|Proper activation||makes sure that Vitamin D does not accumulate in the body|
|Too much activation||Less vitamin D actually gets to cells|
|Too little activation||Vitamin D accumulates to toxic levels ( <1 in 10,000 people)|
Table of contents
- 32+ VitaminDWiki pages with CYP24A1 in title
- 8+ VitaminDWiki pages with both CYP24A1 AND CANCER in the title
- Many cancers increase the activation of the CYP24A1 gene – Feb 2023
- CYP24A1 and Vitamin D - 2011
- Rifampin (an anti-TB drug) reactivated the CYP24A1 gene in one person, stopping Hypercalcemia - May 2022
- CYP24A1 and kidney disease - May 2011
- CYP24A1 as a potential target for cancer therapy.- Jan 2014
- Determinants of vitamin D status: focus on genetic variations.- July 2011
- Search Google Scholar for cyp24a1 "vitamin d" 11,000 items
- CLICK HERE for Clinical Trials of CYP24A1: 25 as of May 2022
- Clinical trials of Genes and Vitamin D 228 as of May 2022
- Wikipedia: P450 enzyme group (CYP24A1 is a member of the group)
- Omega-3 reduces problems due to CYP2E1 – Aug 2017
- Chart: Blood test does not notice when a poor CYP24A1 gene stops Vitamin D from getting to cells
32+ VitaminDWiki pages with CYP24A1 in title
This list is automatically updated
8+ VitaminDWiki pages with both CYP24A1 AND CANCER in the title
This list is automatically updated
Many cancers increase the activation of the CYP24A1 gene – Feb 2023
Vitamin D metabolism in cancer: potential feasibility of vitamin D metabolism blocking therapy
Med Mol Morphol . 2023 Feb 7. doi: 10.1007/s00795-023-00348-x Publisher wants $39 for the PDF
Sakura Kamiya 1, Yuna Nakamori 1 2, Akira Takasawa 1, Kumi Takasawa 1, Daisuke Kyuno 1, Yusuke Ono 1, Kazufumi Magara 1, Makoto Osanai 3
In this review, we discuss the possibility of the vitamin D metabolizing enzyme CYP24A1 being a therapeutic target for various tumors including breast, colorectal and prostate tumors. Given the pleiotropic cellular activity of vitamin D, its deficiency impairs its physiological function in target cells and results in various pathologies including cancer. In addition, accumulated data have shown that elevated expression of CYP24A1 promotes carcinogenesis in various cancer subtypes by decreasing the bioavailability of vitamin D metabolites.
Thus, we propose the potential feasibility of vitamin D metabolism-blocking therapy in various types of human malignancies that express constitutive CYP24A1.
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- Kamiya S, Nakamori Y, Takasawa A, Takasawa K, Kyuno D, Ono Y, Magara K, Osanai M (2023) Suppression of vitamin D metabolizing enzyme CYP24A1 provides increased sensitivity to chemotherapeutic drugs in breast cancer. Oncol Rep, in press.
