Ask about this productRelated genes to: CYP24A1 antibody
- Gene:
- CYP24A1 NIH gene
- Name:
- cytochrome P450 family 24 subfamily A member 1
- Previous symbol:
- CYP24
- Synonyms:
- CP24, P450-CC24
- Chromosome:
- 20q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-09
- Date modifiied:
- 2018-02-28
Related products to: CYP24A1 antibody
Related articles to: CYP24A1 antibody
- The R. dybowskii oviductal tissue undergoes significant expansion during pre-brumation rather than the pre-spawning period, reflecting a unique physiological adaptation for brumation. While vitamin D is known to support growth and reproductive functions in various organisms, its role in seasonal oviductal hypertrophy remains unclear. In this study, the vitamin D metabolic pathway's role in regulating this process was investigated. Morphometric measurements revealed a significant increase in oviductal weight and luminal diameter during pre-brumation compared to pre-spawning, while histological examination showed marked glandular cell hypertrophy in the ampullary region. Correspondingly, 1,25-(OH)₂D₃ was significantly elevated in the oviduct during pre-brumation. Immunohistochemistry revealed that vitamin D metabolic enzymes Cyp2r1, Cyp27b1, Cyp24a1, the vitamin D receptor (Vdr), and the reductase Dhcr7 were localized in both epithelial cells and glandular cells during pre-spawning, but became predominantly restricted to epithelial cells during pre-brumation. qRT-PCR and western blot analyses confirmed higher expression of Cyp2r1, Cyp27b1, Cyp24a1, and Vdr, but reduced expression of Dhcr7 during pre-brumation. To further evaluate potential functional associations, 25-(OH)D₃ and 1,25-(OH)₂D₃ levels were found to be positively correlated with the mRNA expression of steroidogenic (star, cyp11a1) and proliferative (mki67, and pcna) markers across the two periods. Transcriptome analyses further supported these findings, identifying enrichment of differentially expressed genes within the vitamin and steroid hormone biosynthesis pathways. Collectively, these results suggest vitamin D metabolism is locally upregulated in the oviduct during pre-brumation, potentially via autocrine/paracrine mechanisms, and may contribute to seasonal reproductive adaptation in R. dybowskii. - Source: PubMed
Publication date: 2026/05/06
Chen YuanSun JiaweiYao YushanWang YankunShen YongXu MeiyuLiu YuningWeng Qiang - Low vitamin D levels during pregnancy are associated with an increased risk of Gestational Diabetes Mellitus (GDM), potentially mediated by altered vitamin D metabolism. Cytochrome P450 family 24 subfamily A member 1 (CYP24A1) plays a key role in vitamin D catabolism, but its epigenetic regulation in GDM remains unclear. - Source: PubMed
Publication date: 2026/05/06
Milan K LAnuradha MRamkumar K M - Hypercalcemia in infancy is rare and often presents with nonspecific clinical signs, making early recognition challenging. This report describes two infants with severe symptomatic hypercalcemia due to distinct etiologies and highlights the diagnostic value of sterile pyuria as an early clinical clue. - Source: PubMed
Publication date: 2026/03/30
Ahel Ivona ButoracAndritsos VerenikiKošuljandić ĐurđicaSeverinski SrećkoJešić MajaGrozdanić Kristina LovrinovićDekanić Kristina BarabaJambrović JuricaČače Iva Bilić - Calcium (Ca²⁺) homeostasis is tightly regulated by the coordinated actions of the intestine, kidneys and bone. Ca²⁺ transport occurs via either a paracellular pathway, which depends on the expression of select claudins, including claudin-12 (CLDN12) in the tight junction, or a transcellular pathway, involving apical influx through TRPV6. While disruption of paracellular or transcellular pathways impairs transepithelial Ca²⁺ flux, Cldn12-deficient mice and Trpv6 mutant (Trpv6) mice do not display alterations in Ca²⁺ balance as reported previously, perhaps because one pathway compensates for the other. To test this hypothesis, we generated a double knockout mouse (DKO, Cldn12/ Trpv6) to assess Ca²⁺ homeostasis using metabolic cage balance studies, quantitative real-time PCR, and micro-computed tomography (Micro-CT). Despite lacking these key Ca²⁺ transport mechanisms, DKO mice maintained normal blood Ca²⁺. However, PTH and calcitriol were significantly elevated, as were renal Cyp27b1 and Cyp24a1 expression, consistent with hormonal compensation. The proximal colon and cecum exhibited significant compensatory changes in Ca²⁺-regulatory gene expression, including upregulation of the Ca²⁺ buffer S100g and basolateral extrusion mechanism Atp2b1. Notably, the Ca²⁺ channel Trpv5, which is absent from the intestine, became detectable in the proximal colon and cecum, but not in the distal colon or small intestine of DKO mice. Micro-CT of bone revealed reduced trabecular bone volume and thickness, indicating increased bone resorption as a secondary compensatory mechanism. This study highlights the adaptive plasticity of Ca²⁺-regulatory mechanisms and suggests a role for TRPV5 in reabsorbing Ca²⁺ from the proximal colon and cecum when upstream mechanisms of Ca²⁺ absorption are impaired. - Source: PubMed
Publication date: 2026/04/09
Deluque Amanda LimaPan WanlingO'Neill DeborahBogdanovic MilosDimke HenrikDoschak Michael RAlexander R Todd - Despite compelling epidemiological evidence linking vitamin D deficiency to adverse outcomes in chronic obstructive pulmonary disease (COPD), asthma, and cystic fibrosis, randomized controlled trials have consistently failed to demonstrate clinically meaningful benefits from oral vitamin D supplementation. This disconnect between observational associations and interventional evidence represents a significant paradox in pulmonary medicine. Recent meta-analyses have found limited protective or therapeutic effects of oral supplementation on exacerbation rates, lung function, hospitalizations, or quality of life measures. We propose that this therapeutic failure reflects not a lack of vitamin D's efficacy but rather a fundamental limitation in the route of delivery. Oral vitamin D supplementation undergoes hepatic metabolism and systemic dilution before reaching respiratory tissues. High expression of CYP24A1, the vitamin D-inactivating enzyme, in pulmonary vasculature suggests that orally delivered vitamin D may be degraded before reaching the lung lumen. The respiratory epithelium possesses complete machinery for vitamin D activation, and vitamin D receptors are expressed throughout airway epithelial and immune cells, making direct pulmonary delivery mechanistically feasible. Pre-clinical studies demonstrate that nebulized or inhaled vitamin D reduces inflammation, protects epithelial barrier function, and improves lung function in murine models of respiratory disease without producing off-target systemic effects or hypercalcemia. Direct lung delivery of vitamin D represents an unexplored therapeutic strategy that could transform management of chronic respiratory diseases, like COPD, by achieving local therapeutic concentrations while minimizing systemic exposure. Clinical trials investigating safety, dosing optimization, and efficacy are warranted. - Source: PubMed
Publication date: 2026/03/31
Schichlein Kevin DJaspers IlonaDrummond M Bradley