Zinc Finger Protein GLI1 antibody
- Known as:
- Zinc Finger Protein GLI1 (anti-)
- Catalog number:
- orb109412
- Product Quantity:
- 10 Miniblots
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Zinc Finger Protein GLI1 antibody
Related genes to: Zinc Finger Protein 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: Zinc Finger Protein GLI1 antibody
Related articles to: Zinc Finger Protein GLI1 antibody
- We investigated the role of GLI3, a transcription factor highly expressed in the pathogenic THY1CD34 sublining subset of rheumatoid arthritis synovial fibroblasts (RASFs), in regulating their pathogenic behavior. - Source: PubMed
Sato MotohikoSaito TetsuyaKomiya YojiNoda SeijiTagawa YasuhiroYamamoto AkioIwai HideyukiEndo KentaroKoga HideyukiTakahara YasuhiroSugimoto KazutakaSekiya IchiroKawakami EiryoHosoya TadashiYasuda Shinsuke - Primary cilia are increasingly recognized as regulators of cellular signaling and plasticity. Here, we examined their distribution and potential relevance in neuroendocrine (NE) prostate cancer. While typically absent in localized hormone-sensitive prostate tumor cells, we detected primary cilia in neuroendocrine-like cells both and in castration-resistant prostate cancer (CRPC) samples. , cilia were consistently observed in CRPC tumor cells exhibiting FDG-PET positivity and NE features, supporting an association between ciliogenesis, metabolic reprogramming, and disease progression. These aggressive tumors also displayed reduced mitochondrial activity, consistent with a shift away from oxidative metabolism. Building on our work in ccRCC, we identified a GLI1⁺/IFT20⁺ or GLI1⁺/IFT80⁺ signature enriched in ciliated, NE-prone subpopulations. , YAP1 inhibition alone did not induce ciliogenesis, whereas cytoskeletal remodeling with jasplakinolide restored cilium assembly and enabled partial NE transdifferentiation. Single-cell RNA-seq analyses further showed enrichment of ciliogenesis-related genes within NE clusters in CRPC. Together, these observations support a model in which primary cilia are closely associated with NE identity and metabolic adaptation, rather than serving solely as passive markers, and suggest a structural-metabolic axis that may represent a source of biomarkers and therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/05/18
Guo YingboPeng SiyongJamet ThibaudFirlej VirginieIrondelle MarieNau ConstanceGirard Christophe AAsrani KaushalLotan Tamara LHuc RomainSoyeux PascaleRouleau MatthieuLacas-Gervais SandraRovini AmandineLuciano SamanthaHumbert OlivierSchiappa RenaudPujalte-Martin MarcVigneau MathieuPeraldi PascalBost FrédéricLazennec GwendalVacherot FrancisMazure Nathalie M - Hepatocellular carcinoma (HCC) is a lethal malignancy driven by cancer stem cells, which drive progression and therapeutic resistance. Nuclear pore protein ELYS is implicated in tumorigenesis, but its role in HCC stemness remains unclear. - Source: PubMed
Publication date: 2026/06/02
Chen XinZhang QingXie FenZhai HuilanLi ChuanhongZhou WeifengZhang Nuobei - Sweat gland development requires tightly coordinated signaling between multiple gene regulatory networks; however, the timing control of these pathways during postnatal maturation remains poorly defined. X-linked hypohidrotic ectodermal dysplasia (XLHED), caused by pathogenic variants of the ectodysplasin A gene (EDA), exemplifies the clinical consequences of disrupted sweat gland development. In this study, we investigated the postnatal expression dynamics of wingless (WNT), EDA, and sonic hedgehog (SHH) signaling during murine sweat gland maturation. By using immunohistochemical analysis of ventral paw skin from wild-type and Eda-deficient Tabby mice, we demonstrate that phospho-LRP6 (representing the WNT pathway), EDA, and SHH are simultaneously active within a narrowly defined time slot between postnatal day 1 and day 5, corresponding to ductal extension and early secretory maturation of the sweat gland. Disruption of EDA signaling was associated with markedly reduced postnatal WNT activity, suggesting reciprocal regulatory interactions rather than a strictly linear signaling hierarchy. Notably, postnatal SHH activity was accompanied by Gli2, but not Gli1, indicating a gene-specific hedgehog transcriptional program during sweat gland maturation. These findings identify a critical postnatal signaling window and provide insight into why postnatal EDA administration failed to restore sweat gland development in XLHED patients. - Source: PubMed
Publication date: 2026/06/01
Dernai JuleMaier-Wohlfart SigrunPeschel NicolaiDaniel ChristophSchneider HolmPark Jung - Cardiac fibroblast (CF) activation in response to injury or inflammation is a central driver of pathological cardiac fibrosis, contributing to arrhythmias and heart failure. As previously demonstrated, intermittent hypoxia (IH), the hallmark pathophysiological feature of obstructive sleep apnoea (OSA), induces cardiac fibrosis. However, the mechanisms by which IH promotes CF activation and the key molecular mediators involved remain unclear. - Source: PubMed
Publication date: 2026/06/01
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