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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- Cervical squamous cell carcinoma (CESC) is frequently complicated by cisplatin (CDDP) resistance, which is a primary cause of treatment failure and poor prognosis. Here, we identified a CLCF1-ZIC5-CNTFR feedback loop that contributes to CDDP resistance in CESC. We found that ZIC5 was significantly upregulated in CDDP-resistant CESC and correlated with worse overall survival. Functionally, ZIC5 promoted CDDP resistance, in part by enhancing properties associated with cancer stem cells (CSCs) through the transcriptional activation of CNTFR. CLCF1, the ligand for CNTFR, was found to induce ZIC5 expression via STAT3 signaling, thereby forming a CLCF1-ZIC5-CNTFR positive feedback loop. Targeting CNTFR with a neutralizing antibody disrupted this regulatory circuit, leading to a reversal of CDDP resistance and suppression of CSC-associated phenotypes in vitro. Furthermore, combining an anti-CNTFR antibody with CDDP resulted in enhanced antitumor effects in patient-derived xenograft (PDX) and organoid (PDO) models. In summary, our findings suggest that the CLCF1-ZIC5-CNTFR positive feedback loop promotes CDDP resistance in CESC, potentially by sustaining CSC properties. Targeting this pathway, particularly CNTFR, may represent a potential therapeutic strategy for patients with CDDP-resistant CESC. - Source: PubMed
Publication date: 2026/07/25
Jia QinggeLi MingyangLiu JinXu TianqiXu JunpengYuan YuanSui FangYang Xinyuan - Steroid-induced osteonecrosis of the femoral head (SONFH) is the most prevalent type of non-traumatic femoral head necrosis. Exosomes (Exo) secreted from stem cells of human exfoliated deciduous teeth (SHED) play crucial roles in biological processes, particularly in tissue regeneration and repair. Previous studies have demonstrated that exosomes from SHED (SHED-Exo) can alleviate dexamethasone (Dex)-induced osteogenic inhibition in bone marrow mesenchymal stem cells (BMSCs). This study aims to further investigate the molecular mechanism by which SHED-Exo rescues BMSCs osteogenic inhibition. Dex-induced BMSCs were used to construct the SONFH model, and SHED-Exo were used for treatment. Differentially expressed miRNAs (DE miRNAs) were identified by miRNA-seq and miRNA target genes were predicted using the database. Regulation was assessed by transfection of miRNA inhibitor and mimics. Alizarin red staining was used to verify osteogenic differentiation capacity, while qPCR and western blotting were employed to analyze osteogenesis-related proteins (OCN, OPN, and RUNX2), EFNA1, and PI3K/AKT pathways. Modulation using PI3K/AKT inhibitors and EFNA1 small interfering RNAs (siRNA) was performed to probe the molecular mechanism of SHED-Exo therapy. miRNA-seq results identified miR-708-5p as a DE miRNA. qPCR confirmed that its expression was down-regulated after Dex treatment and elevated after SHED-Exo treatment. CNTFR was validated as a miR-708-5p target gene through four database predictions and dual luciferase reporter gene results. Transfection of SHED with miR-708-5p inhibitor and mimics demonstrated that miR-708-5p derived from SHED-Exo negatively regulates CNTFR to promote osteogenesis in BMSCs and increases EFNA1 expression, thereby activating the PI3K/AKT pathway. It was further demonstrated that CNTFR is upstream of EFNA1 and negatively regulates the EFNA1/PI3K/AKT pathway by inhibiting PI3K/AKT and interfering with EFNA1 expression. SHED-Exo carries miR-708-5p into BMSCs, promoting EFNA1 expression by negatively regulating CNTFR, which in turn activates the PI3K/AKT pathway and enhances the osteogenic capacity of BMSCs. - Source: PubMed
Publication date: 2026/07/16
Lv JianBai YuxiMa TianWang XinminXu JieLu YangHou XijunLi JieLiu Fei - Neuroblastoma is characterized by frequent involvement of bone marrow (BM) as a site of cell dissemination and spread. In this study, single-cell RNA sequencing (scRNA-seq) was used to analyze the cellular heterogeneity of a subset of metastatic BM samples collected at initial diagnosis. Comparison of the single-cell data with bulk RNA sequencing further refined the analysis. An enrichment of regulatory T cells relative to a healthy control and activation of the CD24, CD47, and CD200 "don't eat me" signals were documented. Computational analyses highlighted communication between neuroblastoma and myeloid cells via the amyloid precursor protein (APP) and midkine (MK) signaling networks. Within neuroblastoma cells, mutually exclusive adrenergic and transitory cell states were identified, and ten sub-clusters were denoted. In addition, common and unique tumor cell antigens were investigated. CNTFR and CHRNA3, as high-ranking candidates, were validated, confirming their strong selectivity for neuroblastoma cells. Taken together, these findings support the existence of a significant tumor-dependent modulation of the BM ecosystem, which should be considered when introducing immunotherapy. Furthermore, they highlight the potential to investigate new antigens at the single-cell resolution. - Source: PubMed
