ABCD) cohort with single-cell RNA sequencing gene regulatory networks to elucidate the cell type-specific key regulators and molecular mechanisms governing neurocognitive outcome of mTBI, specifically learning and memory performance. Our analysis revealed distinct network regulators in neuronal and glial cell types across hippocampal and cortical brain regions to orchestrate key neurodevelopmental pathways. Examples include APP for synaptic signaling in excitatory neurons, COX5A for mitochondrial function in inhibitory neurons, MOG for myelination in oligodendrocytes in the hippocampus; GRM7 for synaptic signaling in excitatory neurons, SV2A for synaptic signaling in inhibitory neurons, and MOG for myelination in oligodendrocytes in the cortex. These mechanisms also associate with learning and memory through pathway-based polygenic risk score modeling in ABCD. Our findings provide brain region- and cell type-specific insights into the complex regulatory network landscape of mTBI pathology and potential therapeutic candidates at the pathway and network levels. - Source: PubMed
Publication date: 2026/03/13
Cheng MichaelMao MelodyMeng WenjingJacobus JoannaTroyer Emily ADelfel Everett LDennis Emily LWilde Elisabeth AAbildskov Tracyde Souza Nicola LVaida FlorinMax Jeffrey EYang Xia