ArticleLaboratory animal research2022
Loss-of-function mutation in Pcsk1 increases serum APOA1 level and LCAT activity in mice.
Article in Laboratory animal research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Rare Presentation of Heterozygous PCSK1 Deficiency in an Adolescent Male.Case reports in pediatrics · 2026Article
- An optimized luciferin formulation for NanoLuc-based in vivo bioluminescence imaging.Scientific reports · 2025Article
- Functionally characterizing obesity-susceptibility genes using CRISPR/Cas9, in vivo imaging and deep learning.Scientific reports · 2025Article
- Specific circulating miRNAs are associated with plasma lipids in a healthy American cohort.Physiological genomics · 2024Article
- Association ofGenes · 2023Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
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Abstract
backgroundThe convertase subtilisin/kexin family 1 gene (PCSK1) has been associated in various human genetics studies with a wide spectrum of metabolic phenotypes, including early-onset obesity, hyperphagia, diabetes insipidus, and others. Despite the evident influence of PCSK1 on obesity and the known functions of other PCSKs in lipid metabolism, the role of PCSK1 specifically in lipid and cholesterol metabolism remains unclear. This study evaluated the effect of loss of PCSK1 function on high-density lipoprotein (HDL) metabolism in mice.
resultsHDL cholesterol, apolipoprotein A1 (APOA1) levels in serum and liver, and the activities of two enzymes (lecithin-cholesterol acyltransferase, LCAT and phospholipid transfer protein, PLTP) were evaluated in 8-week-old mice with a non-synonymous single nucleotide mutation leading to an amino acid substitution in PCSK1, which results in a loss of protein's function. Mutant mice had similar serum HDL cholesterol concentration but increased levels of serum total and mature APOA1, and LCAT activity in comparison to controls.
conclusionsThis study presents the first evaluation of the role of PCSK1 in HDL metabolism using a loss-of-function mutant mouse model. Further investigations will be needed to determine the underlying molecular mechanism.
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