Source:http://linkedlifedata.com/resource/pubmed/id/11434507
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2001-7-3
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| pubmed:abstractText |
Uteroglobin (UG) is an anti-inflammatory/immunomodulatory protein. Targeted disruption of UG rendered mouse glomerulonephritis resembling immunoglobulin (Ig)A nephropathy (IgAN). Sequence analysis on exon 1 of UG showed several putative binding sites for transcription factors, and polymorphisms in this site might influence the expression level of UG as a competitive protein. We speculated that the single nucleotide polymorphism at the 38th nucleotide (A to G) from the transcription initiation site of UG exon 1 would impact the progression of IgA nephropathy (IgAN). Polymerase chain reaction-restriction fragment length polymorphism and single-strand conformation polymorphism were instituted to determine the genetic polymorphism. Luciferase assay was performed using the gene constructs containing a region 404-bp long located upstream of UG exon 1 initiation site to analyse whether this polymorphism would affect the expression level. UG polymorphism was distributed no differently in patients with IgAN (n = 111) compared to 60 healthy control subjects. An excess of A genotype was found in one patient having progressive disease (P = 0.03) and the risk for the disease progression increased as the number of A alleles increased (P for trend = 0.03) after follow-up for 116 months. The odds ratio for progression with the AA genotype was 4.9 (95% Cl = 1.0-23.9) compared to patients having the GG genotype. Significant interactive effects of hypertension and genetic polymorphisms of UG on the disease progression were observed (P for interaction = 0.001). In the luciferase assay, the gene construct with A at the 38th site showed a decreased activity of 74 +/- 8.4% compared to that showed by G gene construct. Our results suggest that polymorphism at the 5' UTR region of UG exon 1 is an important marker for the progression of IgAN and may modulate the level of protein expression.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
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| pubmed:issn |
0960-314X
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
11
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
299-305
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11434507-5' Untranslated Regions,
pubmed-meshheading:11434507-Adult,
pubmed-meshheading:11434507-Animals,
pubmed-meshheading:11434507-Base Sequence,
pubmed-meshheading:11434507-Case-Control Studies,
pubmed-meshheading:11434507-DNA,
pubmed-meshheading:11434507-Exons,
pubmed-meshheading:11434507-Gene Expression,
pubmed-meshheading:11434507-Gene Frequency,
pubmed-meshheading:11434507-Genetic Markers,
pubmed-meshheading:11434507-Genotype,
pubmed-meshheading:11434507-Glomerulonephritis, IGA,
pubmed-meshheading:11434507-Humans,
pubmed-meshheading:11434507-Kidney Failure, Chronic,
pubmed-meshheading:11434507-Mice,
pubmed-meshheading:11434507-Middle Aged,
pubmed-meshheading:11434507-Molecular Sequence Data,
pubmed-meshheading:11434507-Polymorphism, Genetic,
pubmed-meshheading:11434507-Polymorphism, Restriction Fragment Length,
pubmed-meshheading:11434507-Polymorphism, Single Nucleotide,
pubmed-meshheading:11434507-Polymorphism, Single-Stranded Conformational,
pubmed-meshheading:11434507-Prognosis,
pubmed-meshheading:11434507-Risk Factors,
pubmed-meshheading:11434507-Uteroglobin
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| pubmed:year |
2001
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| pubmed:articleTitle |
Uteroglobin gene polymorphisms affect the progression of immunoglobulin A nephropathy by modulating the level of uteroglobin expression.
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| pubmed:affiliation |
Department of Internal Medicine, Seoul National University College of Medicine, Clinical Research Institute Seoul National University Hospital, Chongno-gu, South Korea.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|