Affinage

GRID1

Glutamate receptor ionotropic, delta-1 · UniProt Q9ULK0

Length
1009 aa
Mass
112.1 kDa
Annotated
2026-06-10
55 papers in source corpus 13 papers cited in narrative 13 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GRID1 encodes GluD1, a glutamate receptor-family protein that functions principally as a postsynaptic organizer of excitatory and inhibitory synapses across multiple brain circuits rather than as a conventional ligand-gated channel (PMID:28696429, PMID:25721396). In midbrain dopamine neurons GluD1 acts downstream of the mGlu1 receptor to generate slow depolarizing currents that drive spontaneous burst firing, an activity abolished by a dominant-negative dead-pore mutant or by Grid1 knockout (PMID:28696429). At synapses GluD1 serves as the postsynaptic component of a NRXN1-CBLN1-GluD1 transsynaptic complex that specifies excitatory connectivity, as shown for VMHvl-to-AgRP/NPY hypothalamic synapses controlling aggression (PMID:36909588). Loss of GluD1 dysregulates postsynaptic receptor composition in a region-specific manner — altering AMPA receptor subunit content, impairing the developmental GluN2B-to-GluN2A NMDAR switch, and perturbing LIMK1-cofilin signaling, dendritic spine density, and synapse number in cortex, hippocampus, striatum, and nucleus accumbens (PMID:22412961, PMID:25721396, PMID:34173171). GluD1 additionally facilitates autophagic flux through direct interactions of its C-terminus with nGOPC/nPIST, BECN1, and LAMP1, and its loss produces overactive Akt-mTOR signaling and impaired autophagy alongside immature excitatory synapses (PMID:35304260, PMID:41147487). Homozygous missense GRID1 variants cause intellectual disability with spastic paraplegia by altering the hinge between the cerebellin- and D-serine-binding domains and impairing mGlu1/5 signaling through Ca2+ and ERK pathways, while distinct variants disrupt cerebellin binding or create constitutively active channels (PMID:37944084, PMID:38418578).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2012 Medium

    Established that GluD1 controls postsynaptic AMPA receptor content and behavior in a region-specific way, defining it as a synaptic regulator rather than a passive structural subunit.

    Evidence Grid1 knockout mouse behavior, synaptoneurosome fractionation, and D-cycloserine pharmacological rescue

    PMID:22412961

    Open questions at the time
    • Did not resolve whether AMPAR changes are direct or secondary to circuit remodeling
    • No molecular mechanism linking GluD1 to receptor subunit trafficking
  2. 2015 Medium

    Showed GluD1 is required for the developmental GluN2B-to-GluN2A NMDAR switch and constrains dendritic spine number via LIMK1-cofilin signaling, connecting GluD1 to spine maturation.

    Evidence Grid1 knockout spine counting, electrophysiology, western blotting, and GluN2B-inhibitor rescue in mPFC and CA1

    PMID:25721396

    Open questions at the time
    • Mechanism coupling GluD1 to LIMK1-cofilin not defined
    • Direct versus indirect control of NMDAR subunit composition unresolved
  3. 2017 High

    Answered how GluD1 contributes to signaling without classical gating: it acts downstream of mGlu1 to produce slow depolarizing currents driving dopamine neuron burst firing.

    Evidence HEK co-expression electrophysiology, dominant-negative dead-pore mutant in midbrain slices, and in vivo recordings in Grid1 knockout mice

    PMID:28696429

    Open questions at the time
    • Structural basis of mGlu1-GluD1 coupling not determined
    • Whether ion flux through GluD1 itself or a downstream conductance carries the current
  4. 2021 Medium

    Extended GluD1 function to inhibitory transmission, showing region-specific loss reduces inhibitory synapse number and presynaptic release with opposing behavioral effects in NAc versus dorsal striatum.

    Evidence Conditional Grid1 knockout, patch clamp with paired-pulse analysis, GAD67 immunofluorescence, and behavioral testing

    PMID:34173171

    Open questions at the time
    • Mechanism by which a postsynaptic protein lowers presynaptic release probability unclear
    • Transsynaptic partner mediating inhibitory effect not identified in this study
  5. 2022 Medium

    Linked GluD1 loss to overactive Akt-mTOR signaling and impaired autophagy accompanying immature excitatory synapses, introducing an autophagy axis to GluD1 biology.

