Ask about this productRelated genes to: GNAL antibody
- Gene:
- GNAL NIH gene
- Name:
- G protein subunit alpha L
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 18p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-20
- Date modifiied:
- 2016-10-05
Related products to: GNAL antibody
Related articles to: GNAL antibody
- The swamp eel (), known for its benthic and nocturnal feeding habits, exhibits a keen sense of smell. To date, the genomic basis for its adaptive evolution of olfactory system was poorly investigated. In this study, we performed comparative genomic analysis to reveal the evolutionary processes underlying the expansion and diversification of olfactory receptor (OR) genes in the swamp eel. A total of 629 gene families were identified to expand in the swamp eel, with five (, , , , and ) distributed in olfactory transduction (KEGG map04740). GO enrichment analysis of these expanded gene families showed biological processes related to sensory perception of smell and detection of chemical stimulus. Among the 287 positively selected genes (PSGs) in the swamp eel, , , , , , , and were linked to signal transduction. A total of 318 OR genes (289 functional genes, 10 partial genes, and 19 pseudogenes) were annotated in the swamp eel genome, significantly surpassing other fish species. Clusters of OR genes were detected on chromosome 4, chromosome 8, chromosome 9, and chromosome 12 in the swamp eel, sharing the same transcriptional orientation, which indicated that tandem duplication was a possible mechanism for the OR gene expansion. Phylogenetic analysis revealed the obvious expansion pattern of OR genes in groups δ and ζ for the swamp eel. Conserved motifs were detected in the OR genes, which indicated the similar functions of OR genes. Our findings unveiled the genomic basis for the olfactory evolution in the swamp eel, providing insights for a better understanding of swamp eel's environmental adaptation and contributing to further investigation of olfactory function in fish. This study enriches the genomic research on the olfactory system of benthic nocturnal fishes and provides a useful evolutionary case for understanding olfactory adaptation to ecological niches in fish. - Source: PubMed
Publication date: 2026/04/29
Zhou ChuangWang ZhongyiZhang ChenhaoSong Zhaobin - Organophosphorus flame retardants (OPFRs) have various health risks. Their recently reported contribution to obesity prevalence earned even more concerns on their hazards. Presently, the obesogenic effects of triphenylphosphine oxide (TPPO), a prevalent OPFR, were investigated in mice. Despite of non-significant influences at 0.1 and 1 µg/(kg·day), TPPO at 10 and 100 µg/(kg·day) significantly increased the body weight gain by 44.5 % and 35.0 % compared with the control, respectively. TPPO at 0.1 µg/(kg·day) stimulated glucose tolerance, while at 100 µg/(kg·day) it declined glucose tolerance. TPPO increased levels of triglycerides and cholesterol. At the low dose, TPPO stimulated high-density lipoprotein cholesterol (HDL-C) in serum and inhibited low-density lipoprotein cholesterol (LDL-C), while at the high dose it inhibited both HDL-C and LDL-C. TPPO stimulated acyl-CoA oxidase 1, long-chain acyl-CoA synthetase, and adipose triglyceride lipase, while it inhibited glycerol-3-phosphateacyl transferases 1, long-chain fatty acid transport protein 1, and acetyl-CoA carboxylase. Simultaneously, TPPO reduced the expressions of Grm3, Gnal, and Cebpa but activated the expression of Ppara in liver. Especially, TPPO's effects on Ppara expressions were different in fat and liver tissues. Moreover, TPPO significantly disturbed the levels of neurotransmitters including acetylcholine, dopamine, 5-hydroxytryptamine and γ-aminobutyric acid and also the composition of the microbiota (e.g., ratio of Firmicutes to Bacteroidetes). Summing up, TPPO caused obesogenic effects through multiple aspects including disturbances on enzyme activities, genetic expression, neural regulation and microbiota composition. Further studies are needed to elucidate the interactions among the multiple aspects. - Source: PubMed
Publication date: 2025/06/28
Liu YoujiaZhou YangyuanGao PinYu ZhenyangYin Daqiang - Endocrine-resistant estrogen receptor-positive (ER) breast cancer often presents with an immune-cold phenotype, yet the upstream regulators driving immune evasion remain unclear. GNAL, a G-protein subunit involved in calcium signaling, has emerged as a potential player in modulating the tumor immune microenvironment, but its role in ER breast cancer has not been systematically investigated. This study aims to systematically investigate GNAL's biological functions, molecular mechanisms, and prognostic relevance in endocrine-resistant ER breast cancer, as well as its role in regulating the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/01/26
