Ask about this productRelated genes to: GNAL Blocking Peptide
- 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 Blocking Peptide
Related articles to: GNAL Blocking Peptide
- 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 - To investigate the protective mechanism of Astragaloside IV (AS-IV) in diabetic retinopathy(DR).A streptozotocin-induced diabetic rat model was established and divided in to three groups: control, DR, and DR + AS-IV. Retinal injury was assessed using optical coherence tomography (OCT). Retinal proteomes were profiled using 4D-DIA proteomics. Candidate genes were validated using quantitative PCR (qPCR).302 differentially expressed proteins were detected. Venn diagram analysis revealed three down-regulated proteins in the DR group: Gnal, Dennd1a, and Snx13, and two up-regulated proteins: Ogn and Mylpf. AS-IV treatment reversed the expression of Dennd1a and Gnal while downregulating Ogn, Mylpf, and Snx13. PPI analysis revealed limited direct connectivity among the five proteins but identified 10 additional interactors, including MYLK, ADCY9, and RAB35. GO analysis indicated involvement in muscle contraction, muscle myosin complex, and phosphatidylinositol phosphate binding and structural molecule activity. KEGG analysis highlighted calcium signalling as a key pathway. Molecular docking demonstrated stable interactions between AS-IV and Dennd1a, Ogn, and Snx13 proteins. qPCR confirmed significant regulation of Dennd1a and Ogn, while Snx13 and Mylpf changes were not significant.AS-IV exhibited protective effects against diabetic retinal injury by modulating Dennd1a and Ogn, implicating calcium signalling and structural pathways in its therapeutic mechanism. - Source: PubMed
Publication date: 2026/01/25
Zhang XingyiLiu Hua