    Evidence Conditional Grid1 knockout, western blotting for Akt-mTOR and autophagy markers (p62, LC3), and synaptic puncta analysis

    PMID:35304260

    Open questions at the time
    • Did not establish direct molecular link between GluD1 and autophagy machinery
    • Causal direction between synapse immaturity and autophagy defect unresolved
  6. 2023 Medium

    Defined GluD1 as the postsynaptic component of a NRXN1-CBLN1-GluD1 transsynaptic complex specifying a hypothalamic excitatory circuit that regulates aggression.

    Evidence Conditional Grid1 deletion in AgRP neurons, chemogenetic/optogenetic manipulation, aggression assays, and epistasis with Nrxn1 and Ube3a (preprint)

    PMID:36909588

    Open questions at the time
    • Preprint, not peer-reviewed
    • Biochemical reconstitution of the tripartite complex not shown in this study
  7. 2024 High

    Connected GRID1 to human Mendelian disease, showing homozygous missense variants cause intellectual disability and spastic paraplegia by altering the cerebellin/D-serine domain hinge and impairing mGlu1/5 Ca2+ and ERK signaling.

    Evidence Patient variant identification, molecular modeling, electrophysiology, Ca2+ and ERK assays, and neuronal morphology in dissociated and slice cultures

    PMID:38418578

    Open questions at the time
    • Variants did not conspicuously alter expression, trafficking, mGlu1 interaction, or cerebellin binding, leaving precise signaling lesion undefined
    • No in vivo model of the human variants
  8. 2024 High

    Resolved how distinct variant classes act, distinguishing cerebellin-binding-disrupting amino-terminal variants from M3-domain variants that produce constitutively active currents, with pentamidine identified as an inhibitor.

    Evidence Mutagenesis of GRID1/GRID2 cDNA, electrophysiology, and biochemical complex-formation assays

    PMID:37944084

    Open questions at the time
    • In vivo consequences of constitutively active variants not tested
    • Therapeutic relevance of pentamidine inhibition not validated in disease models
  9. 2025 Medium

    Provided direct evidence that GluD1 physically engages autophagy machinery, with its C-terminus interacting with nGOPC/nPIST, BECN1, and LAMP1 to promote autophagy and limit AMPAR expression in central amygdala pain circuits.

    Evidence Tat-HRSPN C-terminal peptide intervention, interaction assays with BECN1/LAMP1/nGOPC, autophagy marker blotting, pain models, and mEPSC recordings

    PMID:41147487

    Open questions at the time
    • Interaction assays from a single lab without reciprocal structural validation
    • Stoichiometry and regulation of the GluD1-autophagy interactions unknown
  10. 2025 Medium

    Defined the precise synaptic localization of GluD1, placing it at the core of symmetric (GABAergic) synapses in the lateral habenula, consistent with a role in organizing inhibitory contacts.

    Evidence Pre- and post-embedding immunogold electron microscopy with anterograde tracing in rat and monkey lateral habenula

    PMID:39794140

    Open questions at the time
    • Functional consequence of GABAergic-synapse localization not tested here
    • Transsynaptic partners at these symmetric synapses not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How GluD1's transsynaptic adhesion role, its mGlu1-coupled conductance, and its direct autophagy interactions are integrated into a single molecular mechanism remains unresolved.
  • No structural model unifying ligand-binding, channel, and C-terminal autophagy functions
  • Whether autophagy regulation and synaptic organization are coupled or independent activities
  • Causal mechanism by which a postsynaptic protein controls presynaptic release and inhibitory connectivity

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0098631 cell adhesion mediator activity 2 GO:0060089 molecular transducer activity 1
Localization
GO:0005886 plasma membrane 2 GO:0005764 lysosome 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 2 R-HSA-9612973 Autophagy 2
Partners
BECN1CBLN1CBLN2GOPCGRM1LAMP1NRXN1
Complex memberships
NRXN1-CBLN1-GluD1 transsynaptic complex

