GLI1 Antibody (OALA06145)
- Known as:
- GLI1 Antibody (OALA06145)
- Catalog number:
- oala06145
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GLI1 Antibody (OALA06145)
Related genes to: GLI1 Antibody (OALA06145)
- 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 (OALA06145)
Related articles to: GLI1 Antibody (OALA06145)
- KRAS mutations are a major driver of pancreatic ductal adenocarcinoma (PDAC). RASA2, a RAS GTPase-activating protein, modulates KRAS protein levels in wild-type contexts, suggesting it could play a potential role in PDAC. Here, we systematically investigated the biological function and molecular mechanisms of RASA2 in PDAC. Integrative analyses of multiple datasets and clinical samples demonstrated that RASA2 was consistently upregulated in KRAS-mutant PDAC and significantly associated with poor prognosis and metastatic progression. Gain- and loss-of-function studies revealed that RASA2 markedly enhanced PDAC cell migration and invasion in both KRAS-mutant and KRAS-wild-type models, suggesting that its pro-metastatic activity is largely independent of KRAS mutational status. Transcriptomic and mechanistic analyses revealed that RASA2 activated GLI1 through a TGFβ2-dependent, non-canonical Hedgehog pathway. Mechanistically, RASA2 interacted with RTF1 to promote H2BK120 ubiquitination at the TGFB2 promoter, thereby enhancing TGFβ2 transcription and activating downstream GLI1 signaling. Pharmacological inhibition of TGFβ signaling or genetic silencing of GLI1 effectively suppressed RASA2-driven migratory, invasive, and metastatic phenotypes in vitro and in vivo. Collectively, these findings reveal a mechanism by which RASA2-dependent epigenetic and transcriptional reprogramming promotes metastatic progression and nominate the RASA2- TGFβ2-GLI1 axis as a potential therapeutic target in PDAC. - Source: PubMed
Publication date: 2026/08/14
He TaochenChen QiangdaAn YanfeiXu ZhihangJiang ZhenlaiHan JiandeXie YuqiLi HanyuPang ChaoyuXu JiayiGan WeiWang HaiboJin YunWang WenquanWang Xu-AnWu WenchuanLou WenhuiYin HanlinPu NingLiu Liang - Plexiform fibromyxoma (PFM) is an uncommon, benign mesenchymal tumor typically arising in the gastric antrum and usually characterized by a multinodular, plexiform growth pattern of smooth muscle actin (SMA)-expressing myofibroblastic-like cells. Rare variants with uninodular architecture and absence of SMA expression pose significant diagnostic challenges, as they may mimic gastrointestinal stromal tumors (GISTs) and require comprehensive histopathologic, immunohistochemical, and molecular evaluation to avoid misdiagnosis and inappropriate therapy. - Source: PubMed
Publication date: 2026/05/18
Jarosch ArminDziodzio TomaszGlobke BrigittaÖllinger RobertSchäfer Frederik MaximilianHauptmann KathrinNiyazova SabinaFlörcken AnneHorst DavidAgaimy AbbasSchallenberg Simon - 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