HTR1F Antibody (OALA00633)
- Known as:
- HTR1F Antibody (OALA00633)
- Catalog number:
- oala00633
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HTR1F Antibody (OALA00633)
Related genes to: HTR1F Antibody (OALA00633)
- Gene:
- HTR1F NIH gene
- Name:
- 5-hydroxytryptamine receptor 1F
- Previous symbol:
- -
- Synonyms:
- HTR1EL, 5-HT1F
- Chromosome:
- 3p12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-26
- Date modifiied:
- 2016-02-04
Related products to: HTR1F Antibody (OALA00633)
Related articles to: HTR1F Antibody (OALA00633)
- Wide variation of responses to identical stimuli presented to genetically inbred mice suggests the hypothesis that stochastic non-genetic variation, such as in chromatin state or enhancer activity during neurodevelopment, can mediate such phenotypic differences. However, this hypothesis is largely untested since capturing pre-existing molecular states requires non-destructive, longitudinal recording. Therefore, we tested the potential of Calling Cards (CC) to record transient neuronal enhancer activity during postnatal development in mice, and thereby associate such non-genetic variation with a subsequent phenotypic presentation - degree of seizure response to the pro-convulsant pentylenetetrazol. We show that recorded differences in enhancer activity at 243 loci predict a severe vs. mild response, and that these are enriched near genes associated with human epilepsy. We also validated pharmacologically a seizure-modifying role for two previously unassociated genes, Htr1f and Let7c. This proof-of-principle supports using CC broadly to discover predisposition loci for other neuropsychiatric traits and behaviors. Finally, as human disease is also influenced by non-genetic factors, similar epigenetic predispositions are possible in humans. - Source: PubMed
Publication date: 2026/01/08
Boros Benjamin DGachechiladze Mariam AGuo JuanruGalloway Dylan AMueller Shayna MShabsovich MarkYen AllenChen XuhuaCammack Alexander JShen TaoMitra Robi DDougherty Joseph DMiller Timothy M - The avian cerebellum is pivotal for multisensory integration and motor control during flight, yet its molecular adaptation to prolonged exertion remains incompletely defined. We profiled cerebellar transcriptomes of ten racing pigeons before and after a 300-km homing flight using whole-transcriptome RNA sequencing. Differential expression analysis revealed robust remodeling of metabolic and proteostatic pathways, including upregulation of SLC35D2, consistent with enhanced UDP-GlcNAc flux through the hexosamine biosynthetic pathway aligned with birds' naturally high glycaemia. Increased VLDLR expression links lipid handling to the reelin signalling cascade, suggesting contributions to navigation and synaptic plasticity, whereas downregulation of HTR1F indicates region-specific serotonergic modulation with exercise. Co-expression network analysis (WGCNA) identified modules enriched for endoplasmic reticulum protein processing and stress responses (PLAA, RAD23, ERN1), alongside intensified ribosome and RNA biogenesis, reflecting an elevated demand for protein synthesis and quality control. Functional enrichment (WebGestalt,) highlighted among others ribosome biogenesis, core metabolic pathways, RNA transport. These insights contribute to understanding the genetic and molecular mechanisms underpinning avian navigation and performance, providing a foundation for further research into flight-related neurophysiology. - Source: PubMed
Publication date: 2025/12/29
Stefaniuk-Szmukier MonikaSzmatoła TomaszSteg AnnaSmołucha GrzegorzRopka-Molik Katarzyna - Kidney disease (KD) has emerged as a major global health crisis and leading cause of morbidity and mortality worldwide, impacting over 850 million individuals. Pathophysiological hallmarks of KD encompass renal tubular cell injury/necrosis, tubulointerstitial fibrosis, vascular dysfunction/rarefaction, and mitochondrial dysfunction, all of which are implicated in disease initiation/progression. Unfortunately, there remains a general lack of effective Food and Drug Administration (FDA)-approved therapeutics for the treatment of KD. Thus, the identification of novel and/or repurposed treatment strategies remains of dire importance. Previously, we identified the 5-hydroxytryptamine 1F receptor (HTR1F) as a modulator of renal mitochondrial homeostasis and demonstrated that mice lacking this receptor exhibit hindered renal recovery following mild ischemia/reperfusion-induced acute kidney injury (I/R-AKI). In addition, we reported that treatment with the HTR1F agonist lasmiditan, an FDA-approved therapeutic for acute migraines, expedites renal recovery following I/R-AKI in mice. Here, we show that lasmiditan treatment following moderate-severe I/R-AKI ameliorates acute tubular injury, mitochondrial dysfunction, tubulointerstitial fibrosis, and vascular rarefaction in the renal cortex of mice, which likely contributes to the enhanced recovery observed. Importantly, we also confirm that this lasmiditan-induced renal recovery is contingent on expression. Furthermore, mice lacking the HTR1F exhibit decreased innate renal cortical