Ask about this productRelated genes to: HTR3A Blocking Peptide
- Gene:
- HTR3A NIH gene
- Name:
- 5-hydroxytryptamine receptor 3A
- Previous symbol:
- HTR3
- Synonyms:
- 5-HT3R, 5-HT3A
- Chromosome:
- 11q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-06-16
- Date modifiied:
- 2016-10-11
Related products to: HTR3A Blocking Peptide
Related articles to: HTR3A Blocking Peptide
- Effective therapies for Autism Spectrum Disorder (ASD) are currently limited, and the functional connections between gut microbiota and brain development are not fully elucidated. Using the Katnal2 mutant zebrafish as an ASD-like model, we evaluated whether fecal microbiota transplantation (FMT) from wild-type donors or supplementation with the probiotic Akkermansia muciniphila (A. muciniphila) could ameliorate neurodevelopmental deficits. Assessments included developmental phenotypes, behavior, microbial profiling, neurotransmitter-related gene expression, and short-chain fatty acid (SCFA) signaling in conventionally reared (CR) and germ-free (GF) fish. FMT from wild-type donors and A. muciniphila supplementation significantly improved hatching rates, growth parameters, heart rate, and locomotor activity in Katnal2 mutants, whereas microbiota from Katnal2 mutants induced analogous deficits in wild-type recipients. A. muciniphila successfully colonized the gut, reshaped microbial communities, and reduced anxiety-like behaviors. Mechanistically, A. muciniphila upregulates genes involved in dopamine (th), serotonin (tph1a), and gamma-aminobutyric acid (GABA) synthesis, downregulates the serotonin receptor htr3a, and enhances expression of the SCFA receptor ffar2, independently of total SCFA levels. Correlation analyses linked key developmental, behavioral, and transcriptional changes to altered microbial genera in a sample-specific manner, highlighting compositionally driven neuromodulatory effects of genetic and probiotic interventions. Thus, microbiota-targeted intervention with A. muciniphila rescues neurodevelopmental impairments in ASD models by remodeling the gut-brain axis, supporting its translational potential. - Source: PubMed
Publication date: 2026/03/30
Jia Pan-PanLi YanYang Hao-YuDing YuanGuo Feng-YiWu Ming-FeiJia Jin-QiuPei De-Sheng - Psoriasis is a chronic, immune-mediated inflammatory skin disease with a complex etiology involving genetics, environmental triggers, and immune dysregulation. Research suggests that the endocannabinoid system (ECS) is involved in inflammation and skin homeostasis, prompting interest in its involvement in the pathogenesis of psoriasis. - Source: PubMed
Publication date: 2025/07/26
Turk Jaime NKirchhof Mark G - Serotonin (5-hydroxytryptamine, 5-HT), a pleiotropic biogenic monoamine, modulates immune response through interactions with its distinct receptors (5-HTRs). In this study, thirteen 5-HTRs were identified in the Pacific oyster (Crassostrea gigas) to elucidate their functions in immune response to Vibrio stimulation. Except for the unique ligand-gated cation channels (Cg5-HTR3A-like), the other twelve 5-HTRs (Two Cg5-HTR, Cg5-HTR-like, Cg5-HTR1, Cg5-HTR1A-like, Cg5-HTR1B, Cg5-HTR1B-like, Cg5-HTR2A-like, Cg5-HTR2B, Cg5-HTR4, Cg5-HTR5, and Cg5-HTR6) all belong to G protein-coupled receptor (GPCR) superfamily. Among those twelve 5-HTRs, most are non-canonical members lacking complete seven-transmembrane (7TM) domains; only Cg5-HTR2B and Cg5-HTR6 retain the canonical GPCR architecture. Ten conserved motifs were identified in oyster 5-HTRs, with motif 2 being universal across all receptors and motif 10 unique to Cg5-HTR3A-like, indicating subtype-specific divergence. Molecular docking revealed significant differences in binding affinity and residue interaction among Cg5-HTRs, with Cg5-HTR6 exhibiting the highest binding affinity for 5-HT. Analysis across developmental stages revealed that Cg5-HTR1A-like transcripts were enriched in early gastrula, gastrula and trochophore, Cg5-HTR4, Cg5-HTR1B, and Cg5-HTR-like enriched specifically in the D-shape stage, while Cg5-HTR2B and Cg5-HTR1 transcripts enriched during the pediveliger, spat, and juvenile stages. Furthermore, Cg5-HTR-like