Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several clones containing DMP1 cDNA were isolated from a caiman tooth library by screening with a platypus DMP1 probe. The caiman DMP1 shows little amino acid sequence similarity to mammalian DMP1s for much of its length. A few highly conserved regions can, however, be identified that correspond to the slowly evolving parts of the corresponding mammalian genes. Southern blot analysis using probes comprising either conserved regions or longer segments of the gene indicates that only a single DMP1 locus exists. In coding regions, exon-intron boundaries and reading frames are shared by caiman and mammalian genes with the exception of exons 1 and 5, which are longer in the caiman. The repetitive sequence of the last exon is shared by mammals and caiman as are the high Ser content and acidity due to a high proportion of Asp and Glu residues. The conserved mammalian cell-attachment signal Arg-Gly-Asp is absent in the caiman DMP1. In contrast to the amelogenin gene, the DMP1 gene appears to evolve rapidly in vertebrates.
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PMID:Characterization of dentin matrix protein 1 gene in crocodilia. 1039 3

Dental fluorosis occurs as a result of excess fluoride ingestion during tooth formation. Enamel fluorosis and primary dentin fluorosis can only occur when teeth are forming, and therefore fluoride exposure (as it relates to dental fluorosis) occurs during childhood. In the permanent dentition, this would begin with the lower incisors, which complete mineralization at approximately 2-3 years of age, and end after mineralization of the third molars. The white opaque appearance of fluorosed enamel is caused by a hypomineralized enamel subsurface. With more severe dental fluorosis, pitting and a loss of the enamel surface occurs, leading to secondary staining (appearing as a brown color). Many of the changes caused by fluoride are related to cell/matrix interactions as the teeth are forming. At the early maturation stage, the relative quantity of amelogenin protein is increased in fluorosed enamel in a dose-related manner. This appears to result from a delay in the removal of amelogenins as the enamel matures. In vitro, when fluoride is incorporated into the mineral, more protein binds to the forming mineral, and protein removal by proteinases is delayed. This suggests that altered protein/mineral interactions are in part responsible for retention of amelogenins and the resultant hypomineralization that occurs in fluorosed enamel. Fluoride also appears to enhance mineral precipitation in forming teeth, resulting in hypermineralized bands of enamel, which are then followed by hypomineralized bands. Enhanced mineral precipitation with local increases in matrix acidity may affect maturation stage ameloblast modulation, potentially explaining the dose-related decrease in cycles of ameloblast modulation from ruffle-ended to smooth-ended cells that occur with fluoride exposure in rodents. Specific cellular effects of fluoride have been implicated, but more research is needed to determine which of these changes are relevant to the formation of fluorosed teeth. As further studies are done, we will better understand the mechanisms responsible for dental fluorosis.
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PMID:Chronic fluoride toxicity: dental fluorosis. 2170 Nov 93