Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We have recently reported that the human apolipoprotein A-I (apoA-I) and apolipoprotein C-III (apoC-III) genes are physically linked and that the presence of a DNA insertion in the apoA-I gene is correlated with apoA-I-apoC-III deficiency in patients with premature atherosclerosis.
|
2989400 |
1985 |
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
In addition, the presence of a polymorphic restriction endonuclease site (SacI) in the 3' noncoding region of apoC-III mRNA has been correlated with hypertriglyceridemia in humans.
|
2989400 |
1985 |
Premature coronary artery atherosclerosis
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
These findings indicate that the polymorphism in the region between the apolipoprotein A-I and apolipoprotein C-III genes may be a useful marker for the risk of premature coronary artery disease and familial hypoalphalipoproteinemia.
|
3081805 |
1986 |
Hypoalphalipoproteinemia, Familial
|
0.010 |
Biomarker
|
disease |
BEFREE |
These findings indicate that the polymorphism in the region between the apolipoprotein A-I and apolipoprotein C-III genes may be a useful marker for the risk of premature coronary artery disease and familial hypoalphalipoproteinemia.
|
3081805 |
1986 |
Premature coronary artery atherosclerosis
|
0.020 |
Biomarker
|
phenotype |
BEFREE |
Finally, restriction mapping analysis of DNA from a patient with combined APOA1-APOC3 deficiency and premature coronary artery disease indicated that this patient has a structurally normal APOA4 gene.
|
3095836 |
1986 |
Arteriosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results indicate that absence of transcripts with correct apoAI and apoCIII mRNA sequences causes apoAI and apoCIII deficiency in the plasma of these patients and suggest that these apolipoproteins are involved in cholesterol homeostasis and protection against premature atherosclerosis.
|
3118360 |
1987 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results indicate that absence of transcripts with correct apoAI and apoCIII mRNA sequences causes apoAI and apoCIII deficiency in the plasma of these patients and suggest that these apolipoproteins are involved in cholesterol homeostasis and protection against premature atherosclerosis.
|
3118360 |
1987 |
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A DNA polymorphism of the apolipoprotein C-III gene in extracoronary atherosclerosis.
|
3345637 |
1988 |
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A DNA polymorphism of the apolipoprotein C-III gene in extracoronary atherosclerosis.
|
3345637 |
1988 |
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
DNA polymorphisms in the apolipoprotein C-III and insulin genes and atherosclerosis.
|
3911967 |
1985 |
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
DNA polymorphisms in the apolipoprotein C-III and insulin genes and atherosclerosis.
|
3911967 |
1985 |
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We have recently isolated and characterized the human apo A-I gene and have shown that apo A-I and apolipoprotein C-III (apo C-III) genes are physically linked and that a polymorphism (of unknown frequency in the general population) of the apo A-I gene is inherited as a mendelian trait linked to premature atherosclerosis in an affected family (not the same polymorphism as has previously been reported to be associated with hypertriglyceridaemia).
|
6314145 |
1983 |
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We have recently isolated and characterized the human apo A-I gene and have shown that apo A-I and apolipoprotein C-III (apo C-III) genes are physically linked and that a polymorphism (of unknown frequency in the general population) of the apo A-I gene is inherited as a mendelian trait linked to premature atherosclerosis in an affected family (not the same polymorphism as has previously been reported to be associated with hypertriglyceridaemia).
|
6314145 |
1983 |
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
We have recently isolated and characterized the human apo A-I gene and have shown that apo A-I and apolipoprotein C-III (apo C-III) genes are physically linked and that a polymorphism (of unknown frequency in the general population) of the apo A-I gene is inherited as a mendelian trait linked to premature atherosclerosis in an affected family (not the same polymorphism as has previously been reported to be associated with hypertriglyceridaemia).
|
6314145 |
1983 |
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
The polymorphic sites were the SstI site in the apoCIII 3' untranslated region, whose presence has previously been shown to be associated with hypertriglyceridemia (HTG) in Caucasians, and the MspI site in the third intron of the apoAI gene.
|
7705829 |
1995 |
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Global severity of atherosclerosis at the first angiography was weakly associated with genotypes of the apoCIII-C/T1100 polymorphism, presence of the T1100 allele being associated with 53% lower median score (1.6 vs 0.75; p = 0.09).(ABSTRACT TRUNCATED AT 400 WORDS)
|
7834891 |
1994 |
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Global severity of atherosclerosis at the first angiography was weakly associated with genotypes of the apoCIII-C/T1100 polymorphism, presence of the T1100 allele being associated with 53% lower median score (1.6 vs 0.75; p = 0.09).(ABSTRACT TRUNCATED AT 400 WORDS)
|
7834891 |
1994 |
Hyperlipidemia, Familial Combined
|
0.070 |
GeneticVariation
|
disease |
BEFREE |
By using chemical cleavage mismatch analysis and the single strand conformation polymorphism technique, DNA fragments of the apo CIII gene, including the 5' flanking region and all the exons, were screened for sequence changes underlying the observed association between familial combined hyperlipidaemia (FCHL) and the apo AI-CIII-AIV gene cluster in affected individuals from eight FCHL families.
|
7889654 |
1994 |
Nuchal bleb, familial
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
In FCH the X2 minor allele of the AI-CIII-AIV gene cluster was associated with increased fasting plasma TG, apo CIII, apo AI, and NEFA concentrations and decreased postheparin lipolytic activities.
|
8100834 |
1993 |
Hyperthyroidism
|
0.200 |
Biomarker
|
disease |
RGD |
Role of thyroid hormone in the expression of apolipoprotein A-IV and C-III genes in rat liver.
|
8429259 |
1993 |
Hypothyroidism
|
0.200 |
Biomarker
|
disease |
RGD |
We therefore measured the transcriptional activity of the apoA-IV and apoC-III genes and the abundance of their nuclear RNA and total cellular mRNA in livers of control rats and rats made hyper- and hypothyroid.
|
8429259 |
1993 |
Ataxia Telangiectasia
|
0.010 |
Biomarker
|
disease |
BEFREE |
Among regions with multiple potential candidates is chromosome 11, which includes the apolipoprotein C3 cluster, muscle glycogen phosphorylase, two insulin-dependent diabetes loci, the sulfonylurea receptor, and ataxia telangiectasia.
|
8593945 |
1996 |
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The variant apo CIII promoter is common in the human population and may represent a major contributing factor to the development of hypertriglyceridemia.
|
8675624 |
1995 |
Hypertriglyceridemia
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Polymorphic markers in apolipoprotein C-III gene flanking regions and hypertriglyceridemia.
|
8696957 |
1996 |
Hypertriglyceridemia
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Unlike the human apo CII (HuCII)- and apo CIII (HuCIII)-transgenic mouse models of hypertriglyceridemia, plasma cholesterol was disproportionately elevated (95 +/- 23 vs 73 +/- 23, P = 0.002, fasted and 90 +/- 24 vs 61 +/- 14, P < 0.0001, fed).
|
8698877 |
1996 |