Evidence

Reading pass · 13 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2017 GluD1 functions downstream of mGlu1 receptor to mediate slow depolarizing currents in midbrain dopamine neurons. In HEK cells co-expressing mGlu1 and GluD1, mGlu1 agonist elicits a slow depolarizing current absent in cells expressing either alone; a dominant-negative dead-pore GluD1 mutant abolishes both agonist-evoked and slow postsynaptic mGlu1-dependent currents in dopamine neurons from midbrain slices and in GRID1 knockout mice. In vivo, spontaneous burst firing of dopamine neurons is abolished in GRID1 knockout mice or upon targeted expression of the dominant-negative GluD1 mutant. HEK cell co-expression electrophysiology, dominant-negative mutant expression in midbrain slices, in vivo recordings in GRID1 knockout mice Molecular psychiatry High 28696429
2024 A missense variant in the GluD1 distal amino-terminal domain at a position predicted to interact with Cbln2/Cbln4 disrupts complex formation between GluD1 and Cbln2 in biochemical assays. Additionally, the schizophrenia-associated M3 domain variant GluD1-A650T produces constitutively active receptor currents, analogous to the lurcher mutation in GluD2. Pentamidine potently inhibited constitutive currents of GluD receptor variants (GluD2-T649A IC50 ~50 nM). Electrophysiological assays, biochemical complex formation assays, mutagenesis of GRID1/GRID2 cDNA Human molecular genetics High 37944084
2024 Homozygous missense GRID1 variants (p.Arg161His and p.Thr752Met) identified in patients with intellectual disability and spastic paraplegia impair mGlu1/5 metabotropic glutamate receptor signaling via Ca2+ and ERK pathways and impair dendrite morphology and excitatory synapse density in dissociated and organotypic slice culture neurons. Molecular modeling indicated these mutations alter the hinge between GluD1 cerebellin and D-serine binding domains. Expression, trafficking, physical interaction with mGlu1, and cerebellin binding were not conspicuously altered by these mutations. Molecular modeling, electrophysiological recordings, Ca2+ signaling assays, ERK pathway assays, neuronal culture morphological analysis in dissociated and organotypic slice cultures Molecular psychiatry High 38418578
2012 Deletion of GluD1 (GRID1 knockout mice) leads to hyperactivity, lower anxiety, depression-like behavior, aggression, and social interaction deficits. At the molecular level, synaptoneurosome preparations from GluD1 KO mice show lower GluA1 and GluA2 subunit expression in the prefrontal cortex and higher GluA1, GluK2, and PSD95 expression in the amygdala, indicating GluD1 regulates postsynaptic AMPA receptor content in a region-specific manner. D-Cycloserine rescued social interaction deficits and normalized lower GluA1 expression in prefrontal cortex. GluD1 knockout mouse behavioral analysis, synaptoneurosome biochemical fractionation, pharmacological rescue experiments PloS one Medium 22412961
2015 GluD1 knockout mice exhibit higher dendritic spine number, greater excitatory neurotransmission, higher synapse number, and abnormalities in LIMK1-cofilin signaling in the medial prefrontal cortex and CA1 hippocampus. A lower GluN2A/GluN2B expression ratio was also observed, indicating GluD1 is required for the developmental GluN2B-to-GluN2A NMDAR subunit switch. GluN2B-selective inhibitor Ro-25-6981 partially normalized LIMK1-cofilin signaling and reduced excess spine number. GluD1 knockout mouse spine counting, electrophysiology, western blotting, pharmacological rescue with GluN2B inhibitor Neuropharmacology Medium 25721396
2021 GluD1 loss in medium spiny neurons (MSNs) of the nucleus accumbens (NAc) core leads to reduced inhibitory neurotransmission, evidenced by decreased miniature inhibitory postsynaptic current (mIPSC) frequency and amplitude, increased paired pulse ratio of evoked inhibitory responses (indicating reduced presynaptic release probability), and reduced GAD67 puncta (inhibitory terminals). Local ablation of GluD1 from NAc caused hypolocomotion and altered anxiety- and depression-like behaviors, while ablation from dorsal striatum produced opposite behavioral phenotypes. Conditional GluD1 knockout, whole-cell patch clamp electrophysiology, paired pulse ratio analysis, GAD67 immunofluorescence, behavioral testing Molecular neurobiology Medium 34173171
