Gli1
- Known as:
- Gli1
- Catalog number:
- 044524A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Gli1
Related genes to: Gli1
- 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
Related articles to: Gli1
- GLI1-altered soft tissue tumor is a recently recognized entity featuring GLI1 fusions or amplifications, with predilection for the head and neck region and potential for metastasis. We report an additional case arising in the tongue of a 9-year-old boy with growth hormone insufficiency and epilepsy. Imaging showed an enhancing midline dorsal tongue lesion. Incisional biopsy revealed a multilobulated submucosal proliferation of monomorphic epithelioid-to-ovoid cells with prominent perivascular distribution around branching vessels and focal protrusion into vascular spaces. Tumor cells were GLUT-1 positive and negative for S100, GFAP, pan-cytokeratin, SMA, WT-1, CD31, CD34, STAT6, β-catenin, and HMB-45, with Ki-67 nuclear staining of 10-15% of cells. Next Generation Sequencing of the tumor confirmed ACTB::GLI1 fusion. In light of his neurodevelopmental disorders, further genetic evaluation was performed revealing SHOX deletion within PAR1 with complex Y-chromosomal rearrangement. Although GLI1-altered neoplasms have a distinctive morphology, lack of defining immunophenotype makes molecular confirmation of GLI1-altered soft tissue tumors essential in most cases. These tumors are low-grade sarcomas which are treated with complete local excision and long-term follow-up. - Source: PubMed
Publication date: 2026/05/20
Alshagroud Rana SAlrabiah Reem MAlRasheed Rasha SAldawsari Bader MKoutlas Ioannis G - Autism spectrum disorder (ASD) is a neurodevelopmental disorder marked by repetitive behaviors and difficulties in social interaction and communication. The pathogenesis of ASD remains poorly understood, and no definitive treatment is currently available. This study aimed to systematically identify key genes and signaling pathways involved in autistic-like behaviors by performing genome-wide transcriptional profiling on a neonatal maternal separation (NMS) rat model, thereby revealing the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/28
Zhang QingMa JinhuaXu BoqingLi XiaohuanDai ChunfangZhu LiqiongDing Xiaoting - Cranial sutures are essential for skull growth and tissue homeostasis. Among them, the coronal suture is most frequently affected in syndromic craniosynostosis, yet the mechanisms underlying this preferential involvement remain unclear. Here, we show that the coronal suture mesenchyme undergoes a postnatal lineage transition from mesodermal to cranial neural crest origin, facilitated by dural cell migration into the suture. Mechanistically, this migration is regulated by suture TGFβ signals to Tgfbr2+ dural cells. Loss of dural Tgfbr2 impairs this cell migration into the suture, reduces the Gli1+ suture progenitor pool, and causes premature coronal suture fusion. Furthermore, in Twist1 mice recapitulating human Saethre-Chotzen syndrome, upregulated decorin leads to compromised TGFβ signaling, which impairs dural cell migration, leading to craniosynostosis. Significantly, restoring TGFβ signaling rescues coronal suture patency in Twist1 mice. These findings identify the critical role of TGFβ-mediated dural-suture interactions, particularly dural cell migration, in maintaining coronal suture patency and provide an explanation for the preferential coronal fusion in syndromic craniosynostosis. - Source: PubMed
Publication date: 2026/05/19
Chen PengMeng LinLan LinFeng JifanGuo TingweiGao LuHekmat HanaLy CalistaZhang MingyiCha SaHo Thach-VuChai Yang - Adenomyosis (ADM) is a benign condition associated with various gynecological disorders. However, effective treatment options are limited, highlighting the urgent need for novel therapeutic targets. This study identified abnormal activation of Hedgehog signaling pathway in tamoxifen-induced ADM mice. Inhibition of Hedgehog pathway by GANT61, a Glioma-associated oncogene 1/2 (Gli1/Gli2) inhibitor, significantly reduced the expression of Sonic Hedgehog signaling-related proteins. Ishikawa cells were treated with GANT61 to investigate the effect of Hedgehog signaling pathway inhibition on cell proliferation, migration, and invasion. The expression levels of related proteins were assessed by western blot. Cell phenotype experiments, including colony formation assay, 5-Ethynyl-2'-Deoxyuridine (EdU) assay, wound healing assay, and Transwell assay, were conducted. To validate the in vivo results, an adenomyosis mouse model was established and treated with GANT61. Western blot and immunohistochemistry were performed to measure the expression levels of key proteins. We demonstrated that Hedgehog signaling pathway specifically the Sonic Hedgehog signaling pathway (Shh) is abnormally active in adenomyosis and that GANT61 inhibited Shh signaling pathway, leading to a downregulation of Hedgehog pathway-related proteins and a reduction in cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) both in vivo and in vitro. These findings underscore the pivotal role of Shh signaling pathway in adenomyosis pathogenesis and demonstrate that its inhibition by GANT61 effectively mitigates disease-associated histopathological progression in a mouse model. This study uncovers a novel pathological mechanism and proposes a promising therapeutic strategy for adenomyosis. - Source: PubMed
Publication date: 2026/05/16
Lin ZaifanYan SimiaoRan QingzhenYang QianxinLin HaixinSun JingtongChen YiZhong XiuchiTian YingzhouChen Wanqun - Fuzheng Huayu formula (FZHY) is clinically used for liver fibrosis treatment, but its pharmacological mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/05/12
Hu YonghongZhang ZhengLiang YueTang EnqiWang BibiLiu WeiMu YongpingChen GaofengLiu PingChen Jiamei