- Hanahan D, Weinberg RA (2000) The hallmarks of cancer. Cell 100:57–70
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- Townsend K, Banwell CM, Guy M, Colston KW, Mansi JL, Stewart PM, Campbell MJ, Hewison M (2005) Autocrine metabolism of vitamin D in normal and malignant breast tissue. Clin Cancer Res 11:3579–3586
- Osanai M, Lee G (2016) CYP24A1-induced vitamin D insufficiency promotes breast cancer growth. Oncol Rep 36:2755–2762
- Nakajima M, Yokoi T (2014) MicroRNA: regulation of P450 and pharmacogenetics. In: Padmanabhan S (ed) Handbook of pharmacogenomics and stratified medicine. Academic Press, Cambridge, pp 385–401
- Komagata S, Nakajima M, Takagi S, Mohri T, Taniya T, Yokoi T (2009) Human CYP24 catalyzing the inactivation of calcitriol is post-transcriptionally regulated by miR-125b. Mol Pharmacol 76:702–709
- Matilainen JM, Malinen M, Turunen MM, Carlberg C, Väisänen S (2010) The number of vitamin D receptor binding sites defines the different vitamin D responsiveness of the CYP24 gene in malignant and normal mammary cells. J Biol Chem 285:24174–24183
- Grant WB, Garland CF (2004) A critical review of studies on vitamin D in relation to colorectal cancer. Nutr Cancer 48:115–123
- Giovannucci E (2006) The epidemiology of vitamin D and colorectal cancer: recent findings. Curr Opin Gastroenterol 22:24–29
- Klampfer L (2014) Vitamin D and colon cancer. World J Gastrointest Oncol 6:430–437
- Diaz GD, Paraskeva C, Thomas MG, Binderup L, Hague A (2000) Apoptosis is induced by the active metabolite of vitamin D3 and its analogue EB1089 in colorectal adenoma and carcinoma cells: possible implications for prevention and therapy. Cancer Res 60:2304–2312
- Tangpricha V, Flanagan JN, Whitlatch LW, Tseng CC, Chen TC, Holt PR, Lipkin MS, Holick MF (2001) 25-hydroxyvitamin D-1alpha-hydroxylase in normal and malignant colon tissue. Lancet 357:1673–1674
- Dong LM, Ulrich CM, Hsu L, Duggan DJ, Benitez DS, White E, Slattery ML, Farin FM, Makar KW, Carlson CS, Caan BJ, Potter JD, Peters U (2009) Vitamin D related genes, CYP24A1 and CYP27B1, and colon cancer risk. Cancer Epidemiol Biomarkers Prev 18:2540–2548
- Höbaus J, Hummel DM, Thiem U, Fetahu IS, Aggarwal A, Müllauer L, Heller G, Egger G, Mesteri I, Baumgartner-Parzer S, Kallay E (2013) Increased copy-number and not DNA hypomethylation causes overexpression of the candidate proto-oncogene CYP24A1 in colorectal cancer. Int J Cancer 133:1380–1388
- Jacobs ET, Pelt CV, Forster RE, Zaidi W, Hibler EA, Galligan MA, Haussler MR, Jurutka PW (2013) CYP24A1 and CYP27B1 polymorphisms modulate vitamin D metabolism in colon cancer cells. Cancer Res 73:2563–2573
- Sadeghi H, Nazemalhosseini-Mojarad E, Yassaee VR, Savabkar S, Ghasemian M, Aghdaei HA, Zali MR, Mirfakhraie R (2020) Could CYP24A1 promoter methylation status affect the gene expression in the colorectal cancer patients. Meta Gene 24:100656
- Höbaus J, Fetahu ISh, Khorchide M, Manhardt T, Kallay E (2013) Epigenetic regulation of the 1,25-dihydroxyvitamin D3 24-hydroxylase (CYP24A1) in colon cancer cells. J Steroid Biochem Mol Biol 136:296–299
- Fang Z, Xiong Y, Zhang C, Li J, Liu L, Li M, Zhang W, Wan J (2010) Coexistence of copy number increases of ZNF217 and CYP24A1 in colorectal cancers in a Chinese population. Oncol Lett 1:925–930
- Roff A, Wilson RT (2008) A novel SNP in a vitamin D response element of the CYP24A1 promoter reduces protein binding, transactivation, and gene expression. J Steroid Biochem Mol Biol 112:47–54
