Ask about this productRelated genes to: CNTF antibody
- 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: CNTF antibody
Related articles to: CNTF antibody
- 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 - 4,4'-Diaminobenzophenone (DABP) is an emerging aromatic amine-benzophenone environmental contaminant with potential neurotoxic risk, while its molecular mechanisms remain insufficiently defined. Using an integrative framework combining network toxicology, machine learning-based target prioritization, molecular docking, in vitro neurotoxicity assays, and transcriptomic-metabolomic profiling, we systematically characterized the neurotoxic effects of DABP. Network analysis revealed prominent perturbations in mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase-protein kinase (PI3K-Akt), calcium signaling, and inflammatory pathways. Machine learning approaches consistently identified ciliary neurotrophic factor (CNTF), endothelin 1 (EDN1), semaphorin 3F (SEMA3F), growth arrest and DNA damage-inducible alpha (GADD45A), and FBJ murine osteosarcoma viral oncogene homolog (FOS) as core drivers of DABP-induced neurotoxicity, with SHapley Additive exPlanations (SHAP) enabling quantitative interpretation of their contributions. Molecular docking supported stable interactions between DABP and these targets. Functionally, DABP exposure induced oxidative stress, mitochondrial dysfunction, lipid peroxidation, intracellular iron accumulation, and ferroptosis-related processes in SH-SY5Y cells, accompanied by sustained neuroinflammatory activation. Integrated transcriptomic and metabolomic analyses revealed coordinated dysregulation of inflammatory signaling, metabolic homeostasis, and synaptic-associated pathways. Collectively, this study establishes a systems-level mechanistic framework for DABP-induced neurotoxicity, providing critical insights for environmental neurotoxicity risk assessment and mechanistic toxicology of aromatic amine pollutants. - Source: PubMed
Publication date: 2026/04/19
Zhu JinchaoChen LinglongLi WenjingLiu YanqingIbrahim NayabDong JinruiFan Haojun - Current therapeutic approaches for Alzheimer's disease (AD) demonstrate limited efficacy and fail to address disease progression. In the present study, we present HSN-G1, a novel ginsenoside-enriched pharmaceutical formulation that employs a dual-target mechanism through the modulation of amyloid clearance pathways and cholinergic neurotransmission. HSN-G1 demonstrates a reproducible ginsenoside profile enriched with Re (33.27 mg/g), Rd (25.00 mg/g), and Rg3 stereoisomers (12.18 mg/g), ensuring pharmaceutical-grade reproducibility. HSN-G1 enhanced amyloid-beta (Aβ) clearance in microglial cells, with significantly greater effects observed in SRA-overexpressing cells, suggesting SRA-dependent clearance mechanisms. In APP/PS1 transgenic mice, six-week oral administration of HSN-G1 (100-400 mg/kg) elicited significant dose-dependent improvements in cognitive performance. Male mice exhibited more stable and consistent enhancements in both passive avoidance and spatial memory tests compared to vehicle controls (p < 0.001), while both sexes demonstrated comparable reductions in brain Aβ levels (approximately 45%) and differential increases in acetylcholine (73% in males; 55% in females, p < 0.01). HSN-G1 administration enhanced the expression of neurotrophic factors, with NGF upregulation predominantly observed in males, whereas BDNF, CNTF, and GDNF were consistently elevated across both sexes. These findings establish HSN-G1 as a promising disease-modifying agent with standardized composition and therapeutic efficacy, surpassing the limitations of conventional single-target approaches. The superior efficacy of HSN-G1 compared to existing treatments validates its potential for clinical development, highlighting the significance of sex-specific therapeutic responses in future AD therapeutics. - Source: PubMed
Publication date: 2026/04/22
Ahn Jeong WonYoon Eun-JungKim Hyun SooChoi YunseoJeong JiwonDamodar KongaraYoo Yeong-MinPark DongsunJoo Seong Soo - - Source: PubMed
Publication date: 2026/04/21