and Cg5-HTR1 were primarily expressed in granulocytes, Cg5-HTR1A-like and Cg5-HTR2B in agranulocytes, and Cg5-HTR6 and Cg5-HTR1B in semi-granulocytes. Crucially, following secondary Vibrio splendidus stimulation, the expression levels of Cg5-HTR-like, Cg5-HTR1, Cg5-HTR1A-like, Cg5-HTR1B and Cg5-HTR2B mRNA in hemocytes upregulated significantly, indicating their potential role in immune priming. These findings suggested the potential mechanisms of 5-HTRs in regulating the immune response of hemocytes in C. gigas, which offered insights into the evolutionary conservation and immunoregulation divergence of these receptors in invertebrates. - Source: PubMed
Publication date: 2026/01/31
Xu MinhuiDong MirenGao XiaolongWu WeiWang LinglingWang Chunlin - Diethylhexyl phthalate (DEHP), a common plasticizer, has been associated with hormone disruption and carcinogenesis, but its molecular impact on uterine corpus endometrial carcinoma (UCEC) remains unclear. This study aims to computationally identify a gene signature based on known DEHP-associated toxic targets and evaluates their clinical and immunological relevance in UCEC. DEGs were intersected with DEHP targets from CTD and TargetNet databases. PPI networks, functional enrichment, and survival analyses were conducted. Prognostic genes were identified using Cox and LASSO regression. DEHP risk score models and nomograms were constructed. Immune infiltration was analyzed using ESTIMATE and ssGSEA algorithms. Molecular docking was performed via CB-Dock2. Seventy-five genetic targets linked to DEHP in toxicological databases were identified, and enrichment analyses revealed DEHP-related genes enriched in neurotransmission and hormone signaling pathways. Seven prognostic genes (HTR3A, GRM2, HTR6, THRB, TUBB2B, FOLH1, PGR) correlated with overall survival and histologic grade. The DEHP risk score effectively stratified patients. DEHP-THRB showed strongest binding affinity, suggesting direct toxicological interaction. This study characterizes a computationally derived gene signature associated with DEHP toxicity in UCEC, highlighting their prognostic and immunological significance as potential molecular footprints, while acknowledging that direct exposure inference requires future validation with measured biomonitoring data. - Source: PubMed
Publication date: 2026/01/30
Yin MinuoZhang Huimin - Early life stress (ELS) is a well-known predictor of neuropsychiatric disease and contributes to the development of sensory processing deficits that persist throughout life. Organisms are particularly susceptible to the deleterious effects of stress during critical periods, when neuroplasticity is heightened, and initial representations of the sensory environment are mapped to cortex. When ELS is induced during the auditory cortical (ACx) critical period, it impairs both neural and behavioral responses to a variety of auditory stimuli that rely on temporal processing. Mechanisms by which ELS may alter critical period plasticity are of particular interest in understanding ELS-related pathology, including the 5-HT3R interneuron system, which has been implicated in regulating neural activity during critical periods. Here we examined two principal subpopulations of interneurons in primary ACx: VIP and NDNF cells, which account for a majority of cortical neurons expressing 5-HT3R. The expression of the Htr3a gene during normal development and under ELS conditions was quantified using multiplex fluorescent hybridization. We show that densities of cells expressing NDNF and VIP decrease following ear opening and across the ACx critical period, and that ELS results in the maintenance of elevated cell densities compared to age-matched controls. Further, Htr3a in VIP neurons is developmentally upregulated, and its expression is further increased by ELS beyond normal physiologic levels. Stress-induced shifts in these serotonergic interneurons may contribute to deficits that arise in auditory cortical and perceptual responses via effects on local cortical circuitry. - Source: PubMed
Publication date: 2026/01/05
Moore James TSunthimer Matthew JWhite EthanMellott Jeffrey GRosen Merri J