Ask about this productRelated genes to: NRXN1 antibody
- Gene:
- NRXN1 NIH gene
- Name:
- neurexin 1
- Previous symbol:
- -
- Synonyms:
- KIAA0578, Hs.22998
- Chromosome:
- 2p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2015-09-01
Related products to: NRXN1 antibody
Related articles to: NRXN1 antibody
- Copy number variants (CNVs) in genes encoding metabotropic glutamate receptors (GRMs) have been previously implicated in attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). However, investigations of their role in comorbid ADHD patients suffering from coexisting neurodevelopmental disorders (NDDs), such as anxiety and ASD with or without developmental delay remains limited. To assess the enrichment of CNVs in GRM genes and their molecular interaction networks in a large pediatric cohort with ADHD and comorbid NDDs, we analyzed CNV data from 72,626 pediatric participants recruited through the Center for Applied Genomics at Children's Hospital of Philadelphia. The cohort includes 12,472 individuals diagnosed with ADHD (including 7,967 with other NDD comorbid conditions). CNVs were identified using PennCNV and annotated for overlap with GRM genes and their protein-protein interaction (PPI) networks using data from STRING. We evaluated CNV enrichment in ADHD cases with and without comorbid diagnoses, including autism spectrum disorder (ASD), anxiety, and developmental delay. Significant enrichment of CNVs was observed in GRM-interacting networks among ADHD cases with comorbid NDDs. Specifically, 27 genes interacting with primary GRM genes were significantly enriched in CNVs in these individuals with false discovery rate (FDR) < 0.05, compared to ADHD-only cases or disease-free controls. These included key neurodevelopmental genes such as DLG2, NRXN1, SHANK3, and SYNGAP1, which are involved in synaptic signaling and glutamatergic neurotransmission. In contrast, enrichment of GRM network gene CNVs observed in ADHD-only cases was notably less. Our findings support a distinct genetic profile in ADHD cases with comorbid NDDs, marked by CNV enrichment in glutamatergic signaling pathways involving GRM-interacting genes. These results suggest that GRM network disruptions contribute to the complexity of the phenotype spectrum in ADHD patients suffering from comorbid neurodevelopmental phenotypes and highlight a potential pathway for targeted, genetically informed interventions in these patients. - Source: PubMed
Publication date: 2026/05/07
Glessner Joseph TKhan Munir EChang XiaoLiu YichuanTorkamandi ShahramAbrams DeborahOtieno F GeorgeKim JihoonMahesh YeshwanthLemma MariaMentch FrankLi JinKao CharllyMarch Michael EQu HuiqiConnolly JohnHakonarson Hakon - This study aimed to identify novel exercise-induced myokines and their role in improving insulin sensitivity and reducing inflammation. We identified neuroligin-3 (NLGN3) as an exercise-induced mediator that enhances insulin sensitivity and alleviates inflammation. Exercise-induced NLGN3 upregulation or recombinant NLGN3 administration improved metabolic function in high-fat diet-fed mice via neurexin-1 and -3 (NRXN1/3), but these benefits were lost upon NRXN1/3 ablation. NLGN3 emerges as a key mediator of exercise-driven metabolic benefits and a promising therapeutic target for obesity-associated insulin resistance. - Source: PubMed
Publication date: 2026/05/01
Sinha ArchanaPatra DebarunMishra SubrataVashisth AnkitSharma ShivamDey UpalabdhaRamprasad PallaRoy SoumyajitKumar AdityaTikoo KulbhushanPal DurbaDasgupta Suman - Breast cancer brain metastasis (BCBM) is a major cause of breast cancer-related mortality, but the molecular mechanisms underlying its progression remain poorly understood. Here, we profiled the tumor immune microenvironment of BCBM at single-cell resolution and identified candidate regulators associated with brain metastatic progression. Single-cell RNA sequencing (scRNA-seq) was performed on brain metastatic tissue, adjacent tumor tissue, cerebrospinal fluid, and circulating tumor cells (CTCs) from seven patients, and bulk DNA sequencing was conducted on primary breast tumors, peripheral blood, and brain metastases from 47 patients. Analysis of 131,880 single cells identified 63 distinct cell clusters, including 12 tumor-associated macrophage (TAM) subtypes and 5 metastatic tumor cell (MTC) subtypes. Circulating TAMs displayed an M1-like inflammatory phenotype, whereas tissue-resident TAMs were predominantly M2-like. MTCs exhibited substantial transcriptional heterogeneity, and a neuro-related subtype showed adaptive upregulation of neuronal signaling pathways. Brain metastases also harbored a higher mutational burden than primary tumors, with recurrent mutations in GABRB3 and NRXN1 associated with poorer patient survival. Functional experiments further showed that loss of GABRB3 or NRXN1 impaired tumor growth and brain colonization in xenograft models. These findings nominate GABRB3 and NRXN1 as candidate regulators of brain metastatic fitness in BCBM and support their further evaluation as biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/25
Shi HaoyuanChen JiaxinWu ZishengLiu Dong-XuZhou JinmeiWu XuexueYang AilingLi ShanhuTai YanhongJiang ZefeiHu ZhiyuanZhang MingshanXu XiaojiePan LuWang Tao - Neurexins (NRXNs) are presynaptic adhesion molecules essential for synaptic organization and the regulation of excitatory-inhibitory balance. The molecular diversity of NRXNs arises from alternative promoters and splicing, particularly at splice site 4 (SS4), which dictates ligand binding. Dysregulation of NRXNs has been linked to substance use disorders, but it remains unclear how the expression of NRXN isoforms responds to physiologically relevant amounts of ethanol. - Source: PubMed
Lowe Clara CZimmerman Kip DCervera-Juanes Rita - Ventral midbrain dopaminergic neurons are a key cell type for schizophrenia pathophysiology but information about cell type-specific genomic dysregulation in diseased brains is missing. We generated a unique midbrain functional genomics resource with 97 RNA-seq and 34 Hi-C chromosomal contact libraries for Nurr1 + /NeuN+ dopaminergic and their surrounding Nurr1-/NeuN- nuclei, collected from donors diagnosed with schizophrenia (SCZ), bipolar disorder (BD) and compared to neurotypical controls. Among the 954 dopamine neuron genes specifically dysregulated in SCZ, 331 were downregulated, with selective enrichment for risk-associated synaptic plasticity and neuronal connectivity pathways and embedded within dopamine neuron-specific topologically associated chromosomal domains (TAD). Transcript-resolved analysis revealed 2,350 transcripts with altered expression in SCZ dopamine neurons, affecting key susceptibility genes such as the FOXP1, MAPK10, PCM1 and NRXN1. Therefore, genomic dysregulation in the ventral midbrain of subjects diagnosed with SCZ selectively affects dopaminergic neurons, and includes a unilateral association of genetic risk with down-, but not upregulated transcription at the sites of highly organized chromosomal domains harboring neuron-specific genes with complex transcriptional architectures. - Source: PubMed
Publication date: 2026/04/06
Singh SwadhaIskhakova MarinaLambert Tova YValada AditiShokrian NedaEvans VivianaBendl JaroslavAuluck Pavan KMarenco StefanoWang MinghuiZhang BinHoffman Gabriel EGirdhar KiranRoussos PanosAkbarian Schahram