| Storage |
2 - 8 ℃ |
| Background |
Klotho is a transmembrane protein that, in addition to other effects, provides some control over the sensitivity of the organism to insulin and appears to be involved in aging. Its discovery was documented in 1997 by Kuro-o et al. The name of the gene comes from Klotho or Clotho, one of the Moirai, or Fates, in Greek mythology. The Klotho protein is a novel β-glucuronidase (EC number 3.2.1.31) capable of hydrolyzing steroid β-glucuronides. Genetic variants in KLOTHO have been associated with human aging, and Klotho protein has been shown to be a circulating factor detectable in serum that declines with age.
The binding of certain fibroblast growth factors (FGF's) viz., FGF19, FGF20, and FGF23, to their fibroblast growth factor receptors, is promoted via their interactions as co-receptors with β-Klotho. Klotho-deficient mice manifest a syndrome resembling accelerated human aging and display extensive and accelerated arteriosclerosis. Additionally, they exhibit impaired endothelium dependent vasodilation and impaired angiogenesis, suggesting that Klotho protein may protect the cardiovascular system through endothelium-derived NO production.
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| Alternate Names |
klotho, klotho alpha |
| Assay Type |
Sandwich ELISA |
| Kit Type |
Colorimetric |
| Assay Time |
4.5 hours |
| Sample Type |
serum, plasma |
| Assay Range |
62.5 - 4000 pg/ml |
| Sensitivity |
27.3 pg/ml |
| Specificity |
native and recombinant Klotho protein |
| Recovery |
95.3 - 109% |
| Precision |
Inter assay: 9.3%, Intra-assay: 6.5% |
| Sample Volume |
100 µl |
| Dilution Factors |
undiluted for normal serum |
| Gene ID |
9365 |
| Clinical indications |
α-klotho can suppress oxidative stress and inflammation, thereby reducing endothelial dysfunction and atherosclerosis. Blood plasma α-klotho is increased by aerobic exercise, thereby reducing endothelial dysfunction.
β-klotho activation of FGF21 protein has a protective effect on heart muscle cells. Obesity is characterized by FGF21 resistance, believed to be caused by the inhibition of β-klotho by the inflammatory cell signalling protein (cytokine) tumor necrosis factor alpha.
Klotho is required for oligodendrocyte maturation, myelin integrity, and can protect neurons from toxic effects. Mice deficient in klotho have a reduced number of synapses and cognitive deficits, whereas mice overexpressing klotho have enhanced learning and memory.
It has been found that the decreased klotho expression may be due to DNA hypermethylation, which may have been induced by the overexpression of DNMT3a. Klotho may be a reliable gene for early detection of methylation changes in oral tissues, and can be used as a target for therapeutic modification in oral cancer during the early stages.
Klotho-deficient mice manifest a syndrome resembling accelerated human ageing and display extensive and accelerated arteriosclerosis. Additionally, they exhibit impaired endothelium dependent vasodilation and impaired angiogenesis, suggesting that klotho protein may protect the cardiovascular system through endothelium-derived NO production.
Klotho could play a protective role in Alzheimer's Disease patients
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