ArticleAging cell2019
Noncoding variations in Cyp24a1 gene are associated with Klotho-mediated aging phenotypes in different strains of mice.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 5 citations in OpenAlex.
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- TMEM174 Deficiency Reduces Longevity by Promoting Phosphate-Driven Vascular Calcification.bioRxiv : the preprint server for biology · 2026Article
- Article
- Ezh2-dependent H3K27me3 modification dynamically regulates vitamin D3-dependent epigenetic control of CYP24A1 gene expression in osteoblastic cells.Journal of cellular physiology · 2020Article
- Women in immunology: 2020 and beyond.Nature immunology · 2020Review
- Article
- Phenotypes of Klotho.Aging · 2019Article
- Noncoding variations in Cyp24a1 gene are associated with Klotho-mediated aging phenotypes in different strains of mice.Aging cell · 2019Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
In mutant mice, reduced levels of Klotho promoted high levels of active vitamin D in the serum. Genetic or dietary manipulations that diminished active vitamin D alleviated aging-related phenotypes caused by Klotho down-regulation. The hypomorphic Klotho [kl/kl] allele that decreases Klotho expression in C3H, BALB/c, 129, and C57BL/6 genetic backgrounds substantially increases 1,25(OH)2D3 levels in the sera of susceptible C3H, BALB/c, and 129, but not C57BL/6 mice. This may be attributed to increased basal expression of Cyp24a1 in C57BL/6 mice, which promotes inactivation of 1,25(OH)2D3. Decreased expression of Cyp24a1 in susceptible strains was associated with genetic alterations in noncoding regions of Cyp24a1 gene, which were strongly reminiscent of super-enhancers that regulate gene expression. These observations suggest that higher basal expression of an enzyme required for catabolizing vitamin D renders B6-kl/kl mice less susceptible to changes in Klotho expression, providing a plausible explanation for the lack of aging phenotypes on C57BL/6 strain.
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