Publication date: 2026/06/23
Aveic SanjaDavini AlessandroMenegazzo SaraPantile MarcellaZanon CarloCorrà AnnaFaggin GiovanniCorallo DianaPellin DaniloSantoro LuisaFrasson ChiaraZin AngelicaFrancescato SamuelaRossi BartolomeoNeculaescu Ioana AncutaPigazzi MartinaBuldini BarbaraViscardi ElisabettaBiffi Alessandra - Administration of ciliary neurotrophic factor (CNTF) reduces food intake and body weight in both humans and experimental animals, where it also ameliorates hyperglycemia, hyperinsulinemia, and dyslipidemia. To exert its anti-obesogenic and anti-diabetogenic effects, CNTF targets brain feeding centers as well as multiple peripheral organs inducing the phosphorylation of the transcription factor signal transducer and activator of transcription 3 (p-STAT3). However, data showing which peripheral cytotypes are specifically targeted by exogenous CNTF in vivo in metabolically relevant organs are currently lacking. Here, we first evaluated the gene expression levels of the subunits of the tripartite CNTF receptor (Cntfr) complex, that is, the Cntfrα, the leukemia inhibitory factor receptor β (Lifrβ) and the glycoprotein 130 (gp130), by quantitative real-time PCR in metabolically relevant organs of adult male mice: gastrointestinal (GI) tract, pancreas, liver, visceral and subcutaneous white (WAT) and interscapular brown adipose tissue (iBAT), skeletal muscle and the sciatic nerve. We then quantified p-STAT3 by Western blotting in these organs after intraperitoneal administration of CNTF (0.3 mg/kg) or saline. Finally, we mapped CNTF-responsive cells by immunohistochemistry, followed by morphometric quantification and confocal microscopy in both CNTF- and saline-treated mice. Lifrβ and gp130 were ubiquitously detected across all the investigated organs; the Cntfrα showed the highest expression levels in the skeletal muscle, sciatic nerve, and iBAT, whereas it was found to be expressed to a lesser extent in the other sites. Administration of CNTF led to a significant increase of p-STAT3/STAT3 protein ratio in all organs examined, except the duodenum, and induced a distinctive pattern of cell nuclear p-STAT3 immunoreactivity. Notably, along the analyzed GI tract, CNTF induced nuclear STAT3 phosphorylation in neurons of the submucosal and myenteric plexuses of the enteric nervous system and in contractile cells of the muscularis externa, where the response peaked in the mesenteric gut and colon. In the pancreas, CNTF triggered a higher activation within the endocrine component compared to the exocrine parenchyma. In the liver, CNTF induced STAT3 phosphorylation not only in parenchymal cells but also in sinusoids and resident macrophages. The cytokine activated p-STAT3 in subcutaneous and visceral white adipocytes, but also in brown adipocytes, with a prominent response observed in the beige subcutaneous adipocytes; adipose-resident macrophages and endothelial cells of numerous blood vessels were also CNTF-responsive. Lastly, in skeletal muscle, a major site for glucose/lipid utilization, CNTF induced widespread nuclear p-STAT3 immunoreactivity in muscle fibers and in connective and Schwann cells of the peripheral nerves, including the sciatic nerve, supplying the gastrocnemius. In conclusion, our data indicate that CNTF acts across diverse cytotypes within metabolically relevant organs and tissues, likely fostering its peripheral metabolic effects through this cellular heterogeneity. - Source: PubMed
Publication date: 2026/06/25
Galli ChiaraColleluori GeorgiaPerugini JessicaScopini EdoardoSeveri IleniaGrandin GaiaGiordano Antonio - To identify proteomic signatures underlying 3-year progression from impaired fasting glucose (IFG) to diabetes. - Source: PubMed
Rooney Mary REchouffo Tcheugui Justin BChen JingshaWalker Keenan ABallantyne Christie MBoerwinkle EricKelly Tanika NNdumele Chiadi EPankow James SGrams Morgan EPost Wendy SGanz Peter JWood Alexis CRotter Jerome ISelvin ElizabethCoresh Josef