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 gut-kidney axis has emerged as a critical area of investigation. However, the compartment-specific regulatory mechanisms of gut microbiota metabolites within the glomerular and tubulointerstitial regions of diabetic kidney disease (DKD) remain incompletely understood. - Source: PubMed
Publication date: 2026/08/31
Xie FengweiHe XiongweiChen WenjieLi JiahaoLin SihanBao QihangLi WeiqingCheng JunpengMa YuanWu ZiyuLi Haohuan - Vitamin D (VD) has been widely reported to be associated with the developing of diabetes, potentially through its effects on insulin sensitivity and glucose homeostasis. In this study, we investigated the association between Single nucleotide polymorphisms (SNPs) in genes that are linked to VD pathway (rs10741657 and rs1074165 in CYP2R1, rs6013897 in CYP24A1, and rs10877012 in CYP27B1) and the risk of type 2 diabetes mellitus (T2DM) in the Jordanian population. - Source: PubMed
Publication date: 2026/06/27
Shboul MohammadAl-Wendawi SaraZahra Abdulmalek AbuFathallah Rajaa - Infantile hypercalcemia type 1 (HCINF1) is a rare genetic disorder caused by pathogenic variants in the CYP24A1 gene, which encodes the vitamin D-catabolic enzyme 24-hydroxylase responsible for inactivating 1,25-dihydroxyvitamin D₃. The clinical presentation ranges from severe forms diagnosed in infancy-characterized by hypercalcemia, dehydration, and vomiting-to milder forms that are often identified in adulthood during evaluation for recurrent nephrolithiasis. We present two adult female patients with late-onset HCINF1, both initially referred to a nephrologist for nephrolithiasis and nephrocalcinosis, and one male patient with an infantile presentation who began fluconazole therapy in adulthood. This case series highlights rare late-onset manifestations of HCINF1 associated with recurrent nephrolithiasis, secondary distal renal tubular acidosis (dRTA), and variable degrees of renal function impairment. It emphasizes the importance of considering genetic testing in adults with unexplained hypercalcemia and nephrolithiasis and supports the therapeutic role of fluconazole in selected cases. - Source: PubMed
Publication date: 2026/09/01
Vucenovic Basic NikolinaBeck BodoBalasko AnnemarieVukovic Brinar IvanaFistrek Prlic Margareta - We aim to perform a narrative literature review of gestational hypercalcemia including calcium homeostasis in pregnancy. Additionally, we demonstrate the diagnostic and therapeutic challenges and pitfalls of gestational hypercalcemia. - Source: PubMed
Publication date: 2026/08/19
Martin MiriamHeim CorinMueller MartinMohaupt Markus - Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, typically associated with poor clinical outcomes. Recently, ferroptosis has emerged as a promising therapeutic target for TNBC. ΔA146Ply, a novel pneumolysin variant, has demonstrated potential as an anti-tumor agent; however, its role in regulating ferroptosis remains unclear. This study investigates whether ΔA146Ply exerts anti-TNBC effects by promoting ferroptosis via the CYP24A1-mediated Calcitriol/vitamin D receptor (VDR) pathway. Our in vitro results reveal that ΔA146Ply inhibits MDA-MB-231 cells by inducing ferroptosis. Mechanistically, we demonstrate that CYP24A1 negatively regulates the Calcitriol-VDR pathway and serves as a critical mediator of ferroptosis. In vivo, ΔA146Ply suppresses TNBC tumor growth by downregulating CYP24A1 and promoting ferroptosis. In conclusion, ΔA146Ply exerts anti-TNBC effects by activating ferroptosis through the regulation of the CYP24A1-mediated Calcitriol-VDR pathway. - Source: PubMed
Publication date: 2026/08/30
Yu YeZhang ZhengkunWang DingxueBai XinHe DanJi XuxuYin ZhaoruXu KeyiLiu JiZou Jiaqiong