2022 Conditional deletion of GluD1 from excitatory neurons in corticolimbic regions leads to overactive Akt-mTOR pathway, higher p62, and lower LC3-II/LC3-I ratio in the somatosensory cortex, indicating reduced autophagy. Excitatory synaptic elements were increased in number but showed an immature phenotype with lower GluA1 expression and impaired GluN2B-to-GluN2A developmental switch. Overactive Akt-mTOR signaling and impaired autophagy were also observed in dorsal striatum, prefrontal cortex, and hippocampus. Conditional GluD1 knockout mouse, western blotting for Akt-mTOR pathway components and autophagy markers (p62, LC3), synaptic puncta analysis, behavioral testing Pharmacological research Medium 35304260
2025 GRID1/GluD1 directly facilitates autophagy and reduces AMPA receptor (AMPAR) expression in the central amygdala (CeA). Using a GRID1 C-terminal-derived peptide (Tat-HRSPN), GRID1 was shown to directly interact with autophagy mediators nGOPC/nPIST, BECN1, and LAMP1. During inflammatory and neuropathic pain, GRID1 and CBLN1 are downregulated in CeA alongside impaired autophagic flux and increased excitatory neurotransmission and AMPAR expression. GluD1 is preferentially expressed in PRKCD+ neurons of the CeA where BECN1 and LAMP1 co-localize. GRID1 C-terminal peptide (Tat-HRSPN) application, co-immunoprecipitation/interaction assays with BECN1/LAMP1/nGOPC, western blotting for autophagy markers, pain models (CFA inflammatory, spinal nerve ligation), electrophysiology for mEPSCs, immunofluorescence Autophagy Medium 41147487
2014 GRID1 expression is downregulated in iPS cells derived from both MECP2-mutated and CDKL5-mutated Rett syndrome patients and upregulated during neuronal precursor and mature neuron differentiation, consistent with a role as a postsynaptic adhesion molecule that preferentially induces inhibitory presynaptic differentiation of cortical neurons. iPS cell gene expression profiling, real-time RT-PCR in CDKL5- and MECP2-mutated cells during neuronal differentiation European journal of human genetics Low 24916645
2025 In rodents and non-human primates, GluD1 immunoreactivity in the lateral habenula (LHb) is primarily expressed in dendritic profiles and is strongly localized to the core of symmetric (GABAergic) synapses, with lower perisynaptic presence at asymmetric (glutamatergic) synapses. Axon terminals from the entopeduncular nucleus and lateral hypothalamus show postsynaptic GluD1 immunolabeling in LHb, as determined by anterograde tracing combined with immunogold labeling. Immunoelectron microscopy (pre- and post-embedding immunogold), anterograde tracing combined with immunogold labeling in rat and monkey tissue The Journal of comparative neurology Medium 39794140
2023 The NRXN1-CBLN1-GluD1 transsynaptic complex at VMHvl-to-arcuate AgRP/NPY neuron excitatory synapses regulates aggression. Targeted deletion of GluD1 from arcuate AgRP neurons impairs excitatory synapses from VMHvl neurons onto AgRP/NPY neurons and increases aggression. Heterozygous deficiency of Grid1 synergizes with increased UBE3A to further increase aggression, placing GluD1 as a postsynaptic component of the NRXN1-CBLN1-GluD1 transsynaptic complex required for this hypothalamic circuit. Conditional Grid1 deletion in AgRP neurons, chemogenetic/optogenetic activation, behavioral aggression assays, epistasis with Nrxn1 and Ube3a genetic manipulations bioRxivpreprint Medium 36909588
2024 Grid1 knockdown in hypothalamic neurons (via lentiviral vector) decreases Grid1 and Rfrp-3 mRNA expression but increases Gnrh mRNA. ICV injection of LV-Grid1 in prepubertal rats causes earlier vaginal opening, increased Gnrh mRNA, decreased Rfrp-3 mRNA, decreased progesterone concentration, and altered follicular development, indicating GluD1 modulates puberty onset via Gnrh and Rfrp-3 regulation in the hypothalamus. Lentiviral Grid1 knockdown in hypothalamic neurons, ICV injection in prepubertal female rats, qRT-PCR, hormone measurement (progesterone), histological ovary analysis The Journal of veterinary medical science Low 38479882
2025 HDAC5 inhibitor T2943 promotes H3K14 acetylation at the Grid1 promoter region, enhancing GRID1 transcription and expression. GRID1 knockdown blocks the antidepressant behavioral effect of T2943 in mice, establishing GRID1 as a downstream effector of HDAC5-dependent chromatin remodeling in the antidepressant response. CUT&Tag chromatin profiling, GRID1 knockdown, behavioral tests (forced swim, sucrose preference), HDAC5 inhibitor pharmacology Scientific reports Low 39915556

