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)
- 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 - Metastatic castration-resistant prostate cancer (mCRPC) remains a lethal disease state with limited durable responses to existing therapies, including taxane-based chemotherapy. Resistance mechanisms are multifactorial and incompletely addressed by current treatments. Drug repurposing offers an accelerated pathway for the development of novel therapeutic strategies in treatment-resistant disease. - Source: PubMed
Publication date: 2026/08/06
Souza Luciano OPapoutsi Despoina GMoreira José M A - Next-generation HER2-targeted therapies including tyrosine kinase inhibitors (TKIs) and antibody-drug conjugates (ADCs) improve survival of HER2-positive cancer patients. However, mechanisms of primary and acquired resistance remain unclear. Here, we reported that primary HER2-specific targeted therapy (tucatinib) resistant or sensitive breast cancers derived from clinical trial patients exhibited differential protein profiles. Prolonged tucatinib exposure induced autophagy pathway enrichment in HER2-positive breast cancer cells. Integrated high-throughput analyses identified A-kinase anchoring protein (AKAP)13 as a critical molecule involved in both primary and acquired resistance and an independent predictor of poor prognosis. Silencing of AKAP13 significantly diminished novel HER2-targeted therapies resistance. Mechanistically, AKAP13 inhibits autophagosome formation by suppressing the expression of ULK1, a kinase essential for autophagy initiation. ULK1 transcription is driven by GLI1, which binds to the ULK1 promoter via its arginine-592 residue. We further elucidated that the RhoGEF domain of AKAP13 activates RhoA, which subsequently triggers the activation of PKA anchored to AKAP13. The activated PKA then inhibits the nuclear translocation of GLI1, thereby repressing its transcriptional activity on ULK1. In vivo and in vitro experiments demonstrated the synergistic efficacy of tucatinib and AKAP13 inhibitor A13. In the validation phase, organoids were constructed using tissue obtained via puncture from patients resistant to trastuzumab deruxtecan, confirming upregulation of AKAP13 and A13-mediated reversal of resistance to novel HER2-targeted therapies. Collectively, these findings highlight the role of AKAP13 in drug resistance and propose A13 as a promising therapeutic strategy for HER2-positive breast cancer. Model diagram of this study and proposed molecular mechanisms. - Source: PubMed
Publication date: 2026/08/06
Guo QingChen XinyuWu LinfengRen ChanghaoJian YourongLin MingxiJin YiziZeng ChengZhou TengYan YuxinRuan YuanyuanZhang Jian - Hedgehog (HH) signaling plays a complex role in epithelial-stromal interactions, but its effects on gastrointestinal stem cells mediated by heterogeneous stromal cell populations remain incompletely defined. Here, we investigate how stromal HH signaling regulates gastric stem cells and tumorigenesis in a segment-specific manner. - Source: PubMed
Publication date: 2026/08/05
Li PingChe ManjuDeng QiGuo RuiFeng LiuchunLiu HuijuanWu QiangWang ZhengtingLi Baojie