CNTF, affinity purified antibody, goat, 100 ug.
- Known as:
- CNTF, antigenic enriched (anti-), caprine, 100 ug.
- Catalog number:
- GT15028-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- CNTF affinity purified antibody goat 100 .
Related genes to: CNTF, affinity purified antibody, goat, 100 ug.
- 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, affinity purified antibody, goat, 100 ug.
Related articles to: CNTF, affinity purified antibody, goat, 100 ug.
- 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 - 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