- Chai L, Ni J, Ni X, Zhang N, Liu Y, Ji Z, Zhao X, Zhu X, Zhao B, Xin G, Wang Y, Yang F, Sun L, Zhu X, Bao W, Shui X, Wang F, Chen F, Yang Z (2021) Association of CYP24A1 gene polymorphism with colorectal cancer in the Jiamusi population. PLoS ONE 16:e0253474
- Sadeghi H, Nazemalhosseini-Mojarad E, Yaghoob-Taleghani M, Amin-Beidokhti M, Yassaee VR, Aghdaei HA, Zali MR, Mirfakhraie R (2018) miR-30a promoter variation contributes to the increased risk of colorectal cancer in an Iranian population. J Cell Biochem. https://doi.org/10.1002/jcb.28047 - DOI
- Luo W, Karpf AR, Deeb KK, Muindi JR, Morrison CD, Johnson CS, Trump DL (2010) Epigenetic regulation of vitamin D 24-hydroxylase/CYP24A1 in human prostate cancer. Cancer Res 70:5953–5962
- Deeb KK, Luo W, Karpf AR, Omilian AR, Bshara W, Tian L, Tangrea MA, Morrison CD, Johnson CS, Trump DL (2011) Differential vitamin D 24-hydroxylase/CYP24A1 gene promoter methylation in endothelium from benign and malignant human prostate. Epigenetics 6:994–1000
- Novakovic B, Sibson M, Ng HK, Manuelpillai U, Rakyan V, Down T, Beck S, Fournier T, Evain-Brion D, Dimitriadis E, Craig JM, Morley R, Saffery R (2009) Placenta-specific methylation of the vitamin D 24-hydroxylase gene: implications for feedback autoregulation of active vitamin D levels at the fetomaternal interface. J Biol Chem 284:14838–14848
- Ramnath N, Nadal E, Jeon CK, Sandoval J, Colacino J, Rozek LS, Christensen PJ, Esteller M, Beer DG, Kim SH (2014) Epigenetic regulation of vitamin D metabolism in human lung adenocarcinoma. J Thorac Oncol 4:473–482
- Miller GJ, Stapleton GE, Hedlund TE, Moffat KA (1995) Vitamin D receptor expression, 24-hydroxylase activity, and inhibition of growth by 1alpha,25-dihydroxyvitamin D3 in seven human prostatic carcinoma cell lines. Clin Cancer Res 1:997–1003
- Ruijter E, van de Kaa C, Miller G, Ruiter D, Debruyne F, Schalken J (1999) Molecular genetics and epidemiology of prostate carcinoma. Endocr Rev 20:22–45
- Ahn J, Albanes D, Peters U, Schatzkin A, Lim U, Freedman M, Chatterjee N, Andriole GL, Leitzmann MF, Hayes RB, For the Prostate, Lung, Colorectal, and Ovarian Trial Project Team (2007) Dairy products, calcium intake, and risk of prostate cancer in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev 16:2623–2630
- Tannour-Louet M, Lewis SK, Louet JF, Stewart J, Addai JB, Sahin A, Vangapandu HV, Lewis AL, Dittmar K, Pautler RG, Zhang L, Smith RG, Lamb DJ (2014) Increased expression of CYP24A1 correlates with advanced stages of prostate cancer and can cause resistance to vitamin D3-based therapies. FASEB J 28:364–372
- Farhan H, Wahala K, Cross HS (2003) Genistein inhibits vitamin D hydroxylases CYP24 and CYP27B1 expression in prostate cells. J Steroid Biochem Mol Biol 84:423–429
- Swami S, Krishnan AV, Moreno J, Bhattacharyya RB, Peehl DM, Feldman D (2007) Calcitriol and genistein actions to inhibit the prostaglandin pathway: potential combination therapy to treat prostate cancer. J Nutr 137(1 Suppl):205–210
- Zhang Q, Kanterewicz B, Buch S, Petkovich M, Parise R, Beumer J, Lin Y, Diergaarde B, Hershberger PA (2012) CYP24 inhibition preserves 1a,25-dihydroxyvitamin D(3) anti-proliferative signaling in lung cancer cells. Mol Cell Endocrinol 355:153–161
