ArticleFrontiers in genetics2012
Population-Based Resequencing of LIPG and ZNF202 Genes in Subjects with Extreme HDL Levels.
Article in Frontiers in genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Identification and functional characterisation of DNA methylation differences between East- and West-originating Finns.Epigenetics · 2024Article
- Endothelial lipase variant T111I does not alter inhibition by angiopoietin-like proteins.Scientific reports · 2024Article
- HDL Cholesterol Metabolism and the Risk of CHD: New Insights from Human Genetics.Current cardiology reports · 2017Review
- Monogenic causes of elevated HDL cholesterol and implications for development of new therapeutics.Clinical lipidology · 2013Article
- Genetic and structure-function studies of missense mutations in human endothelial lipase.PloS one · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial lipase (LIPG) and zinc finger protein 202 (ZNF202) are two pivotal genes in high density lipoprotein (HDL metabolism). We sought to determine their genetic contribution to variation in HDL-cholesterol levels by comprehensive resequencing of both genes in 235 individuals with high or low HDL-C levels. The selected subjects were 141 Whites (High HDL Group: n = 68, [Formula: see text] Low HDL Group: n = 73, [Formula: see text]) and 94 Hispanics (High HDL Group: n = 46, [Formula: see text] Low HDL Group: n = 48, [Formula: see text]). We identified a total of 185 and 122 sequence variants in LIPG and ZNF202, respectively. We found only two missense variants in LIPG (T111I and N396S) and two in ZNF202 (A154V and K259E). In both genes, there were several variants unique to either the low or high HDL group. For LIPG, the proportion of unique variants differed between the high and low HDL groups in both Whites (p = 0.022) and Hispanics (p = 0.017), but for ZNF202 this difference was observed only in Hispanics (p = 0.021). We also identified a common haplotype in ZNF202 among Whites that was significantly associated with the high HDL group (p = 0.013). These findings provide insights into the genetics of LIPG and ZNF202, and suggest that sequence variants occurring with high frequency in non-exonic regions may play a prominent role in modulating HDL-C levels in the general population.
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