GLI1 antibody
- Known as:
- GLI1 (anti-)
- Catalog number:
- orb10718
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- GLI1 antibody
Related 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
- Aberrant activation of the Sonic Hedgehog (SHH)-glioma-associated oncogene 1 (GLI1) signaling pathway is a determinant driver of basal cell carcinoma (BCC) and SHH-subgroup medulloblastoma (MB). Here, we demonstrate the role of S-palmitoylation and depalmitoylation of GLI1 in the regulation of incidence and progression of MB. High expression of acyltransferase ZDHHC13 in MB induces S-palmitoylation of human GLI1 at Cys1034, stabilizes GLI1 by preventing its ubiquitin-dependent proteasomal degradation, and in turn activates this signaling pathway to promote the progression of MB. Conversely, the deacylase ABHD17A depalmitoylates GLI1 at Cys1034, destabilizes GLI1, and in turn inactivates this signaling pathway. As a result, conditional knockout of Zdhhc13 in cerebellar granule neuron precursors (GNPs) significantly alleviates the severity of MB induced by constitutively active Smoothened (Smo-M2) overexpression and markedly extends overall survival, whereas knockout of Abhd17a increases the incidence of MB induced by Patched-1 ablation, rather than its progression. Together, these findings uncover the dynamic regulation of GLI1 palmitoylation and depalmitoylation by the ZDHHC13 and ABHD17A and subsequent GLI1 stabilization and destabilization as a hitherto uncharacterized mechanism controlling SHH/GLI1 signaling and may provide additional targets for therapeutic intervention of MB. - Source: PubMed
Publication date: 2026/06/29
Shen TingyuBao HangyangWang JirongJi XingGu WeizhongTang ChaoHe QiangqiangLuo JiahaoTan DanYao JialiXu ChengyunGong YingWu XimeiZhang Shi-HongZeng Ling-Hui - Desert Hedgehog (Dhh) mutations cause Leydig cell dysfunction, yet the mechanisms governing Leydig lineage commitment through Dhh-mediated receptor selectivity, transcriptional effector specificity, and steroidogenic coupling remain elusive. In this study, using CRISPR/Cas9-mediated gene knockout and stem Leydig cells (SLCs) transplantation, we identified a critical Dhh/Patched 2 (Ptch2)/Glioma-associated oncogene homolog 1 (Gli1)/steroidogenic factor 1 (Sf1) signaling axis essential for SLC differentiation in Nile tilapia (). Dhh deficiency resulted in defective adult Leydig cells and androgen insufficiency. Rescue experiments involving 11-ketotestosterone administration and a Dhh agonist treatment, combined with SLCs transplantation, demonstrated that Dhh regulates SLC differentiation, not survival. In vitro knockout of and in SLCs revealed that Ptch2 likely acts as the functional receptor for Dhh. This was further supported by in vivo genetic rescue experiments, where mutation did not impair testicular development, yet completely rescued the testicular defects in mutants-consistent with Ptch2 acting as an inhibitory receptor whose loss alleviates Dhh pathway suppression. Luciferase assays in Gli-knockout SLCs demonstrated that Gli1 acts as the primary transcriptional effector and transactivates expression. Additionally, functional transplantation assays confirmed that Sf1 is indispensable for SLC differentiation, as Sf1-overexpressing SLCs rescued differentiation, whereas -mutant SLCs failed. Overall, our work delineates the Dhh-Ptch2-Gli1-Sf1 axis and provides fundamental insights into the endocrine regulation of Leydig cell lineage development. - Source: PubMed
Publication date: 2026/06/29
Zhao ChangleChen YongxunLiu LeiLiu XiangXiao HeshengWang FeilongHuang QinDai XiangyanTao WenjingWang DeshouWei Jing - Vismodegib (VDG), a Smoothened inhibitor approved for basal cell carcinoma, has potential for repurposing in other tumors in which Hedgehog (Hh) signaling contributes to malignancy. However, systemic VDG treatment is associated with relevant adverse effects, and its effective delivery to cutaneous targets remains challenging, supporting the exploration of drug delivery systems for its administration. - Source: PubMed
Publication date: 2026/06/05
Calienni Maria NataliaSandoval-Acuña CristianPotomová PetraYbarra David EmanuelTruksa JaroslavMontanari Jorge - Sonic hedgehog (SHH) signaling pathway serves as a critical regulator for embryonic development and tumorigenesis. Medulloblastoma (MB) is one of the most common malignancy in cerebella of pediatric populations, and mutation and aberrant activation of key components in SHH signaling pathway drive the oncogenesis of MB, accompanied by activation of the effector transcription factor GLI1. We have previously uncovered that phosphorylation of human GLI1 on Ser937 controls the oncogenesis of MB. To explore further the post-translational modifications in GLI1, we performed proteomics analysis and found that GLI1 interacted with RING family ubiquitin E3 ligase RNF138. RNF138 directly polyubiquitinated GLI1 on lysine residues K815 and K942 and in turn destabilized GLI1 to inactivate SHH signaling. As a result, low expression of RNF138 in human MB correlated with high GLI1 protein level, whereas overexpression of RNF138 downregulated GLI1 to suppress the growth of human MB Daoy cells xenografts. Taken together, these results uncover GLI1 polyubiquitination by RNF138 as a hitherto uncharacterized mechanism governing SHH signaling and may serve as an additional therapeutic target in SHH-driven malignancies. - Source: PubMed
Publication date: 2026/06/28
Bao HangyangShen TingyuXu YanaLu MeipingWang JirongGu WeizhongHe QiangqiangLuo JiahaoTan DanYao JialiXu ChengyunWu XimeiZhang ShihongZeng Ling-Hui - Diabetes mellitus and cancer represent two major global health burdens. This paper systematically reviews and analyzes recent research advances on the relationship between diabetes and cancer risk, encompassing both epidemiological and molecular mechanism studies. Epidemiological data indicate that the association between diabetes and cancer exhibits significant organ specificity, geographic and population variability, as well as type-specific differences. Diabetes mellitus significantly increases the risk of hepatocellular carcinoma, pancreatic cancer, breast cancer, and colorectal cancer, yet exhibits a unique inverse association with prostate cancer risk. At the molecular level, hyperinsulinemia directly promotes tumor cell proliferation by activating the PI3K/AKT/mTOR and Ras/MAPK/ERK signaling pathways through the insulin/IGF-1 axis. Concurrently, hyperglycemia creates a favorable microenvironment for tumorigenesis by enhancing the Warburg effect, promoting advanced glycation end-product (AGE) accumulation, and inducing oxidative stress and chronic inflammation. Beyond the classical pathways of hyperinsulinemia and hyperglycemia in diabetes, recent research has explored novel directions, including tumor microenvironment remodeling, epigenetics, and immunometabolism. These discoveries encompass emerging mechanisms such as exosomes acting as long-range messengers of systemic metabolic disorders, novel key signaling molecules (e.g., inhibin subunit βB (INHBB) and fibrinogen C domain containing 1 (FIBCD1)), and the remodeling of Schwann cells within the tumor microenvironment. These mechanisms, coupled with potential intervention targets like INHBB, glioma-associated oncogene 1 (Gli-1), FIBCD1, and estrogen-related receptor alpha (ERRα), offer novel clinical approaches for tumor screening, treatment, and prevention. - Source: PubMed
Publication date: 2026/06/26
Huang YuxuanJu ShuhanLi Shanyi