Proteins CNTF , Human
- Known as:
- Proteins CNTF , Human
- Catalog number:
- C098
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CNTF Human
Related genes to: Proteins CNTF , Human
- Gene:
- CNTF NIH gene
- Name:
- ciliary neurotrophic factor
- Previous symbol:
- -
- Synonyms:
- HCNTF
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-07
- Date modifiied:
- 2016-10-05
Related products to: Proteins CNTF , Human
Related articles to: Proteins CNTF , Human
- Macular telangiectasia type 2 (MacTel type 2) is a rare, chronic neurodegenerative macular disease that typically occurs bilaterally in the second half of life. Patients report paracentral scotomas and reading difficulties early in the disease course. Over time, limitations in daily life progressively increase. - Source: PubMed
Publication date: 2026/08/27
Jung MalteBucher Felicitas - N-methyl-D-aspartate (NMDA) excitotoxicity drives mitochondrial dysfunction and retinal ganglion cell (RGC) loss in blinding retinal disorders. Ciliary neurotrophic factor (CNTF) is neuroprotective, but its short half-life limits long-term therapy. Here, we investigated whether mitochondrial homeostasis mediates the sustained protection of a CNTF-loaded chitosan hydrogel. In vitro, free CNTF and the hydrogel equally protected RGCs against NMDA, effects completely abolished by the mitochondrial uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). In vivo, free CNTF provided only transient rescue, whereas the hydrogel sustained RGC survival, mitochondrial integrity, and visual function for 28 days, with persistent upregulation of mitochondrial biogenesis genes. Adeno-associated virus-mediated DRP1 overexpression-induced mitochondrial fission fully reversed the hydrogel's benefits, mirroring CCCP inhibition. Collectively, intact mitochondrial homeostasis is essential for the long-term neuroprotection of the CNTF-chitosan hydrogel, which extends CNTF retention without altering its mitochondrial-dependent mechanism. This hydrogel represents a promising long-acting treatment for retinal excitotoxicity. - Source: PubMed
Publication date: 2026/08/12
Jiang HuitingGuo XunhuiBai YuanyuanMa XinyueDuan HongmeiLi XiaoguangYang Zhaoyang - Ciliary neurotrophic factor (CNTF), a pleiotropic cytokine with central and peripheral actions, has been implicated in obesity, insulin resistance, and aging, yet its role in skeletal muscle and cardiometabolic health remains unclear. This study examined skeletal muscle CNTF mRNA expression in relation to adiposity and glucose tolerance in older adults and assessed the effects of six-month weight loss (WL) and aerobic exercise training (AEX) interventions on its expression. Sixty-seven adults (age, 60.75 ± 7.58) underwent a vastus lateralis muscle biopsy, VOmax testing, dual-energy X-ray absorptiometry (DXA) scan, a resting metabolic rate (RMR) and substrate oxidation assessment, and a 3-h oral glucose tolerance test with glucose and insulin area under the curve (AUC) calculation. A subset completed 6 months of either a WL program ( = 21) or a supervised 3 times per week AEX intervention ( = 20). At baseline, skeletal muscle CNTF expression was inversely associated with RMR, fat oxidation, 3-h glucose AUC, and insulin AUC, but not with BMI, percent body fat, or VOmax. WL reduced body weight, fat mass, glucose AUC, insulin AUC, and basal muscle CNTF expression, whereas AEX increased VOmax and reduced fat mass without altering body weight, glucose AUC, insulin AUC, or basal CNTF. Insulin-stimulated CNTF expression increased after both WL and AEX, and the intervention-induced change in glucose disposal (M) was positively associated with the change in insulin-stimulated CNTF. In older adults, skeletal muscle CNTF is associated with glucose intolerance but is not associated with body composition or aerobic fitness. Improvements in insulin sensitivity are associated with increases in muscle CNTF during hyperinsulinemia. Further work is needed to determine the mechanism for muscle CNTF change during hyperinsulinemia after weight loss and exercise training, and its role in glucose metabolism and obesity in older adults. - Source: PubMed
Publication date: 2026/08/21
Ryan Alice SLi GuoyanLynch ColleenJaber Sausan MBigman Galya - Resting myokine abundance cannot distinguish adaptive signaling from compensation, tissue injury, altered receptor availability, or non-muscle contribution. We conducted a targeted narrative review of PubMed/MEDLINE, Embase, Web of Science Core Collection, and Scopus through 30 June 2026 to examine ciliary neurotrophic factor (CNTF), cardiotrophin-like cytokine factor 1 (CLCF1), and muscle metabolism across basal, insulin-stimulated, exercise, recovery, and training states. CNTF has the better-established CNTFRα-LIFR-gp130 receptor model, and pharmacological studies link it to AMPK activation, glucose uptake, ceramide handling, and insulin responsiveness. CLCF1 depends partly on CRLF1-associated extracellular availability, whereas its receptor usage and tissue source in skeletal muscle remain incompletely resolved. One recent study provides important preclinical and exploratory human evidence for exercise-responsive CLCF1, but direct human studies pairing CNTF/CLCF1 kinetics with muscle metabolomics or isotope-resolved flux are lacking. We, therefore, present neurotrophic secretory flexibility as a testable, hypothesis-generating construct rather than a validated biological system or biomarker. Its minimum evaluation requires synchronized measurements of extracellular ligand, receptor-proximal signaling, and metabolic output within the same physiological challenge. Targeted and untargeted metabolomics, lipidomics, quality-controlled annotation, paired tissue and plasma sampling, and stable isotope tracing can determine whether putative coupling is reproducible, muscle-relevant, and altered by aging. - Source: PubMed
Publication date: 2026/08/09
Tong FeiChen YiruiGui HongxinLi AoweiLi HongyuPei YusenWu ZimuWang Mengyang - Ischemic stroke is one of the most prevalent neurological disorders, with primary injury typically localized to the neocortex. However, secondary damage often extends to anatomically distant regions, particularly the hippocampus. One of the early neuroendocrine responses to cerebral ischemia is activation of the hypothalamic-pituitary-adrenal (HPA) axis. Increased release of corticosterone (CORT) by the adrenal glands into the bloodstream leads to its accumulation in the hippocampus. We hypothesize that this process may contribute to the hippocampal damage and underlie delayed cognitive and affective impairments following stroke. To test this, we investigated the levels of neurotrophic factors reflecting the neuroprotective potential of the hippocampus using two established middle cerebral artery occlusion (MCAO) models that differ in their effects on CORT production: the Koizumi et al. (1986) model (MCAO1) and the Longa et al. (1989) model (MCAO2). Although both models produced comparable neurological deficits, mortality rates, and infarct volumes, they differed markedly in endocrine and hippocampal responses. Significant increases in circulating CORT and its accumulation in both ipsilateral and contralateral hippocampus were observed only in MCAO1. Moreover, correlations between the CORT levels (in the blood and hippocampus) and both rat body weight and neurological deficit were stronger in MCAO1 than in MCAO2. In both acute models, brain-derived neurotrophic factor (BDNF) levels were elevated in the ipsilateral hippocampus, whereas the content of glial cell line-derived neurotrophic factor (GDNF) remained unchanged. In contrast, ciliary neurotrophic factor (CNTF) increased in the ipsilateral hippocampus only in MCAO2. These findings suggest that differential activation of the HPA axis and consequent variations in corticosteroid signaling in the hippocampus selectively modulate the neurotrophic response during the acute phase following MCAO. - Source: PubMed
Onufriev Mikhail VMoiseeva Yulia VNovikova Margarita RKostryukov Pavel AGulyaeva Natalia V