AMTN
- Known as:
- AMTN
- Catalog number:
- 001542A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMTN
Related genes to: AMTN
- Gene:
- AMTN NIH gene
- Name:
- amelotin
- Previous symbol:
- -
- Synonyms:
- UNQ689, RSTI689
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-12-06
- Date modifiied:
- 2014-11-18
Related products to: AMTN
Related articles to: AMTN
- The cocrystal strategy is an effective approach to reducing the sensitivity of high-energy CL-20 while maintaining its superior detonation performance. However, the microscopic mechanism by which guest molecules stabilize the host lattice remains insufficiently understood. Using density functional theory (DFT) and molecular dynamics (MD) simulations, we compare the the geometric structures and electronic properties, SAPT analysis, Hirshfeld surfaces, and radial distribution functions of the CL-20/1-amino-3-methyl-1,2,3-triazolium nitrate (1-AMTN) cocrystal with those of pure CL-20. The results show that 1-AMTN introduction increases the total density of states (DOS), and significantly reduces the band gap from 3.251 eV to 2.222 eV. Although a narrower band gap is generally correlated with higher electronic excitation sensitivity, further SAPT, Hirshfeld surface, and RDF analyses reveal that the cocrystal exhibits strengthened O-H…O hydrogen-bond networks and denser van der Waals contacts. Quantitative Hirshfeld analysis shows that the combined O…H/H…O polar contacts exceed 59% in the cocrystal, accompanied by newly emerged N…H interactions. Energy decomposition indicates that electrostatic and dispersion forces cooperatively dominate the lattice stabilization. Collectively, 1-AMTN enhances the supramolecular non-covalent interactions, providing additional binding energy that likely counterbalances the electronic sensitivity risk, which serves as the microscopic origin of the experimentally observed desensitization. This work elucidates the essential role of guest molecules in cocrystal stabilization and provides theoretical guidance for the rational design of low-sensitivity, high-energy cocrystals. - Source: PubMed
Publication date: 2026/08/12
Simin ZhuHan ZhangZhuqing ZhangKaiqiang HeXinyu Wang - Metabolic stress during enamel development may influence ameloblast differentiation and enamel formation, although the underlying mechanisms remain poorly understood. In this study, we investigated transcriptional and cellular responses to palmitic acid (PA) in the human ameloblast-like cell line HAM3 using a custom quantitative reverse transcription polymerase chain reaction panel based on amelogenesis imperfecta-related genes. PA exposure under both sustained low-dose conditions (50 μM for 24 h) and acute high-dose conditions (500 μM for 4 h) induced coordinated transcriptional changes associated with enamel maturation and cellular stress responses. Expression of the maturation-associated gene AMTN was detectable at baseline and consistently upregulated following PA exposure, whereas that of the epithelial transcription factor gene BCL11B was selectively suppressed under acute high-dose conditions. PA also induced expression of stress-responsive genes including GDF15 and HMOX1. In parallel, immunoblotting demonstrated increased levels of cleaved caspase-3 and LC3-II, while immunofluorescence analysis revealed accumulation of p62-positive structures, consistent with stress-associated apoptosis and altered autophagy-related processes. These findings suggest that PA-induced metabolic stress promotes a stress-associated pseudo-maturation-like transcriptional state in ameloblast-like cells while activating coordinated cellular stress responses. This study provides a potential framework linking metabolic stress environments to altered enamel development. - Source: PubMed
Publication date: 2026/06/30
Nakagawa MimaIwawaki YukiIwata TakeoTanaka EijiYoshida KayaKudo YasuseiMiyoshi KeikoMizusawa Noriko - The expression of gingival junctional epithelium (JE)-associated genes, including amelotin (), odontogenic ameloblast-associated protein (), and follicular dendritic cell-secreted protein (), has been reported to increase during gingival inflammation. However, the associations between the expression levels of JE-associated genes and periodontal clinical parameters remain unclear. This study aimed to investigate this association. - Source: PubMed
Publication date: 2026/04/14
Matsuzaki MisakiOchiai YoshitoMorita TakumiIgarashi KazumaWada MasatomoSaito YumiYamaguchi ArisaYamazaki-Takai MizuhoTakai HidekiOgata YorimasaNakayama Yohei - Ameloblasts are specialized epithelial cells responsible for enamel formation, a process that requires tightly coordinated matrix secretion, proteolytic turnover, and hydroxyapatite crystal growth. Although genetically regulated, amelogenesis is susceptible to environmental modulation by agents such as fluoride and amoxicillin. Calcium and vitamin D supplementation have been proposed as potential protective factors against fluoride-induced enamel alterations. This study investigated whether combined exposure to fluoride and amoxicillin impairs ameloblast viability and enamel formation, and whether vitamin D and calcium supplementation can mitigate these effects. Using a rat incisor model, enamel structure, ameloblast apoptosis, and matrix protein dynamics were evaluated through ultrastructural analysis, histology, immunohistochemistry, TUNEL assay, and proteomic profiling. Fluoride exposure, particularly when combined with amoxicillin, resulted in disorganization of enamel prisms and increased apoptotic activity in ameloblasts, as evidenced by caspase-3 and TUNEL labeling, especially during the early maturation stage. Immunohistochemistry revealed reduced KLK4 levels within ameloblasts, whereas proteomic analysis demonstrated increased KLK4 abundance in the enamel matrix, suggesting altered intracellular trafficking and impaired proteolytic turnover. Additionally, the abundance of AMBN, AMTN, and ODAM, proteins essential for enamel crystal nucleation and maturation, was reduced in treated groups. Vitamin D and calcium supplementation neither significantly restored enamel organization nor normalized matrix protein alterations under the experimental conditions tested. Overall, these results indicate that fluoride exposure, particularly when combined with amoxicillin administration, disrupts ameloblast homeostasis, matrix proteolysis, and enamel prism organization, resulting in structurally compromised enamel, with no beneficial effects from vitamin D and calcium supplementation. - Source: PubMed
Publication date: 2026/05/25
Porto I Mda Silva A A SDos Santos J V ASilva B MGiacomin E Bda Fonseca G SGerlach R F - Amelotin (AMTN), a protein involved in enamel formation, is induced in retinal pigment epithelial (RPE) in patients with dry age-related macular degeneration (AMD) and is associated with calcification in drusen. To examine the effects of constitutive expression of human AMTN in RPE we created a transgenic (TG) mouse model that expresses human AMTN specifically in the RPE using the regulatory components of the mouse Rpe65 gene. This led to several AMD-like abnormalities in RPE but did not produce calcified depositions. Reasoning that other aspects of cell stress or damage may be needed for calcification we tested moderate laser injury of the retina in young TG and WT mice. TG mice, but not WT, developed AMTN-dependent deposits containing AMTN, cholesterol, and calcium phosphate/HAP in the laser lesions, reminiscent of deposits seen in dry AMD drusen. While laser lesions in WT mice healed normally, those in TG mice progressed, obliterating adjacent photoreceptors and recruiting microglia. This shows that chronic expression of AMTN can induce pathologies in RPE and that when coupled with injury can form structures similar to calcified drusen. These deposits are associated with increased retinal damage and inflammation. The model presents a system to test possible therapeutic effects of inhibition or suppression of AMTN in RPE in vivo. - Source: PubMed
Publication date: 2026/05/13
Rajapakse DinushaFan JianguoDaily DannikaDong LijinPeterson KatherineFariss RobertWistow Graeme