Human Polyclonal GLI1 Ab
- Known as:
- Human Polyclonal GLI1 Antibody
- Catalog number:
- a8387
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal GLI1
Related genes to: Human Polyclonal GLI1 Ab
- 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: Human Polyclonal GLI1 Ab
Related articles to: Human Polyclonal GLI1 Ab
- Genetic variants near Hedgehog interacting protein () have been consistently associated with increased risk for chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide. However, 's role in COPD pathogenesis remains elusive. Canonically, HHIP is a negative regulator of the Hedgehog pathway and downstream and activation. The Hedgehog pathway plays an important role in wound healing, specifically in activating transcription factors that drive the epithelial-mesenchymal transition (EMT), which in its intermediate state (partial EMT) is necessary for the collective movement of cells closing a wound. Herein, we use a systems biology approach to propose a mechanism to explain HHIP's role in faulty epithelial wound healing, which could contribute to the development of emphysema, a key feature of COPD. Using two different Boolean models, we show dysfunctional HHIP results in a lack of negative feedback on GLI, triggering a full EMT, where cells become mesenchymal and do not properly close the wound. We validate these Boolean models with experimental evidence gathered from published scientific literature. Finally, we show evidence supporting our hypothesis in single-cell and single-nucleus RNA-Seq data from different COPD cohorts and heterozygous knockout mice. Overall, our analyses suggest that aberrant wound healing due to dysfunctional HHIP, combined with chronic epithelial damage through cigarette smoke exposure, may be a primary cause of COPD-associated emphysema. - Source: PubMed
Publication date: 2026/05/26
Deritei DávidAnamika Wardatul JannatZhou Anny XiaoboYun Jeong HSauler MaorCho Michael HSilverman Edwin KRavasz Regan ErzsébetGlass Kimberly - DNAJC9, an HSP40 family member with histone chaperone function, exhibits unclear roles in cervical cancer. DNAJC9 is specifically overexpressed in malignant cervical cancer cells, and downregulation of DNAJC9 inhibits proliferation, induces G1/S arrest, and suppresses tumorigenicity. GLI1 has been identified as a key downstream effector of DNAJC9, and GLI1 rescue reverses proliferation defects. Mechanistically, DNAJC9 promotes the p300-H3 interaction to sustain H3K27ac at the GLI1 enhancer and facilitate GLI1 transcription, driving proliferation. Furthermore, DNAJC9 expression correlates positively with GLI1 in clinical specimens, suggesting that the DNAJC9-GLI1 axis is a potential prognostic marker and therapeutic target. - Source: PubMed
Publication date: 2026/05/25
Xie ZhongyiDi LongjiangHe XingkaiHuang MingzhuQian JinqinYang HuiChen JiayiLu XiaopengZhu Wei-Guo - 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