CNTF (27_72) (Human) _ 100ug
- Known as:
- CNTF (27_72) (Human) _ 100ug
- Catalog number:
- 002-93
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Phoenix Peptide
- Gene target:
- CNTF (27_72) (Human) _ 100ug
Related genes to: CNTF (27_72) (Human) _ 100ug
- 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
- Gene:
- TRERF1 NIH gene
- Name:
- transcriptional regulating factor 1
- Previous symbol:
- BCAR2
- Synonyms:
- TReP-132, HSA277276, RAPA, dJ139D8.5
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-26
- Date modifiied:
- 2016-10-05
Related products to: CNTF (27_72) (Human) _ 100ug
Related articles to: CNTF (27_72) (Human) _ 100ug
- 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
- Carbon nanotube fibers (CNTFs) enable real-time dual-stage monitoring of CNT/epoxy nanocomposites via single-step embedding during manufacturing. Although highly sensitive, CNTF responses can be influenced by environmental and processing factors that introduce sensor artifacts and response lag. Here, we quantitatively assess, for the first time, the accuracy of CNTF sensing in multifunctional epoxy nanocomposites. CNTFs were fabricated via the wet-pulling of single-walled CNT (SWCNT) thin films (18, 39, and 59 nm thickness) and embedded in epoxy containing 0.005 and 0.5 wt. % single- and multiwalled CNTs (MWCNTs). Electrical measurements were conducted using 2- and 4-point techniques. CNTFs showed negligible measurement inaccuracy of less than 10% and 10% for MW- and SWCNT nanocomposites, respectively. Owing to their virtually contact-resistance-free behavior, CNTFs achieve 1-2 orders of magnitude higher accuracy than standard surface-applied electrodes. These results establish CNTFs as high-fidelity, low-artefact sensors capable of monitoring multifunctional epoxy nanocomposites better than existing techniques. - Source: PubMed
Publication date: 2026/03/27
Shadrov Sergei PButt Hassaan AVildanova Aliya RAgafonova Ekaterina EDmitrieva Veronika AKondrashov Vladislav AYan YaotianQi JunleiWang ZeyuKrasnikov Dmitry VAkhavan OmidNasibulin Albert G - - Source: PubMed
Publication date: 2026/04/16
Wang YanjieNusinowitz StevenYang Xian-Jie