- Ly LH, Zhao XY, Holloway L, Feldman D (1999) Liarozole acts synergistically with 1alpha,25-dihydroxyvitamin D3 to inhibit growth of DU 145 human prostate cancer cells by blocking 24-hydroxylase activity. Endocrinology 140:2071–2076
- Zhao J, Tan BK, Marcelis S, Verstuyf A, Bouillon R (1996) Enhancement of antiproliferative activity of 1alpha,25-dihydroxyvitamin D3 (analogs) by cytochrome P450 enzyme inhibitors is compound- and cell-type specific. J Steroid Biochem Mol Biol 57:197–202
- Rao A, Woodruff RD, Wade WN, Kute TE, Cramer SD (2002) Genistein and vitamin D synergistically inhibit human prostatic epithelial cell growth. J Nutr 132:3191–3194
- Rodriguez GC, Turbov J, Rosales R, Yoo J, Hunn J, Zappia KJ, Lund K, Barry CP, Rodriguez IV, Pike JW, Conrads TP, Darcy KM, Maxwell GL, Hamilton CA, Syed V, Thaete LG (2016) Progestins inhibit calcitriol-induced CYP24A1 and synergistically inhibit ovarian cancer cell viability: an opportunity for chemoprevention. Gynecol Oncol 143:159–167
- Lee LR, Teng PN, Nguyen H, Hood BL, Kavandi L, Wang G, Turbov JM, Thaete LR, Hamilton CA, Maxwell GL, Rodriguez GC, Conrads TP, Syed V (2013) Progesterone enhances calcitriol antitumor activity by upregulating vitamin D receptor expression and promoting apoptosis in endometrial cancer cells. Cancer Prev Res (Phila) 6:731–743
- Lou YR, Tuohimaa P (2006) Androgen enhances the antiproliferative activity of vitamin D3 by suppressing 24-hydroxylase expression in LNCaP cells. J Steroid Biochem Mol Biol 99:44–49
- Yee SW, Campbell MJ, Simons C (2006) Inhibition of Vitamin D3 metabolism enhances VDR signaling in androgen-independent prostate cancer cells. J Steroid Biochem Mol Biol 98:228–235
- Josephia R, Muindi W-D, Yingyu M, Engler KL, Kong RX, Trump DL, Johnson CS (2010) CYP24A1 inhibition enhances the antitumor activity of calcitriol. Endocrinol 151:4301–4312
- Dovnik A, Dovnik NF (2020) Vitamin D and ovarian cancer: systematic review of the literature with a focus on molecular mechanisms. Cells. https://doi.org/10.3390/cells9020335 - DOI
CYP24A1 and Vitamin D - 2011
25-Hydroxyvitamin D-24-hydroxylase (CYP24A1): its important role in the degradation of vitamin D.
Arch Biochem Biophys. 2012 Jul 1;523(1):9-18. doi: 10.1016/j.abb.2011.11.003. Epub 2011 Nov 12.
Jones G1, Prosser DE, Kaufmann M.
Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada K7L 3N6. gj1 at queensu.ca
CYP24A1 is the cytochrome P450 component of the 25-hydroxyvitamin D(3)-24-hydroxylase enzyme that catalyzes the conversion of 25-hydroxyvitamin D(3) (25-OH-D(3)) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) into 24-hydroxylated products, which constitute the degradation of the vitamin D molecule. This review focuses on recent data in the CYP24A1 field, including biochemical, physiological and clinical developments. Notable among these are: the first crystal structure for rat CYP24A1; mutagenesis studies which change the regioselectivity of the enzyme; and the finding that natural inactivating mutations of CYP24A1 cause the genetic disease idiopathic infantile hypercalcemia (IIH). The review also discusses the emerging correlation between rising serum phosphate/FGF-23 levels and increased CYP24A1 expression in chronic kidney disease, which in turn underlies accelerated degradation of both serum 25-OH-D(3) and 1,25-(OH)(2)D(3) in this condition. This review concludes by evaluating the potential clinical utility of blocking this enzyme with CYP24A1 inhibitors in various disease states.
