Ask about this productRelated genes to: GLI1 antibody
- Gene:
- GLI1 NIH gene
- Name:
- GLI family zinc finger 1
- Previous symbol:
- GLI
- Synonyms:
- -
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-01-15
Related products to: GLI1 antibody
Related articles to: GLI1 antibody
- - Source: PubMed
Publication date: 2026/09/02
Mackey TristanSalovesh StephanieTsung Andrew JCarter AlexisMordeson JackPatel Purvi - Nicotine from tobacco products, secondhand smoke, and emerging delivery systems remains a major but underappreciated driver of gastric carcinogenesis (GC). Although reactive oxygen species (ROS) have long been implicated in tumor biology, current models incompletely explain how chronic nicotine selectively reprograms gastric epithelial signaling. This review advances the concept of redox rewiring, whereby nicotine establishes a persistent oxidative state that orchestrates multiple oncogenic programs spatially compartmentalized NOX signaling. - Source: PubMed
Publication date: 2026/09/01
Liu XileiJiang QinhanXie BoxuanZhang ZhongweiZhou JianmingZhou TongWang Huai - Odontogenic keratocyst (OKC) is a developmental odontogenic cyst that may occur sporadically (OKCsp) or in association with nevoid basal cell carcinoma syndrome (NBCCS) (OKC-sy). NBCCS is an autosomal dominant disorder characterised by morphological abnormalities and an increased predisposition to several neoplasms, including basal cell carcinomas. Mutations in the tumour suppressor gene PTCH1 have been reported in patients with OKC and NBCCS. PTCH1 participates in a signalling cascade that culminates in the translocation of GLI transcription factors to the nucleus, thereby activating target genes involved in cell proliferation. Aberrant GLI1 expression has been associated with increased proliferation in lung adenocarcinoma and other cancers. - Source: PubMed
Publication date: 2026/09/01
Oyarzún-Puga EstebanEscobar-López EnricoVelozo-Papez LuisEspinoza-Santander IrisOrtega-Pinto Ana - Wogonoside, a major flavone 7-O-glucuronide from Scutellaria baicalensis Georgi, has long been used as a quality-control marker for Scutellariae Radix and related traditional herbal formulations. Emerging evidence suggests that wogonoside is not merely an analytical marker or an inactive glucuronide, but a pharmacologically active constituent and potential precursor of bioactive metabolites. In preclinical models, it exhibits anti-inflammatory, antioxidant, anti-angiogenic, anti-fibrotic, antitumor, cardioprotective, neuroprotective, and renoprotective activities. These effects are associated with the regulation of key signaling networks involved in inflammation, oxidative stress, inflammasome activation, autophagy, angiogenesis, fibrosis, and regulated cell death. Representative mechanisms include modulation of TLR4/NF-κB/NLRP3, Nrf2/HO-1, PI3K/AKT/mTOR, AMPK/mTOR, Wnt/β-catenin, Hedgehog/SMO/Gli1, and ferroptosis-related SLC7A11/GPX4 signaling. Recent target-validation studies have identified several candidate molecular targets, including SMO, NF-κB p65, HNF4α, NEK7, GPX4, TLR4, and CD39. However, the strength of evidence varies, and direct target engagement remains to be confirmed for many of these proteins. Pharmacokinetic studies reveal complex disposition characteristics, including intestinal microbial deglycosylation to wogonin, intestinal and hepatic re-glucuronidation, transporter-mediated efflux, enterohepatic or enteric recycling, and frequent multiple-peak plasma profiles. These properties support the value of wogonoside as both a quality-control marker and a dynamic exposure-related marker in Scutellaria-containing preparations. This review summarizes current advances in the chemical analysis, pharmacokinetics, biotransformation, molecular pharmacology, and disease-specific actions of wogonoside, and discusses key challenges for future development, including variable bioavailability, metabolite contribution, target specificity, pharmacokinetic-pharmacodynamic relationships, and clinical translation. - Source: PubMed
Publication date: 2026/08/30
Xie MingLiu JiaPu RuiQiu XiangWang JiahaoZhang KeyanHua HaibingLi Xiandeng - Uterine leiomyomas (ULMs) are the most common benign gynecological tumors affecting women in reproductive age. Symptoms such as abnormal uterine bleeding, pelvic pain, and infertility may occur, leading to a significant decline in patients' quality of life. In addition, ULMs represent the second leading indication for gynecological surgery in Brazil, imposing a substantial economic burden on the public healthcare system. However, despite their high prevalence and clinical impact, there is still no curative clinical treatment for these tumors, and the molecular mechanisms underlying their development and clinical behavior remain poorly understood. Recent studies have demonstrated the involvement of the Sonic Hedgehog (SHH) signaling pathway in uterine mesenchymal tumors. Therefore, the aim of this study was to investigate the expression profile and regulation of the SHH and Wnt signaling pathways in ULMs, as well as to evaluate their potential role in tumor progression through integrative analyses of promoter methylation, mRNA expression, and microRNA-mediated regulation. Initially, 106 genes related to SHH, Wnt signaling pathways were examined in ULM, compared to normal myometrium (MM) by real-time PCR. Interactions among SHH pathway genes were assessed through multivariate analysis. In addition, methylation profiles of nine key SHH-related genes were evaluated using methylation-specific assays, and the expression of 84 microRNAs (miRNAs) was analyzed in association with differentially expressed genes potentially involved in tumorigenesis. Differential expression analysis identified 23 dysregulated genes, including 13 upregulated and 10 downregulated genes. Multivariate analysis suggested that SHH pathway activation in ULMs occurs independently of SHH-PTCH1 binding and may involve GLI1, CCND1, and BCL-2. Significant DNA methylation alterations were detected in PTCH1, SMO, GLI1, GLI3, GREM1, and WNT1. Furthermore, 16 miRNAs were differentially expressed, eight of which showed significant correlations with their predicted target genes. Collectively, these findings suggest that ULM pathogenesis involves a complex regulatory network integrating SHH and Wnt signaling pathways, epigenetic modifications, and microRNA-mediated post-transcriptional regulation. These results provide novel insights into the molecular mechanisms underlying ULM development and identify candidate regulatory elements that may serve as potential biomarkers or therapeutic targets in future functional studies on uterine fibroids. - Source: PubMed
Publication date: 2026/08/29
Purcino Grazielle Marques DuarteFerreira Kelly PedrozoBozzini NiloBaracat Edmund ChadaCarvalho Katia Candido