vasculature, exacerbated rarefaction, and markedly increased mortality rates following moderate-severe I/R-AKI. These findings not only underscore the importance of expression and agonism in renal repair and recovery but also further highlight the repurposing potential of lasmiditan for the treatment of AKI and/or KD onset/progression. In the present study, we confirmed that lasmiditan-induced renal recovery following moderate-severe bilateral ischemia/reperfusion-induced acute kidney injury (I/R-AKI) in mice is dependent on the expression. Furthermore, lasmiditan treatment ameliorated acute tubular injury, mitochondrial dysfunction, tubulointerstitial fibrosis, and renal cortical vascular rarefaction postinjury, likely contributing to this enhanced recovery. Interestingly, we also found that mice lacking the HTR1F display decreased innate renal cortical vasculature, exacerbated rarefaction, and exhibit markedly increased mortality following moderate-severe I/R-AKI. - Source: PubMed
Publication date: 2025/10/08
Thompson Austin DMcAlister Kai WScholpa Natalie EJanda JaroslavHortareas JohnGeorgieva Teodora GSchnellmann Rick G - (5-Hydroxytryptamine Receptor 1F) encodes a G protein-coupled receptor involved in serotonin signaling. Although dysregulated expression has been implicated in certain malignancies, its biological functions and clinical significance across cancer types remain largely unexplored. We performed an integrative pan-cancer analysis of transcriptomic and pharmacogenomic datasets covering 34 cancer types (PAN-CAN cohort, N = 19,131; normal tissues, G = 60,499). Drug sensitivity and molecular docking analyses were conducted using the GSCALite database. The protein-protein interaction (PPI) network of was constructed via the STRING database. Additionally, we evaluated the effects of overexpression on proliferation and invasion in human lung squamous cell carcinoma (LUSC) cell lines NCI-H520 and NCI-H226. expression was significantly upregulated in 17 cancer types and was associated with poor prognosis, with LUSC showing an AUC of 0.912 for 1-year survival prediction. In LUSC, 695 genes were upregulated and 67 downregulated in response to overexpression. expression correlated with immune-related genes, immune checkpoints, tumor-infiltrating immune cells, tumor mutation burden (TMB), microsatellite instability (MSI), and drug responses. Genomic alterations, including amplification and deletion, were positively associated with expression. Drug sensitivity analysis identified compounds such as sotrastaurin (-10.2 kcal/mol), austocystin D (-9.7 kcal/mol), and tivozanib (-9.3 kcal/mol) as potentially effective inhibitors based on predicted binding affinity. Functional enrichment analyses (GO, KEGG) and GSEA revealed that is primarily involved in cell cycle regulation, DNA replication, cellular senescence, and immune-related pathways. Functional validation showed that overexpression promotes proliferation of LUSC cells via the MAPK signaling pathway. Our integrative analysis highlights as a potential biomarker associated with prognosis, immune modulation, and drug sensitivity across multiple cancer types. These findings provide a foundation for future experimental and clinical studies to explore -targeted therapies. - Source: PubMed
Publication date: 2025/09/11
Gao YanjunZhang ZiyueYe DafuLi QingqingWen YingmeiMa ShaowenZheng BoChen LeiYao Yi - It has been shown previously that repeated positive fighting experience in daily agonistic interactions is accompanied by the development of psychosis-like behavior, with signs of an addiction-like state associated with changes in the expression of genes encoding the proteins involved in the main neurotransmitter events in some brain regions of aggressive male mice. Fighting deprivation (a no-fight period of 2 weeks) causes a significant increase in their aggressiveness. This paper is aimed at studying-after a period of fighting deprivation-the involvement of genes (associated with neurotransmitter systems within the nucleus accumbens) in the above phenomena. The nucleus accumbens is known to participate in reward-related mechanisms of aggression. We found the following differentially expressed genes (DEGs), whose expression significantly differed from that in controls and/or mice with positive fighting experience in daily agonistic interactions followed by fighting deprivation: catecholaminergic genes , , , , , and ; serotonergic genes , , , and ; opioidergic genes , , and ; and glutamatergic genes , , , , , , , and . The expression of DEGs encoding proteins of the GABAergic system in experienced aggressive male mice mostly returned to control levels after fighting deprivation, except for . In light of the conceptual paradigm for analyzing data that was chosen in our study, the aforementioned DEGs associated with the behavioral pathology can be considered responsible for consequences of aggression followed by fighting deprivation, including mechanisms of an aggression relapse. - Source: PubMed
Publication date: 2025/09/03
Kudryavtseva Natalia NSmagin Dmitry ARedina Olga EKovalenko Irina LGalyamina Anna GBabenko Vladimir N