Human Ciliary Neurotrophic Factor,CNTF ELISA Kit
- Known as:
- Human Ciliary Neurotrophic Factor,CNTF Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-1203
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Ciliary Neurotrophic Factor CNTF ELISA Kit
Related genes to: Human Ciliary Neurotrophic Factor,CNTF ELISA Kit
- 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: Human Ciliary Neurotrophic Factor,CNTF ELISA Kit
Related articles to: Human Ciliary Neurotrophic Factor,CNTF ELISA Kit
- Myocardial ischemia (MI) remains a major clinical challenge, and the therapeutic potential of electroacupuncture (EA) is constrained in practice by repeated needle insertion, poor repeatability of acupoint localization, and limited long-term patient compliance. To overcome these barriers, we developed a minimally invasive implantable electroacupuncture (IEA) system based on carbon nanotube fiber (CNTF) electrodes via a minimally invasive, ultrasound-guided procedure to establish a "single-implantation, long-term stimulation" strategy, delivering both sustained mild stimulation and conventional electroacupuncture at the Neiguan (PC6) acupoint. Results demonstrated that CNTFs with a diameter of 20-30 μm, a conductivity of (2.64 ± 0.95) × 10⁵ S/m, a charge storage capacity of 13.09 ± 2.79 mC/cm², and an impedance of 133.48 ± 69.88 Ω at 1 kHz represented the balanced trade-off for performance. Within the 14-day observation period, CNTF implantation at PC6 did not induce obvious local inflammatory infiltration or pathological tissue alterations. In a rat model of isoproterenol-induced MI, the IEA system markedly improved cardiac electrophysiology attenuated cardiac remodeling and reduced serum cTnT levels demonstrating superior therapeutic effects compared with conventional EA. Kinetic analysis of electrophysiological data revealed that daily IEA facilitated faster effect accumulation and consolidation, favoring acute- or subacute-phase management, whereas alternate-day IEA achieved a higher therapeutic ceiling, suggesting its superiority for maximizing long-term functional recovery. These results provided a rationale for session-frequency-personalized therapy. Furthermore, the cardioprotective effect was mediated through the downregulation of the FXR/SHP apoptotic pathway, validated by pharmacological inhibition. This work established a safe, effective, and stable platform that merged advanced bioelectronic materials with traditional acupuncture theory, providing a promising translational solution for the chronic, home-based rehabilitation of heart disease or other diseases, particular for elderly, paralyzed, or those with limited mobility and access to clinical care. - Source: PubMed
Publication date: 2026/06/10
Fu QixuanNing SiminYu AotianLiu QingGuo YuhangHe JialingLi MengZhou JiulongXiao YeliWang YunjuanShang YuanyuanCao AnyuanLiu Cun-ZhiLiu BaoyanXu Wenjing - Neurodegenerative diseases of the retina result from diverse insults, including genetic mutations, metabolic deficiencies, vascular compromise, and inflammatory injury. These processes converge on dysfunction of the neurovascular unit, where neurons, glia, and vascular cells cooperate to maintain retinal health. Thus, neuroprotection must be considered in a broader context that incorporates support of glial and vascular elements in addition to neurons. In this chapter, we review both classical and emerging neuroprotective strategies in retinal disease. We summarize preclinical and clinical studies of trophic factor-based approaches, including ciliary neurotrophic factor (CNTF), brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3), fibroblast growth factor 2 (FGF2), insulin-like growth factor-1 (IGF-1), and transforming growth factor-β (TGF-β), outlining mechanisms, efficacy, limitations, and safety. We also highlight nonclassical agents such as mesencephalic astrocyte-derived neurotrophic factor (MANF) and the lipid mediator erucamide, which act through distinct pathways to modulate stress responses and neurovascular stability. Additional approaches, including stem cell-based therapies, extracellular vesicles, metabolic supplementation, and lifestyle interventions, are discussed. Finally, we emphasize the importance of human-derived models such as retinal explants and organoids to overcome translational barriers. Collectively, these studies suggest that multimodal strategies may offer meaningful neuroprotection and preserve vision in progressive retinal disease. - Source: PubMed