CYP24A1: biochemistry and catalytic properties
CYP24A1: crystal structure, homology modeling and mutagenesis studies
CYP24A1: physiological role
CYP24A1: regulation by 1,25-(OH)2D3, PTH and FGF-23
CYP24A1: pharmacological role
CYP24A1: human polymorphisms and genome-wide linkage studies
CYP24A1: pathological role and implications in disease
CYP24A1 and genetically-linked idiopathic infantile hypercalcemia
CYP24A1 and genetically-linked hypophosphatemia
CYP24A1: involvement in chronic kidney disease
CYP24A1: involvement in pathogenesis and treatment of hyperproliferative disorders
Download the PDF from Sci-Hub via VitaminDWiki
Rifampin (an anti-TB drug) reactivated the CYP24A1 gene in one person, stopping Hypercalcemia - May 2022
Long-term efficacy and safety of rifampin in the treatment of a patient carrying a CYP24A1 loss-of-function variant
J Clin Endocrinol Metab . 2022 May 15;dgac315. doi: 10.1210/clinem/dgac315 PDF is behind a $39 paywall
Alessandro Brancatella 1, Daniele Cappellani 1, Martin Kaufmann 2, Antonella Semeraro 1, Simona Borsari 1, Chiara Sardella 3, Fulvia Baldinotti 4, Maria Adelaide Caligo 4, Glenville Jones 2, Claudio Marcocci 1 3, Filomena Cetani 3
Background: Pharmacological therapy may be useful in the treatment of moderate to severe hypercalcemia in patients with infantile hypercalcemia-1 (HCINF1) due to pathogenic variants in the cytochrome P450 24 subfamily A member 1 (CYP24A1). Rifampin is an antituberculosis drug that is a potent inducer of cytochrome P450 3 subfamily A member 4 (CYP3A4), involved in an alternative catabolic pathway of vitamin D. The efficacy of rifampin in improving hypercalcemia was previously reported but many questions remain on the long-term efficacy and safety. Aim of the study is to test the long-term efficacy and safety of rifampin in a patient with HCINF1.
Methods: We report clinical, biochemical and imaging features of a 23-year-old man affected by HCINF1 with moderate hypercalcemia (12.9 mg/dL), symptomatic nephrolithiasis, nephrocalcinosis and impaired kidney function (eGFR 60 mL/min/1.73 m2) treated with rifampin for an overall period of 24 months. Kidney, liver and adrenal function were evaluated at every follow-up visit.
Results: In 2 months, rifampin induced a normalization of serum calcium (9.6 mg/dL) associated with an improvement of kidney function (eGFR 92 mL/min/1.73 m2) stable during the treatment. After 15 months, rifampin was temporally withdrawn because of asthenia, unrelated to impairment of adrenal function. After three months, the timing of drug administration was shifted from the morning to the evening, obtaining the remission of asthenia. At the end of follow-up, the nephrolithiasis disappeared and the nephrocalcinosis was stable.
Conclusions: Rifampin could represent an effective choice to induce a stable reduction of calcium levels in patients with HCINF1, with a good safety profile.
CYP24A1 and kidney disease - May 2011
Curr Opin Nephrol Hypertens. 2011 May 22.
PMID: 21610497 full text online
CYP24A1 as a potential target for cancer therapy.- Jan 2014
Anticancer Agents Med Chem. 2014 Jan;14(1):97-108.
Sakaki T, Yasuda K, Kittaka A, Yamamoto K, Chen TC1.
Increasing evidence has accumulated to suggest that vitamin D may reduce the risk of cancer through its biologically active metabolite, 1α,25(OH)2D3, which inhibits proliferation and angiogenesis, induces differentiation and apoptosis, and regulates many other cellular functions. Thus, it is plausible to assume that rapid clearance of 1α,25(OH)2D3 by highly expressed CYP24A1 could interrupt the normal physiology of cells and might be one cause of cancer initiation and progression. In fact, enhancement of CYP24A1 expression has been reported in literature for many cancers. Based on these findings, CYP24A1-specific inhibitors and vitamin D analogs which are resistant to CYP24A1-dependent catabolism might be useful for cancer treatment. CYP24A1-specific inhibitor VID400, which is an azole compound, markedly enhanced and prolonged the antiproliferative activity of 1α,25(OH)2D3 in the human keratinocytes. Likewise, CYP24A1-resistant analogs such as 2α-(3-hydroxypropoxy)-1α,25(OH)2D3 (O2C3) and its C2-epimer ED-71 (Eldecalcitol), and 19nor- 2α-(3-hydroxypropyl)-1α,25(OH)2D3 (MART-10) showed potent biological effects. Our in vivo studies using rats revealed that MART-10 had a low calcemic effect, which is a suitable property as an anticancer drug. Much lower affinity of MART-10 for vitamin D binding protein (DBP) as compared with 1α,25(OH)2D3 may be related to its more potent cellular activities.
