CNTFR
- Known as:
- CNTFR
- Catalog number:
- Y213623
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CNTFR
Related genes to: CNTFR
- Gene:
- CNTFR NIH gene
- Name:
- ciliary neurotrophic factor receptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-22
- Date modifiied:
- 2016-10-05
Related products to: CNTFR
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- Cholestatic liver disease (CLD) is characterized by disrupted bile acid (BA) homeostasis and excessive accumulation of toxic bile acids in the liver. While both genetic and acquired factors are known to contribute to its pathogenesis, the full spectrum of underlying pathological mechanisms remains incompletely understood, and treatment options are limited. Cardiotrophin-like cytokine factor 1 (CLCF1), a CNTFR ligand, plays a pivotal role in energy metabolic homeostasis, yet its role in cholestasis remains unclear. Here, we show that hepatic CLCF1 expression is markedly upregulated in cholestatic patients and mouse models (all mice used in this study were male). Hepatocyte-specific Cntfr deletion exacerbates DDC-induced cholestasis and fibrosis, whereas AAV-mediated hepatic Clcf1 overexpression attenuates cholestatic liver injury and fibrosis in both Abcb4 knockout (Mdr2) and DDC-fed mice. Mechanistically, CLCF1 suppresses BA synthesis enzymes independently of hepatic FXR-SHP signaling, and selectively enriches FXR-agonistic BAs (e.g., LCA) in the gut, activating the intestinal FXR-FGF15 axis. Gut-restricted FXR antagonism partially reverses CLCF1-mediated hepatoprotection, underscoring the gut-liver axis as a critical effector. Furthermore, CLCF1 remodels the microbiota to favor Firmicutes, enhancing BA excretion. Altogether, our data demonstrate that CLCF1 mitigates CLD through suppressing BA synthesis and enhancing BA excretion. CLCF1 may represent a promising therapeutic avenue for cholestasis. - Source: PubMed
Publication date: 2026/03/16
Liu ManSu YingxiHu YujieShen MengBao SurigugeGong YanqingJi YinglanWang LingfeiZhang YujieWang XiaoyiYang HuiChang YongshengZhou Lu - Esophageal squamous cell carcinoma (ESCA) represents a prevalent, highly aggressive malignancy of the digestive tract. Notably, both its proliferation and metastatic dissemination are facilitated by the tumor microenvironment (TME). One intriguing option for non-invasive biomarkers has been found to be miRNA. MicroRNA-21-5P is an essential regulator of biological processes such as the growth, migration, invasion, and metastasis of some malignancies. The prediction software successfully identified CNTFR as the putative target gene for miR-21-5P. To confirm this interaction, a luciferase reporter gene test was conducted to assess the binding of miR-21-5P to CNTFR. By using quantitative polymerase chain reaction (RT-qPCR), in comparison to normally adjacent tissues, the tumor tissues of patients with ESCA exhibited elevated relative expression amounts of miR-21-5P and decreased relative expression amounts of CNTFR. Furthermore, miR-21-5P mimics were able to drastically lower the CNTFR gene level, as demonstrated by RT-qPCR and western blot. On the other hand, esophageal cancer cells' expression of CNTFR can be markedly elevated by miR-21-5P inhibitors. Within the context of this research, the association between miR-21-5p and CNTFR was established through bioinformatics, luciferase reporter gene, CCK-8, EdU, transwell, flow cytometry, qRT-PCR, and WB analysis. In summary, our work identifies the miR-21-5p suppresses CNTFR expression to promote ESCA cell proliferation, invasion, and migration; these findings highlight the miR-21-5p/CNTFR axis as a promising candidate for non-invasive diagnostic biomarker development and targeted therapeutic strategy optimization in ESCA. - Source: PubMed
Publication date: 2026/02/12
Deng YuhanCui YixiaoWu ZhenhuaZhu YiWusiman ShabahaitiXu KemingLuo ChangqiSun Xiaohong - Cardiotrophin-like cytokine factor 1 (CLCF1) is an essential gene that shows exceptional sequence conservation among vertebrates. CLCF1 loss-of-function mutations cause Crisponi/cold-induced sweating syndrome-2, a disorder with severe and complex phenotypes, underscoring the non-redundant roles of CLCF1. Initially identified as a member of the interleukin-6 (IL-6) cytokine family with activity in neurons and immune cells, CLCF1 is now recognized for broader roles in thermoregulation, glomerular function, myelopoiesis, oncogenesis, and muscle fitness. Despite growing interest in the multifaceted biology of CLCF1, the mechanisms regulating its transcription, translation, secretion, receptor binding, and signaling remain incompletely understood. This review integrates data from multiple open databases and functional studies to outline the current state of knowledge regarding CLCF1 regulatory landscape, receptor interactions, and downstream signaling. It also highlights recent discoveries about the CLCF1 interactome and intracellular functions and underlines its emerging potential as a therapeutic target. - Source: PubMed
Publication date: 2026/02/07
Rousseau MarineCôté FranceChemtob SylvainGauchat Jean-FrançoisPasquin SarahLesage Sylvie - Dilated cardiomyopathy (DCM) is a severe form of cardiomyopathy. The study aims to investigate the impact of metabolic and lifestyle factors on DCM and to identify new potential therapeutic targets. - Source: PubMed
Publication date: 2025/12/30
Wang HuiWang YihuiHuang DezhiJiang XiaoLi CaiyunXia XutingLiu GuichunShi JianchenLi Xinhui - - Source: PubMed
Publication date: 2025/12/02
Kovács PatrikBrazda PeterHajdú TiborHarsányi BoglárkaJuhász KrisztiánTakács RolandVágó JuditWang ZhangzhengCoveney ClareBoocock David JMatta Csaba