GLI2 antibody - middle region (ARP31885_T100)
- Known as:
- GLI2 (anti-) - middle region (ARP31885_T100)
- Catalog number:
- arp31885_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GLI2 antibody - middle region (ARP31885_T100)
Ask about this productRelated genes to: GLI2 antibody - middle region (ARP31885_T100)
- Gene:
- GLI2 NIH gene
- Name:
- GLI family zinc finger 2
- Previous symbol:
- -
- Synonyms:
- THP2, HPE9, THP1
- Chromosome:
- 2q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2016-10-05
Related products to: GLI2 antibody - middle region (ARP31885_T100)
Related articles to: GLI2 antibody - middle region (ARP31885_T100)
- - Source: PubMed
Publication date: 2026/04/23
Wang ZheYang ZeChen YongZhao XiaojingGao DengfengWang NancyWilliams Albert - Glaucoma, a leading global cause of blindness, is characterized by progressive retinal neuronal loss. NOP2/Sun RNA methyltransferase 4 (NSUN4), a writer of 5-methylcytosine (m5C) RNA modifications, has established roles in methylation and mitoribosome assembly, yet its function in retinal cell survival remains unexplored. In this study, integrated methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-seq analysis in an NMDA-induced retinal injury model revealed widespread mRNA hypomethylation enriched in the Sonic Hedgehog (SHH) signaling pathway, accompanied by significant downregulation of Nsun4. To investigate the underlying mechanisms, we utilized the R28 retinal cell line, a widely accepted model for studying retinal neuroprotection. In glutamate-stimulated R28 cells, NSUN4 overexpression mitigated excitotoxic injury, attenuating Ca² ⁺ overload, mitochondrial dysfunction, and apoptosis. Mechanistically, NSUN4 enhanced m5C methylation on key SHH pathway transcripts (Shh, Gli1, and Gli2). Crucially, the neuroprotective effect of NSUN4 was abolished upon pharmacological inhibition of the SHH pathway using Vismodegib, confirming that pathway activation is essential for NSUN4-mediated protection. Clinically, NSUN4 levels were significantly reduced in the aqueous humor of patients with primary open-angle glaucoma compared to controls. Together, these findings establish NSUN4 as an m5C-dependent activator of the SHH pathway that protects retinal cells against excitotoxic injury, nominating it as a novel candidate for glaucoma neuroprotection. - Source: PubMed
Publication date: 2026/04/15
Li YahongLi DianGeng ChaoWei RuihuaDuan Yajian - Eccrine porocarcinoma (EPC), a rare malignant eccrine gland tumour, remains molecularly understudied. Transcriptomic studies of EPC and benign eccrine poroma (EP) have identified recurrent fusions and expression changes, but differences distinguishing malignant EPC from benign EP are unclear. RNA was extracted from formalin-fixed, paraffin-embedded (FFPE) samples (13 EPCs and 49 EPs) from Helsinki Biobank and Finnish Clinical Biobank Tampere. RNA sequencing characterized transcriptomic profiles. Histopathological features were assessed on haematoxylin-eosin-stained sections, and fusion genes were evaluated by NUT and YAP1 immunohistochemistry. EPCs and EPs clustered into two transcriptomic groups regardless of tumour subtype, primarily distinguished by differential expression of genes involved in skin metabolism. The metabolism-high group showed higher expression of genes associated with immune-related processes, mesothelin, and Ras-MAPK signalling. The metabolism-low group contained a subgroup enriched for Hedgehog pathway-associated genes, such as GLI1, GLI2, HHIP, LRP2, and PTCH2. All samples with the YAP1-NUTM1 fusion pattern belonged to the metabolism-low group and showed elevated NUTM1 expression in the heatmap. RNA sequencing revealed transcriptomic subgroups in EPC/EP partly linked to fusions. The results underscore the necessity for further investigation into the disrupted signalling pathways, which may facilitate the development of targeted therapies. - Source: PubMed
Puttonen MayaKilpinen Samivon Willebrand MariaOjala KalleBöhling TomKoljonen VirveSihto Harri - Esophageal squamous cell carcinoma (ESCA) constitutes a major global health burden, with immune evasion and therapeutic resistance posing significant challenges. This study aims to elucidate the molecular mechanisms underlying ESCA immune escape and resistance to neoadjuvant therapy, focusing on the role of ADAMDEC1 in regulating the tumor microenvironment (TME) and immune evasion. - Source: PubMed
Publication date: 2026/04/07
Cheng JiweiMa HaiboQian XinXing Wenqun - Well-differentiated and dedifferentiated liposarcoma (WDLPS and DDLPS) exhibit markedly different clinical behaviors, with DDLPS showing greater aggressiveness, higher recurrence and metastasis rates, and worse outcomes. Using single-nucleus multiome sequencing, epigenomic profiling, and spatial transcriptomics, we characterized cellular and epigenetic heterogeneity between these subtypes at single-cell and spatial resolution. We found distinct phenotypic states reflecting altered lineage differentiation and plasticity: DDLPS is dominated by early-differentiated progenitor-like cells, sclerotic WDLPS displays broader mesenchymal lineage plasticity, and adipocytic WDLPS contains abundant committed adipocytes. The DDLPS immune microenvironment was dominated by immunosuppressive macrophages, whereas WDLPS harbored more T cells and inflammatory macrophages. Notably, sclerotic WDLPS displayed intermediate cellular and molecular features, suggesting it may represent a distinct WDLPS subtype. Importantly, we identified novel gene regulatory circuits underlying each state, including FABP4/PPARG programs in adipocytic WDLPS, GLI2/TCF7L2/RBPJ/KLF7 programs in sclerotic WDLPS, and KLF7/FOSL2/SP3/GLI2/RBPJ programs in DDLPS. H3K27ac-marked enhancers were enriched near adipocytic marker genes in WDLPS and mesenchymal markers in DDLPS. Together, these findings reveal the cellular heterogeneity of tumor and immune compartments across liposarcoma subtypes and identify regulatory programs driving their differentiation states. - Source: PubMed
Publication date: 2026/03/25
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