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Bipolar I disorder and schizophrenia: a 440-single-nucleotide polymorphism screen of 64 candidate genes among Ashkenazi Jewish case-parent trios. American journal of human genetics 328 16380905
2012 Evaluation of copy number variations reveals novel candidate genes in autism spectrum disorder-associated pathways. Human molecular genetics 154 22543975
2011 The unfolded protein response (UPR)-activated transcription factor X-box-binding protein 1 (XBP1) induces microRNA-346 expression that targets the human antigen peptide transporter 1 (TAP1) mRNA and governs immune regulatory genes. The Journal of biological chemistry 127 22002058
2012 Genome-wide association study of comorbid depressive syndrome and alcohol dependence. Psychiatric genetics 109 22064162
2012 Deletion of glutamate delta-1 receptor in mouse leads to aberrant emotional and social behaviors. PloS one 101 22412961
2009 A MicroRNA gene is hosted in an intron of a schizophrenia-susceptibility gene. Schizophrenia research 82 19264453
2014 GluD1 is a common altered player in neuronal differentiation from both MECP2-mutated and CDKL5-mutated iPS cells. European journal of human genetics : EJHG 60 24916645
2009 Dissection of phenotype reveals possible association between schizophrenia and Glutamate Receptor Delta 1 (GRID1) gene promoter. Schizophrenia research 57 19346103
2007 A case-control association study between the GRID1 gene and schizophrenia in the Chinese Northern Han population. Schizophrenia research 57 17490860
2015 Essential role of GluD1 in dendritic spine development and GluN2B to GluN2A NMDAR subunit switch in the cortex and hippocampus reveals ability of GluN2B inhibition in correcting hyperconnectivity. Neuropharmacology 55 25721396
2015 Genetic assessment of additional endophenotypes from the Consortium on the Genetics of Schizophrenia Family Study. Schizophrenia research 55 26597662
2011 The phenotype of recurrent 10q22q23 deletions and duplications. European journal of human genetics : EJHG 51 21248748
2017 GluD1, linked to schizophrenia, controls the burst firing of dopamine neurons. Molecular psychiatry 49 28696429
2020 GluD1 knockout mice with a pure C57BL/6N background show impaired fear memory, social interaction, and enhanced depressive-like behavior. PloS one 46 32078638
2015 LPA signaling initiates schizophrenia-like brain and behavioral changes in a mouse model of prenatal brain hemorrhage. Translational psychiatry 36 25849980
2010 Novel gene rearrangements in transformed breast cells identified by high-resolution breakpoint analysis of chromosomal aberrations. Endocrine-related cancer 33 19858224
2012 Glutamate receptor δ 1 (GRID1) genetic variation and brain structure in schizophrenia. Journal of psychiatric research 30 23017809
2017 Exome sequencing of a large family identifies potential candidate genes contributing risk to bipolar disorder. Gene 29 29248581
2020 Whole-exome and RNA sequencing of pulmonary carcinoid reveals chromosomal rearrangements associated with recurrence. Lung cancer (Amsterdam, Netherlands) 27 32417679
2017 Molecular Genetic Influences on Normative and Problematic Alcohol Use in a Population-Based Sample of College Students. Frontiers in genetics 27 28360924
2015 CREB-BDNF pathway influences alcohol cue-elicited activation in drinkers. Human brain mapping 25 25939814
2021 An emerging map of glutamate delta 1 receptors in the forebrain. Neuropharmacology 18 33992669
2017 Two novel candidate genes identified in adults from the Newfoundland population with addictive tendencies towards food. Appetite 18 28115213
2021 Glutamate Delta-1 Receptor Regulates Inhibitory Neurotransmission in the Nucleus Accumbens Core and Anxiety-Like Behaviors. Molecular neurobiology 17 34173171
2022 Glutamate delta 1 receptor regulates autophagy mechanisms and affects excitatory synapse maturation in the somatosensory cortex. Pharmacological research 16 35304260
2016 Evidence for genetic regulation of the human parieto-occipital 10-Hz rhythmic activity. The European journal of neuroscience 16 27306141
2015 Polymorphisms of PRLHR and HSPA12A and risk of gastric and colorectal cancer in the Chinese Han population. BMC gastroenterology 15 26302849
2024 Clinical features, functional consequences, and rescue pharmacology of missense GRID1 and GRID2 human variants. Human molecular genetics 13 37944084
