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Single nucleotide polymorphisms in the AMELX and AMBN genes may be genetic variants that contribute to developmental defects of enamel in primary dentition of Polish children.
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the calcium level was associated with genetic variations in AMELX, AMNB and ESRRB. AMELX and AMNB are involved in enamel mineralization. Mutations in both these genes are responsible for the amelogenesis imperfecta phenotype (OMIN), which supports their link with enamel alterations as well as enamel mineralization.
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these results indicate that AMBN enhances IL-1beta production in LPS-treated U937 cells through ERK1/2 phosphorylation and caspase-1 activation, suggesting that AMBN upregulates the inflammatory response in human macrophages and plays an important role in innate immunity.
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Association between caries experience (caries-free versus caries affected) depending on asthma status and SNPs was tested. Logistic regression showed an association between AMBN rs4694075 and caries experience. Ameloblastin is associated w/caries in asthmatic children.
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Protein interaction between Ambn and Psma3 can facilitate redistribution of ameloblastin domains within forming enamel.
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Authors perform an evolutionary analysis of mammalian AMBN sequences in order to predict functionally important sites of the protein and to identify candidate disease-associated mutations responsible for the protein function and identify AMBN as a candidate for amelogenesis imperfect in humans.
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Report shows for the first time that AMBN mutations cause non-syndromic human amelogenesis imperfecta and confirms that mouse models with disrupted Ambn function are valid.
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two genetic variants (rs2337359 upstream of TUFT1 and missense rs7439186 in AMBN) involved in gene-by-fluoride interactions.
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We found a trend for association between variation in AMBN and MIH in both cohorts, which may suggest that variation in the regulation of AMBN is a mechanism that leads to MIH.
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AMBN ribbons exhibited lengths ranging from tens to hundreds of nm. Deletion analysis and NMR spectroscopy revealed that N-terminal segment encoded by exon 5 comprises two short independently structured regions and plays a role in self-assembly of AMBN
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AMBN does not influence osteogenic activity in vitro under the conditions used
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Findings suggest a role for this protein in early bone formation and repair.
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ameloblastin is expressed in osteoblasts and functions as a promoting factor for osteogenic differentiation via a novel pathway through the interaction between CD63 and integrin beta1
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found to induce, directly and indirectly, signal transducer and activator of transcription (STAT) 1 and 2 and downstream factors in the interferon pathway
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The identification of a fibronectin-binding domain in ameloblastin might permit interesting applications for dental implantology.
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The frequently detected AMBN alterations in ameloblastomas are polymorphisms, which appear to be unrelated to the occurrence of ameloblastomas.
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a bipolar calcium-binding molecule [with] a possible role in protein-protein interactions
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Mutation of ameloblastin gene is associated with calcifying epithelial odontogenic tumor.
