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Study provides evidence for a transmission disequilibrium of allele T of rs2248359 in T2DM family. Maternal derived copy of the variant allele T is the principal risk factor for T2DM offspring. Individuals with CT genotype and T2DM parents may be more likely to suffer from vitamin D deficiency.
rs2248137 CYP24A1 is associated with vitamin D status and multiple sclerosis.
The role of methylation in the regulation of CYP24A1 expression in human colorectal cancer showed that DNA methylation is involved in the regulation of CYP24A1 expression in a cell-dependent manner.
SREBP1 trans-activates CYP24A1 expression through SREBP binding elements present in the promoter.
There was no significant difference in CYP24A1 expression between epileptic patients and normal subjects.
No significant differences were found between ischemic stroke patients and controls in terms of CYP24A1 rs927650 and CYP2R1 rs10741657 genotype frequencies. Polymorphic allele frequencies of CYP24A1 rs927650 and CYP2R1 rs10741657 were 0.414 and 0.660 in stroke patients, respectively.
There were no associations between CYP24A1 polymorphisms and overall cancer risks
colorectal cancer (CRC) patients had a higher frequence of insufficient vitamin D and a higher concentration of active vitamin D. These concentration were higher between patients with polymorphic genotypes variants of ApaI and BsmI, CYP24A1 and CYP27B1. Polymorphic genotypes cause a lower correlation between the forms of vitamin D.
Single nucleotide polymorphisms in CYP24A1 has a statistically significant association with risk of the colonic polyps, colon cancer, and ulcerative colitis in a Chinese population.
The loss of peripheral catabolism of vitamin D metabolites in patients with an inactivating mutation of CYP24A1 is responsible for persistent high levels of 1,25-dihydroxyvitamin D especially after sun exposure and a charge of native vitamin D.
Dietary habits, lifestyle, and polymorphisms in VDR (ApaI), CYP24A1 (rs6013897, rs158552, rs17217119) and CYP27B1 (rs10877012) were associated with a higher risk of colorectal cancer
The local regulation of vitamin D in sinonasal tissue during chronic rhinosinusitis may be independent of serum 25(OH)D levels. Vitamin D may be dysregulated at multiple levels, with decreased transcription of the metabolic gene CYP27B1 and increased transcription of the catabolic gene CYP24A1.
High CYP24A1 expression is associated with Lung Adenocarcinoma.
More recent evidence has identified loss of function mutations in CYP24A1 in association with hypercalcemia, hypercalciuria and nephrolithiasis in humans. [review]
Uremic serum increased the intracellular expression of IL-6, IFN-gamma, TLR7, TLR9, VDR, CYP27b1 and CYP24a1
Biallelic mutations in CYP24A1 or SLC34A1 were associated with infantile idiopathic hypercalcemia with vitamin D hypersensitivity
CYP24A1 association with the susceptibility of esophageal squamous cell carcinoma in a Northern Chinese population.
CYP24A1 was expressed in a >2-fold higher fraction of spermatozoa from normal than infertile men.
Our results indicate that CYP24A1, central in the degradation of the physiologically active 1,25[OH]2D, is important in the association of lower levels of 25[OH]D and increased risk of SLE.
Findings offer direct evidence that Cyp24a1 functions as an oncogene in PTC, where its overexpression activates multiple signaling cascades to promote malignant progression.
CYP24A1 activity is not essential for intramembranous bone formation.
results link CYP24 activity to the pathophysiology of FGF23-dependent renal phosphate wasting states and implicate pharmacologic CYP24 inhibition as a therapeutic adjunct for their treatment.
Gsalpha is required in proximal tubules for suppressing renal vitamin D 24-hydroxylase mRNA levels and for maintaining normal serum 1,25(OH)2D.
Data suggest that control of CYP24A1 increase during diabetes has a beneficial effect on senescence induction and caspase-3 increased expression.
the mechanism through which 1,25(OH)(2)D(3) induces the CYP24A1 enzyme
The expression of vitamin D 24-hydroxylase gene was directly regulated by serum calcium rather than 25-hydroxyvitamin D 1 alpha-hydroxylase.
Ureteral obstruction leads to the alteration of renal vitamin D metabolic enzyme expression and calcium transporter abundance, which may secondarily induce the abnormality of vitamin D endocrine system and bone health.
Results show that Inhibition of 24-OHase activity modulates serum calcitriol PK in normal C3H/HeJ mice.
Cyp24a1 deficiency delays fracture repair and strongly suggest that vitamin D metabolites hydroxylated at position 24, such as 24,25(OH)2D3, play an important role in the mechanisms leading to normal fracture hea
1,25(OH)2D is the preferred substrate for CYP24 in murine kidney mitochondria.
findings demonstrate that regulation of both the 25-hydroxyvitamin D-1 alpha-hydroxylase and 25-hydroxyvitamin D-24-hydroxylase genes by phosphorus is disordered in hypophosphatemic mice at the level of renal mRNA expression
the absence of CYP24A1 or vitamin D receptor retards catabolism of 1alpha,25(OH)2D3 and 25(OH)D3
xenobiotics and drugs can modulate CYP24 gene expression and alter vitamin D(3) hormonal activity and calcium homeostasis through the activation of pregnane X receptor
CYP24A1 can activate and inactivate vitamin D prodrugs in skin and other target cells in vitro
Data show that activation of steroid and xenobiotic receptor does not induce cytochrome P450, family 24 (CYP24)-mediated expression, but inhibits vitamin D receptor-mediated CYP24 promoter activity.
methylation silencing of CYP24 contributes to selective calcitriol-mediated growth inhibition in endothelial cells
Data demonstrate that VDR mediates the anti-proliferative and pro-apoptotic effects of vitamin D metabolites and analogs, but that the potency of a vitamin D compound to induce CYP24 does not accurately predict its potency in mediating growth regulation.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This mitochondrial protein initiates the degradation of 1,25-dihydroxyvitamin D3, the physiologically active form of vitamin D3, by hydroxylation of the side chain. In regulating the level of vitamin D3, this enzyme plays a role in calcium homeostasis and the vitamin D endocrine system. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
1,25-@dihydroxyvitamin D3 24-hydroxylase
, 1,25-dihydroxyvitamin D(3) 24-hydroxylase, mitochondrial
, cytochrome P450 24A1
, cytochrome P450, subfamily XXIV (vitamin D 24-hydroxylase)
, cytochrome P450-CC24
, exo-mitochondrial protein
, vitamin D 24-hydroxylase
, vitamin D(3) 24-hydroxylase
, 25-hydroxyvitamin D-24-hydroxylase
, cytochrome P450, 24
, cytochrome P450, 24a1
, 25-hydroxyvitamin D3 24-hydroxylase
, Cytochrom P450 (25-hydroxyvitamin D24-hydroxylase)
, cytochrome P450, subfamily 24
, 25-hydroxyvitamin D3-24-hydroxylase