2020 RNA-Seq Analysis of Genetic and Transcriptome Network Effects of Dual-Trait Selection for Ethanol Preference and Withdrawal Using SOT and NOT Genetic Models. Alcoholism, clinical and experimental research 11 32090358
2018 Methylation pattern variation between goats and rats during the onset of puberty. Reproduction in domestic animals = Zuchthygiene 11 29577480
2024 GRID1/GluD1 homozygous variants linked to intellectual disability and spastic paraplegia impair mGlu1/5 receptor signaling and excitatory synapses. Molecular psychiatry 10 38418578
2023 Detection of Candidate Genes Associated with Fecundity through Genome-Wide Selection Signatures of Katahdin Ewes. Animals : an open access journal from MDPI 10 36670812
2021 Whole-genome methylation analysis reveals novel epigenetic perturbations of congenital scoliosis. Molecular therapy. Nucleic acids 10 33717649
2019 Non-del(5q) myelodysplastic syndromes-associated loci detected by SNP-array genome-wide association meta-analysis. Blood advances 10 31738830
2020 Gene discovery for high-density lipoprotein cholesterol level change over time in prospective family studies. Atherosclerosis 9 32109663
2021 Whole-exome sequencing identifies biosignatures that predict adverse survival outcomes in surgically treated patients with oral cavity squamous cell carcinoma. Oral oncology 7 34700279
2020 Whole-genome sequence analysis reveals candidate genomic footprints and genes associated with reproductive traits in Thoroughbred horse. Reproduction in domestic animals = Zuchthygiene 6 31858623
2025 Trans-synaptic signaling through GRID1/glutamate receptor delta-1 and CBLN1/cerebellin-1 facilitates autophagic flux in central amygdala and prevents chronic pain. Autophagy 5 41147487
2024 Genome-Wide Association Studies and Runs of Homozygosity Reveals Genetic Markers Associated with Reproductive Performance in Korean Duroc, Landrace, and Yorkshire Breeds. Genes 5 39596622
2025 Novel histone deacetylase-5 inhibitor T2943 exerts an anti-depressive effect in mice by enhancing GRID1 expression. Scientific reports 4 39915556
2025 Ultrastructural Localization of Glutamate Delta Receptor 1 in the Rodent and Primate Lateral Habenula. The Journal of comparative neurology 3 39794140
2024 Grid1 regulates the onset of puberty in female rats. The Journal of veterinary medical science 3 38479882
2023 Association between 14 candidate genes, PM2.5, and affective disorders: a study of the Taiwan Biobank. BMC public health 3 38012695
2026 Glutamate Delta 1 Receptor in Synapses, Circuits, and Disease. The European journal of neuroscience 2 41636022
2025 Design and verification of a 25 K multiple-SNP liquid-capture chip by target sequencing for dairy goat. BMC genomics 2 40234771
2025 Rare phenotypes of white coat color in Simmental calves: genetic causes of syndromic forms of albinism and depigmentation. Molecular genetics and genomics : MGG 2 40913728
2025 GluD1 at the synaptic crossroads: from domain structure to circuit dysfunction. Acta pharmacologica Sinica 2 41345253
2023 UBE3A and transsynaptic complex NRXN1-CBLN1-GluD1 in a hypothalamic VMHvl-arcuate feedback circuit regulates aggression. bioRxiv : the preprint server for biology 2 36909588
2023 A pharmacogenetic study of perampanel: association between rare variants of glutamate receptor genes and outcomes. Frontiers in genetics 2 38075685
2022 Genetic variation as a long-distance modulator of RAD21 expression in humans. Scientific reports 2 35906355
2026 Multi-omics reveals co-regulation of hepatic bile acid metabolism in laying hens by host genetics and the cecal Anaerostipes. Poultry science 1 41544443
2025 Molecular Mechanism of the Grid Gene Family Regulating Growth Size Heteromorphism in Cynoglossus semilaevis. Animals : an open access journal from MDPI 1 40281964
2025 Neurotransmitter Genes in the Nucleus Accumbens That Are Involved in the Development of a Behavioral Pathology After Positive Fighting Experiences and Their Deprivation: A Conceptual Paradigm for Data Analysis. International journal of molecular sciences 1 40943499
2022 Genome-wide association study of fasting proinsulin, fasting insulin, 2-hour postprandial proinsulin, and 2-hour postprandial insulin in Chinese Han people. Endokrynologia Polska 1 35971929
2026 Trans-ancestry GWAS of hot flashes reveals potent treatment target and overlap with psychiatric disorders. Communications medicine 0 41495267

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