Zeng JingTian DongchenZhang JiahuiWang GuixinLi YingxiYu YueTian YaoHe JinxianShen WeiyuChen Zhaohui - Dystonia due to loss-of-function variants in the GNAL gene in DYT-GNAL and 18p-deletion (18pdel) syndrome has been reported to respond well to pallidal deep brain stimulation (GPi-DBS) occasionally, but long-term data is scarce. GNAL is implicated in dopamine receptor function, which may explain anecdotal reports of hypokinesia in DYT-GNAL and 18pdel-associated dystonia, a phenomenon that has not yet been systematically reviewed. We retrospectively evaluated a cohort of three patients with GNAL variants treated with GPi-DBS, documenting individual long-term outcomes spanning up to 25 years. Dystonia severity was assessed using the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) and the Burke - Fahn - Marsden Dystonia Rating Scale (BFMDRS). We also documented bradykinetic symptoms and levodopa response. A literature review was added focusing on DBS outcomes and the effects of levodopa in DYT-GNAL and 18pdel-associated dystonia. In our patients, TWSTRS severity subscale I was reduced by 63% in early (≤ 12months; 20.7 to 7.7 points) and 81% in late follow-up (> 12months; 20.7 to 4 points) after GPi-DBS χ. BFMDRS decreased by 67% and 44%; each with a Kendall's coefficient of 0.78, indicating a high degree of concordance in improvement trajectories. Two patients exhibited bradykinesia, which was levodopa-responsive in one. GPi-DBS responses have been reported for another ten DYT-GNAL and two 18pdel-patients. Bradykinesia prompted levodopa challenges in 15 patients, resulting in improvement in five. Long-term follow-up data from three DYT-GNAL patients treated with DBS showed sustained improvement in dystonia, particularly in cervical symptoms. Bradykinesia may be an inherent clinical feature of GNAL-related dystonia, warranting further investigation. - Source: PubMed
Publication date: 2026/02/03
Reimer JohannaSchumann FriederikeLohmann KatjaRiemer Thomas GKrauss Joachim KSchneider Gerd-HelgeKühn Andrea AKrause Patricia - Gastric cancer (GC) remains a leading cause of cancer mortality, yet the causal roles of microRNAs (miRNAs) in its pathogenesis are poorly characterized. While observational studies implicate miRNAs in GC progression, confounding biases and tissue-specific limitations hinder causal inference and clinical translation. We conducted a 2-sample Mendelian randomization (MR) analysis using genetic instruments derived from plasma miRNA expression quantitative trait loci (eQTLs). Summary-level data for miRNA-eQTLs were obtained from a study by Huan et al. (involving 5239 individuals and 280 miRNAs), while genetic associations with GC were sourced from 3 independent genome-wide association studies (ebi-a-GCST90018849, ebi-a-GCST90018629, and bbj-a-119) accessed via the IEU OpenGWAS Project. Instrumental variables were constructed using miRNA-eQTLs that reached significance at a false discovery rate (FDR < 0.1. Causal estimates were primarily generated using inverse-variance weighted regression, supplemented by MR-Egger regression to assess and adjust for potential pleiotropy. Sensitivity analyses, including leave-one-out validation, were performed to evaluate the robustness of the findings. Experimentally validated targets were analyzed for differential expression, prognostic relevance, and somatic mutations. Functional enrichment and pan-cancer analyses were conducted to delineate oncogenic mechanisms. MR analysis revealed 5 plasma miRNAs with consistent causal effects on GC risk: hsa-miR-127-3p, hsa-miR-370-3p, hsa-miR-382-5p, hsa-miR-409-3p, and hsa-miR-654-5p. All 5 miRNAs conferred increased risk (ORs 1.021-1.037, all ≤0.0025) across the 3 cohorts (ebi-a-GCST90018849, ebi-a-GCST90018629, bbj-a-119). These miRNAs collectively targeted 549 genes, of which 76 were differentially expressed in GC tissues. Seventeen dysregulated targets showed prognostic significance, with enrichment in immune regulation (T/B cell receptor signaling) and cancer pathways. In GC, miR-409-3p overexpression independently predicted poor survival (H = 1.55, P = .0098) and inversely correlated with multiple targets (XKR4, F2, ATAD5, GNAL, GDNF, UNC13A, and ELL2). Pan-cancer analysis revealed oncogenic roles for causal miRNAs in 16 malignancies, with miR-409-3p showing GC-specific prognostic significance. This MR study establishes plasma miRNAs as causal mediators of gastric carcinogenesis, with miR-409-3p emerging as a key prognostic biomarker. The identified miRNA-target networks highlight actionable pathways for therapeutic intervention, bridging genetic epidemiology with functional genomics in GC precision oncology. - Source: PubMed
Lin YejueLuo Ming