AMELX
- Known as:
- AMELX
- Catalog number:
- 001520A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMELX
Related genes to: AMELX
- Gene:
- AMELX NIH gene
- Name:
- amelogenin X-linked
- Previous symbol:
- AMG, AIH1
- Synonyms:
- -
- Chromosome:
- Xp22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2018-04-26
Related products to: AMELX
Related articles to: AMELX
- This study aimed to explore whether zona-associated residual sperm may contribute to exogenous contamination and cause sex bias in PCR-based sex classification of ovine early-stage embryos, based on the amplification of the gene. Primers targeting the conserved regions of the ovine and genes were designed, and a nested PCR system using AMEL and genes was established. Group A comprised 17 female and 33 male embryos, corresponding to a female-to-male ratio of 0.52:1, whereas Group B comprised 23 female and 27 male embryos, corresponding to a female-to-male ratio of 0.85:1. DAPI staining revealed sperm-morphology structures or structures containing sperm-derived DNA adjacent to the zona pellucida of ovine early-stage embryos. Sequence alignment of PCR amplicons showed consistency with the and reference genes. In conclusion, these results support our research hypothesis that zona-associated residual sperm may serve as a potential source of contamination and interfere with PCR-based embryonic sex determination. - Source: PubMed
Publication date: 2026/09/14
Ma QiangqiangChen YingDong HongWang LiqinFu XuefengAbudureyimu GulimireZhang JiaxinZhang WeiTian JinboWu YangshengLin Jiapeng - Amelogenesis imperfecta (AI) is a group of rare, inherited disorders characterized by abnormal enamel formation. While identifying the genes and mutations that cause the disease is important, understanding its molecular pathogenesis is essential to developing precision and personalized medicine, which aim to stop disease onset, slow its progression, and provide a range of treatment options. Previously, we identified mutations that affect the conserved alternative splicing of the gene, leading to the inclusion of normally skipped exon 4 and resulting in a characteristic AI phenotype. - Source: PubMed
Publication date: 2026/07/01
Cho Eui-SicKim Youn JungSeymen FigenKoruyucu MineHu Jan C-CSimmer James PKim Jung-Wook - Enamel, the outermost mineralized tissue of the tooth, is produced by specialized dental epithelial cells called ameloblasts. Unlike human enamel, which lacks regenerative capacity, the mouse incisor grows throughout life, driven by adult stem cells residing in the labial cervical loop (LaCl). To maintain tissue homeostasis, dental epithelial stem cells produce transit-amplifying cells (TACs) that commit to preameloblasts (PABs), migrate distally, and differentiate into enamel-forming ameloblasts. The full dental epithelial differentiation trajectory coexists within a single mouse incisor, making it an accessible model for studying adult tissue repair and regeneration. We have shown that the genome organizer SATB1 is enriched in PABs and is required for their differentiation into ameloblasts. Here, we investigated the injury response of PABs following mouse incisor tip trimming. Injured wild-type (wt) incisors exhibited an expanded PAB zone with intensive proliferation, reduced SATB1 in the ameloblast lineage, associated with a spatial delay in the deposition of the dentin/enamel matrix compared to uninjured controls. Trimming of Satb1 cKO mouse incisor failed to elicit this response, highlighting SATB1's role in PAB's response to injury. Compared with wt controls, injured wt incisors and both Satb1 cKO groups showed increased Ki67 immunoreactivity in LaCl mesenchymal and epithelial compartments, along with reduced Col1a1 expression in PAB microenvironment. In vitro, SATB1-transduced ameloblast lineage cells (ALCs) cultured on increasing concentrations of type I collagen exhibited reduced Ki67 but elevated Amelx/Ambn expression. There findings indicate that SATB1 is required for epithelial TACs to exit the cell cycle and transition toward PABs. Incisor tip injury delays PAB differentiation by stimulating LaCL mesenchymal proliferation and altering ECM remodeling within the PAB niche. - Source: PubMed
Publication date: 2026/08/14
Campbell AlexiaLin KevinNgu JakeAhlstrand Cierra RoseKohwi-Shigematsu TerumiZhang Yan - Autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI; OMIM#130900) is a hereditary enamel defect caused by truncation mutations in FAM83H, though the underlying pathogenic mechanisms remain incompletely understood. This study aimed to identify novel FAM83H mutations in a Chinese family with ADHCAI and to investigate their functional consequences on enamel formation. - Source: PubMed
Wang YueChen HongfeiLai JiyongHuang XueqingHuang Yanyu - Autism Spectrum Disorder (ASD) screening requires multimodal biomarkers to capture the heterogeneous neurological and behavioral phenotypes. Current screening approaches remain siloed across EEG analysis and conversational assessment, limiting integrated diagnostic architecture. Privacy-preserving machine learning frameworks for mental health screening are underdeveloped, particularly for multilingual deployment contexts. This paper presents NeuroCon-AutismNet, a candidate multimodal architecture integrating diffusion-regularized EEG synthesis, multilingual conversational screening, and formal differential privacy as architectural proof-of-concept. No diagnostic discrimination capability is claimed; all validation is scoped to synthetic evaluation. - Source: PubMed
Publication date: 2026/07/24
Revathy JM KarthigaYogarayan SumendraBalusamy Balamurugan