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
- Transplanted neural precursor cells (NPCs) can support repair after spinal cord injury (SCI) but often face poor survival and limited differentiation within the hostile post-injury microenvironment. We tested whether subacute activation of Sonic hedgehog (Shh) signaling improves NPC engraftment and functional recovery over the duration of 6 weeks. Female Wistar rats underwent T9/T10 clip-contusion SCI and were assigned to vehicle, Shh-only, NPC-only, Shh + NPC, or sham groups ( = 8 per SCI arm, = 5 sham, total = 37). GFP + NPCs (4 × 10) were grafted at 7 days post injury. Recombinant Shh or vehicle was delivered intrathecally via osmotic pumps for 7 days thereafter. Outcome measures included pathway activation (GLI1, SMO), NPC differentiation (NeuN, Olig2, Nestin, GFAP), astrogliosis (GFAP), CSPG deposition, immune cell infiltration (CD3, Iba1), apoptosis (cleaved Caspase-3), and locomotion (BBB, Gridwalk, CatWalk) over 6 weeks. Shh delivery increased GLI1/SMO expression and, when combined with NPCs, significantly elevated NPC-derived neurons and oligodendrocytes while preserving undifferentiated NPCs. Combined therapy reduced astrogliosis, CSPG deposition, T-cell and macrophage/microglial densities, cyst size and apoptotic cells compared with controls. These histological benefits were accompanied by improved locomotor scores in BBB, Gridwalk and selected CatWalk parameters. Our findings highlight the synergistic effects of Shh pathway activation and NPC transplantation in promoting neuroregeneration after SCI. The data support Shh as an adjunct to NPC transplantation for SCI repair. - Source: PubMed
Publication date: 2026/08/04
Tail MohamedZheng GuoliZhang HaoWang HaoHarms Anna-KathrinHatami MaryamSkutella ThomasUnterberg AndreasZweckberger KlausYounsi Alexander - R-CHOP-treated diffuse large B-cell lymphoma (DLBCL) shows heterogeneous outcomes. High-risk relapsed/refractory (R/R) patients, especially activated B-cell (ABC) and double-/triple-hit subtypes, have poor prognosis, highlighting an urgent need to uncover the underlying aggressive molecular mechanisms. Epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties drive its invasion, metastasis, and drug resistance. This study investigated the regulatory role and mechanism of Hedgehog (Hh) pathway key factor GLI1 in DLBCL. Immunohistochemistry detected GLI1, Bmi1, and SOX2 expression in DLBCL tissues. DLBCL cell lines (HBL-1, SUDHL-2) were treated with pan-GLI inhibitor GANT61, or transfected with GLI1 overexpression/silencing plasmids combined with Bmi1 intervention. CCK-8, flow cytometry, RT-qPCR, Western blot, Co-IP, tumor sphere, and immunofluorescence assays were performed. In vivo xenograft experiments were conducted to verify GANT61's anti-tumor effect. GLI1 was aberrantly activated in DLBCL tissues and positively correlated with Bmi1/SOX2. GANT61 inhibited DLBCL cell proliferation, induced G0/G1 arrest and apoptosis, reversed EMT, and reduced CSC-related molecules. Co-IP confirmed GLI1-Bmi1 interaction. GLI1 overexpression enhanced proliferation, EMT, and CSC properties, while GLI1 silencing exerted opposite effects. Bmi1 inhibitor reversed GLI1's pro-tumor effects, and Bmi1 agonist partially restored GLI1 silencing-induced inhibition. In vivo, GANT61 significantly reduced tumor volume/weight in HBL-1 xenografts with good tolerability. GLI1 modulates EMT-like plasticity and stem cell traits in DLBCL via direct protein interaction with Bmi1, confirming a functional regulatory connection between these two molecules that forms the core Hh-GLI1-Bmi1 regulatory pathway. Targeting this axis provides a novel therapeutic strategy for DLBCL. Key words: Hedgehog signaling pathway; Diffuse large B-cell lymphoma (DLBCL); Epithelial-mesenchymal transition (EMT); Cancer stem cell properties; GLI1-Bmi1 axis; GANT61; Xenograft model. - Source: PubMed
Publication date: 2026/07/31
Xiao HuifangLi ChuntuanHan YanGao JingjingXu WenqianXin PengliangZhu Xiongpeng - - Source: PubMed
Publication date: 2026/08/12
Yan XichanYang YinongGuan HaichenZhang XuemeiLi LiYu Penghui - Chronic obstructive pulmonary disease (COPD) ranks among the leading causes of morbidity and mortality globally. Genomic susceptibility factors are acknowledged as critical modulators of disease variability and progression. The Sonic Hedgehog (SHH) pathway regulates epithelial tissue healing, mucin synthesis, and airway remodeling. GLI1 polymorphic variants may influence the manifestations of COPD. - Source: PubMed
Publication date: 2026/08/10
Mahajan NidhiChopra VishalGarg KrantiSharma Siddharth - Docetaxel (DTX) resistance remains a major barrier in metastatic prostate cancer, often driven by ABCB1 efflux and activation of survival pathways. We investigated the therapeutic impact of itraconazole (ITZ), a multifunctional antifungal agent with activity against Hedgehog/GLI signalling and ABCB1 efflux, in DTX-resistant prostate cancer xenograft models (PC3 and DU145). Tumour growth was analysed longitudinally, metastatic burden assessed by hCD44-positive micrometastasis enumeration, and pharmacodynamic responses evaluated through Ki-67 indexes, necrotic fractions, and Gli1 expression. Neither DTX alone, ITZ alone, nor their combination reduced primary tumour growth or cumulative tumour burden. However, the combination suppressed development of lung micrometastases in both models. ITZ and DTX + ITZ reduced Ki-67 and Gli1 levels, demonstrating inhibition of proliferation and Hedgehog signalling despite the absence of tumour shrinkage. ITZ monotherapy was well tolerated, whereas DTX-containing regimens produced expected systemic toxicity. These results indicate antimetastatic and pathway-modulating activity of ITZ in resistant prostate cancer and support its further evaluation as a rational adjunct to taxanes in treatment contexts where metastatic control is a key therapeutic objective. - Source: PubMed
Publication date: 2026/08/07
Souza Luciano OBartels AnnetteMoreira José M A