Wei GuoqinPham HelenaRandall-Jarrard EmmaEade KevinFriedlander Martin - In the adult mammalian central nervous system (CNS), failure of axon regeneration limits recovery after traumatic injury or in neurodegenerative disease. Local protein translation has been implicated in the regulation of axon growth in highly compartmentalized neurons. 3' untranslated regions (3'UTRs) of mRNAs play critical roles in RNA localization and modification. Here we studied the regulation of 3'UTRs in growth cone and axon regeneration. - Source: PubMed
Publication date: 2026/05/29
Bian MinjuanHuie Emma LXia XinNahmou MichaelMaxfield Savana ALi LiangLiu LiangLuo ZimingTsien ChristinaHealzer Katherine JChang Heather VRussano KristinaGoldberg Jeffrey L - To find the pathways of neuropathic pain after brachial plexus avulsion injury, we screen out key molecules or related signal pathways. Serum samples were collected from 20 patients with brachial plexus injury (BPI) and 10 healthy controls. A BPI rat model was constructed, divided into control, sham, and operated groups. Subtype injuries (upper, lower, complete avulsion) were further modeled. Protein profiles were analyzed using Raybiotech GSH-INF-3 and AAH-NEU-2 antibody microarrays. In clinical samples, 5 cytokines (MMP-3, CNTF, GM-CSF, IL-18, TGF-β) were differentially expressed between BPI patients and healthy controls, among which IL-18, CRP, and GM-CSF were elevated in the pain group compared to the painless group. In rats, serum cytokines showed no significant differences; however, nerve tissue analysis revealed increased levels of IL-6, IL-13, MCP-1, and TNF-α in the operated BPI group compared to the sham group. Histological and immunohistochemical analyses showed progressively severe nerve degeneration and inflammatory responses in upper, lower, and complete injury models. There were signal pathways related to autoimmune diseases screened out, such as IL-17 signaling pathway, inflammatory bowel disease, and Th1 and Th2 cell differentiation. This study suggests that cytokines may affect neuropathic pain in inflammatory pathway and neuroimmune pathway. - Source: PubMed
Publication date: 2026/05/11
Tu ZhehuiQin BengangGu Liqiang - : Inherited retinal diseases (IRDs) represent a genetically heterogeneous group of disorders caused by mutations in over 280 genes with more than 3100 identified variants. While gene-specific replacement therapies have achieved landmark success with voretigene neparvovec (Luxturna) for biallelic -associated retinal dystrophy, developing individual therapies for each genetic subtype remains impractical. This review examines gene-agnostic therapeutic approaches utilizing neuroprotection and immunomodulation that target common pathophysiological mechanisms shared across multiple IRD genotypes. : We reviewed the literature on neuroprotective and immunomodulatory gene therapy strategies for IRDs, focusing on neurotrophic factors and complement system modulation. : Neuroprotective approaches delivering neurotrophic factors-including pigment epithelium-derived factor (PEDF), ciliary neurotrophic factor (CNTF), rod-derived cone viability factor (RdCVF), brain-derived neurotrophic factor (BDNF), fibroblast growth factors (FGFs), glial cell line-derived neurotrophic factor (GDNF), and proinsulin-have demonstrated photoreceptor preservation across multiple preclinical IRD models regardless of the underlying genetic mutation. The recent FDA approval of CNTF cell-based gene therapy (Encelto) for macular telangiectasia type 2 validates this therapeutic paradigm. Complement system inhibition represents another gene-agnostic strategy, with intravitreal complement inhibitors approved for geographic atrophy secondary to age-related macular degeneration and gene therapy approaches targeting C3, C5, or delivering soluble complement regulators under investigation for IRDs. Combination strategies simultaneously addressing multiple pathogenic pathways may offer synergistic benefits. : Gene-agnostic approaches targeting neuroprotection and immunomodulation offer a therapeutic paradigm capable of benefiting patients across the spectrum of IRD genotypes, potentially transforming treatment for conditions where mutation-specific therapies remain unavailable. - Source: PubMed
Publication date: 2026/03/30
Rowe Lucas WBecerra S PatriciaMacLaren Robert EAvery Robert LWykoff Charles CHo Allen CRegillo Carl DEliott DeanOsborne AndrewBinley Katie MCiulla Thomas A