GLI1 Antibody (OALA06145)
- Known as:
- GLI1 Antibody (OALA06145)
- Catalog number:
- oala06145
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GLI1 Antibody (OALA06145)
Related genes to: GLI1 Antibody (OALA06145)
- 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 (OALA06145)
Related articles to: GLI1 Antibody (OALA06145)
- Enamel is asymmetrically distributed in mouse incisors, which grow throughout life, and this continuous renewal is driven by dental epithelial stem cells (DESCs). In this study, we report that ablation of Isl1 in the dental epithelium using Pitx2-Cre leads to impaired development of the mandibular incisors. In Isl1 mutant embryos, the mandibular incisors exhibited a significant reduction in size and length compared to wild-type controls. A significant decrease in the proliferation of epithelial and mesenchymal cells was also detected in Isl1 mutant incisors, and cell apoptosis was markedly increased in the lateral cervical loop of Isl1 mutant incisors at E17.5. Ameloblasts and enamel were present on all surfaces of the mandibular incisor, including the labial side. Transcriptome analysis and in situ hybridisation revealed that Isl1 deletion induced significant upregulation of Hedgehog pathway components (Shh, Ptch1, Gli1) and FGF signalling mediators (Fgf3, Etv4, Etv5), while downregulating dental epithelial stem cell markers Sox2 and Lgr5. Our results showed that ISL1 co-localised with SOX2 in the lingual and lateral dental epithelium of mandibular incisors, and the expression of Sox2 was regulated by Isl1. Our results demonstrate that Isl1 sustains DESC viability and orchestrates ameloblast lineage commitment via SOX2-mediated regulation during incisor morphogenesis. - Source: PubMed
Publication date: 2026/08/27
Qu YapingLiu HuizhouWang YanGao ShanhuiHuang HuarongLi JianyingQiu MengshengLi Feixue - Soft tissue sarcomas (STSs) are a heterogeneous group of rare mesenchymal malignancies with overlapping morphological and immunohistochemical features, often making definitive diagnosis challenging. Recent advances in next-generation sequencing (NGS) have enabled the identification of recurrent molecular alterations that contribute to tumor classification, prognostic stratification, and precision oncology approaches. This retrospective study aimed to evaluate the diagnostic and clinical impact of molecular profiling in pediatric soft tissue sarcomas using the Oncomine Childhood Cancer Research Assay (OCCRA) panel. Fifty-five frozen tumor samples representing 24 distinct soft tissue sarcoma subtypes were obtained from the Pediatric Oncology Institute -IOP/GRAACC/UNIFESP Biobank (B-053). Molecular analysis was performed using NGS to identify gene fusions, single nucleotide variants (SNVs), copy number variations (CNVs), and insertions/deletions (InDels). Clinically relevant molecular alterations were identified in 70% (37/55) of cases, including 18 fusion transcripts, 13 SNVs, 8 CNVs, and 6 InDels. Recurrent and diagnostically relevant alterations included ::, ::, :, ::, ::, ::, ::, :: and :: fusions, as well as amplifications involving , , , , , and . Pathogenic variants affecting genes involved in tumor suppression and chromatin remodeling, including , , , , , and , were also detected. Importantly, molecular profiling had significant diagnostic impact in several histologically ambiguous tumors, enabling molecular reclassification and refinement of previously inconclusive or inaccurate pathological diagnoses. In multiple cases, NGS transformed descriptive histopathological interpretations into genetically defined sarcoma entities, including -rearranged spindle cell neoplasms, -rearranged sarcomas, synovial sarcoma, low-grade fibromyxoid sarcoma, and clear cell sarcoma. Furthermore, the identification of actionable alterations highlighted potential opportunities for targeted therapies and precision medicine approaches. Our findings demonstrate that comprehensive molecular profiling significantly enhances diagnostic accuracy in pediatric soft tissue sarcomas, particularly in morphologically challenging cases. The integration of NGS into routine sarcoma diagnostics enables biologically informed tumor classification and supports personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/08/12
Tesser-Gamba FrancineMendes Thais BiudeLima Fernanda TeresaAbib Simone de Campos VieiraCaran Eliana Maria MonteiroToledo Silvia Regina Caminada de - Early-onset colorectal cancer (EOCRC), defined as colorectal cancer diagnosed before 50 years of age, is increasing worldwide and may exhibit molecular features distinct from late-onset colorectal cancer (LOCRC). This study aimed to identify EOCRC-associated genes and evaluate the functional relevance of the leading candidate. - Source: PubMed
Publication date: 2026/08/04
Lee Chung-YingPan Hsu-JuiLee Yu-ChengNguyen Hieu DucNi Yi-ChunYee Ke XinNguyen Man ThiWu Yung-FuLee Kuen-Haur - Glioma-associated oncogene homologue 1-altered mesenchymal tumours (GLI1-AMT) are rare, recently characterised soft tissue neoplasms driven by GLI1 fusions or amplifications. They predominantly arise in the head and neck, though their full clinicopathological presentation remains variable.A female in her 30s with a year-long history of progressive dysphagia was found to have a GLI1-AMT of the upper oesophageal sphincter, the first known case at this site. She underwent laser excision of the mass with adjuvant radiotherapy with no disease recurrence to date.Literature review identified 42 additional cases in the head and neck, most commonly affecting the tongue. Genetic alterations include GLI1 amplifications, frequently co-amplified with CDK4 and MDM2, and fusions, typically with ACTB, PTCH1 or MALAT1. Immunohistochemical staining patterns are inconsistent, though CD56, S100 and MDM2 are frequently positive.Classification of GLI1-AMT has evolved over recent years, and research is needed to refine diagnostic criteria and elucidate the behaviour of this spectrum of neoplasms. - Source: PubMed
Publication date: 2026/08/25
Hebert SagePeters MalloryCuevas-Ocampo AreliDewan Karuna - The periodontal ligament (PDL) contains heterogeneous mesenchymal stem/progenitor cells that contribute to periodontal homeostasis and regeneration. However, the developmental origin and behavior of α-smooth muscle actin (αSMA)-positive cells remain poorly understood. This study investigated the spatiotemporal distribution of αSMA-positive cells during tooth development and their response to altered mechanical loading following extraction of the opposing mandibular molars in mice. Before tooth eruption, αSMA-positive cells were widely distributed throughout the dental follicles but became progressively restricted to the apical PDL during root formation and eruption. In contrast, c-kit immunoreactivity gradually disappeared from the apical PDL, whereas Gli1/tdTomato-positive cells partially co-localized with αSMA-positive cells. Following extraction of the opposing molars, the αSMA-positive area and the number of PCNA-positive cells transiently increased, while endomucin-positive blood vessels became dilated in the apical PDL. These findings demonstrate that αSMA-positive cells undergo dynamic developmental redistribution and rapidly respond to altered mechanical loading. Furthermore, the partial co-localization of αSMA and Gli1 suggests that at least a subset of αSMA-positive cells may represent a resident mechanosensitive mesenchymal progenitor population involved in periodontal homeostasis and remodeling, providing new insight into the biological basis of periodontal remodeling during orthodontic tooth movement and periodontal regeneration. - Source: PubMed
Publication date: 2026/08/21
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