Source:http://linkedlifedata.com/resource/pubmed/id/12847143
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
2003-7-8
|
| pubmed:databankReference | |
| pubmed:abstractText |
NFS/N-sld mice harbor a spontaneous autosomal recessive mutation, sld (sublingual gland differentiation arrest) and histologically display attenuated mucous cell expression in sublingual glands (Hayashi et al. Am J Pathol 132: 187-191, 1988). Because altered serous demilune cell expression is unknown, we determined the phenotypic expression of this cell type in mutants. Moreover, we evaluated whether absence of glycoconjugate staining in 3-day-old mutant glands is related to disruption in apomucin gene expression and/or to posttranslational glycosylation events. Serous cell differentiation is unaffected, determined morphologically and by serous cell marker expression (PSP, parotid secretory protein; and Dcpp, demilune cell and parotid protein). Conversely, apical granules in "atypical" exocrine cells of mutant glands are PSP and mucin negative, but contain abundant SMGD (mucous granule marker). Age-related appearance of mucous cells is associated with expression of apomucin gene products, whereas SMGD expression is unaltered. "Atypical" cells thus appear specified to a mucous cell fate but do not synthesize mucin glycoproteins unless selectively induced postnatally, indicating the sld mutation disrupts apomucin transcriptional regulation and/or decreases apomucin mRNA stability.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
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| pubmed:issn |
1531-2267
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
7
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| pubmed:volume |
14
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
95-106
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:12847143-Animals,
pubmed-meshheading:12847143-Cell Differentiation,
pubmed-meshheading:12847143-Female,
pubmed-meshheading:12847143-Gastric Mucins,
pubmed-meshheading:12847143-Gene Expression Regulation,
pubmed-meshheading:12847143-Genes, Recessive,
pubmed-meshheading:12847143-Glycosylation,
pubmed-meshheading:12847143-Male,
pubmed-meshheading:12847143-Mice,
pubmed-meshheading:12847143-Mice, Inbred Strains,
pubmed-meshheading:12847143-Mice, Mutant Strains,
pubmed-meshheading:12847143-Microscopy, Electron,
pubmed-meshheading:12847143-Molecular Sequence Data,
pubmed-meshheading:12847143-Mucous Membrane,
pubmed-meshheading:12847143-Mutagenesis,
pubmed-meshheading:12847143-Protein Processing, Post-Translational,
pubmed-meshheading:12847143-Rabbits,
pubmed-meshheading:12847143-Rats,
pubmed-meshheading:12847143-Sublingual Gland
|
| pubmed:year |
2003
|
| pubmed:articleTitle |
The sld mutation is specific for sublingual salivary mucous cells and disrupts apomucin gene expression.
|
| pubmed:affiliation |
University of Rochester Medical Center, Center for Oral Biology and the Department of Pharmacology and Physiology, Rochester, New York 14642-8611, USA.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|