Based on these results, we conclude that
- (1) high affinity for VDR,
- (2) resistance to CYP24A1-dependent catabolism,
- (3) low affinity for DBP, and
- (4) low calcemic effect
may be required for designing potent vitamin D analogs for cancer treatment. PMID: 23869781
Determinants of vitamin D status: focus on genetic variations.- July 2011
PMID: 21654390 full text online
Search Google Scholar for cyp24a1 "vitamin d" 11,000 items
- Vitamin D receptor (VDR) and metabolizing enzymes CYP27B1 and CYP24A1 in breast cancer - Dec 2020 https://doi.org/10.1007/s11033-020-05780-1
- Bone Metastases of Diverse Primary Origin Frequently Express the VDR (Vitamin D Receptor) and CYP24A1 - Nov 2022 https://doi.org/10.3390/jcm11216537 FREE PDF
- Genetic Polymorphism of Vitamin D Family Genes CYP2R1, CYP24A1, and CYP27B1 Are Associated With a High Risk of Non-alcoholic Fatty Liver Disease: A Case-Control Study - Nov 2021 FREE PDF
- Genetic Variants in CYP2R1, CYP24A1 and VDR Modify the Efficacy of Vitamin D<sub>3</sub> Supplementation for Increasing Serum 25-Hydroxyvitamin D Levels in a Randomized Controlled Trial. - July 2014
- Development of novel Vitamin D Receptor-Coactivator Inhibitors.Feb 2014
- Common variants in CYP2R1 and GC genes predict vitamin D concentrations in healthy Danish children and adults.Feb 2014 full text online
- Genetic Predictors of Circulating 25-Hydroxyvitamin D and Risk of Colorectal Cancer. Aug 2013
- Stress and vitamin D: Altered vitamin D metabolism in both the hippocampus and myocardium of chronic unpredictable mild stress exposed rats. April 2013
- Colonic vitamin D metabolism: Implications for the pathogenesis of inflammatory bowel disease and colorectal cancer. July 2011
- Vitamin D-Related Genetic Variants, Interactions with Vitamin D Exposure, and Breast Cancer Risk among Caucasian Women in Ontario. July 2011
- Mutations in CYP24A1 and Idiopathic Infantile Hypercalcemia June 2011 free text here and online
- Inherited variation in vitamin D genes is associated with predisposition to autoimmune disease type 1 diabetes. May 2011 full text on-line
- Functional significance of vitamin D receptor FokI polymorphism in human breast cancer cells.- with free paper
- CYP24A1 Is an Independent Prognostic Marker of Survival in Patients with Lung Adenocarcinoma. Feb 2011
- Effects of 25-hydroxyvitamin D3 on proliferation and osteoblast differentiation of human marrow stromal cells require CYP27B1/1?-hydroxylase.
- Gender differences in 1,25 dihydroxyvitamin D3 immunomodulatory effects in multiple sclerosis patients and healthy subjects.
- Vitamin D pathway gene variants and prostate cancer prognosis.
- Cytochromes P450 are essential players in the vitamin D signaling system.
- CYP24A1 inhibition enhances the antitumor activity of calcitriol.
- Epigenetic regulation of vitamin D 24-hydroxylase/CYP24A1 in human prostate cancer.
- Common genetic determinants of vitamin D insufficiency: a genome-wide association study. Lancet
- Efficacy of a potent and safe vitamin D receptor agonist for the treatment of inflammatory bowel disease.
- Epigenetic regulation of vitamin D converting enzymes.
- The vitamin D / CYP24A1 story in cancer.
- Polymorphisms in vitamin D metabolism related genes and risk of multiple sclerosis.
- Asthma and genes encoding components of the vitamin D pathway. - free text
CLICK HERE for Clinical Trials of CYP24A1: 25 as of May 2022
Clinical trials of Genes and Vitamin D 228 as of May 2022
Wikipedia: P450 enzyme group (CYP24A1 is a member of the group)
https://en.wikipedia.org/wiki/Cytochrome_P450 June 2017
|CYP1||drug and steroid (especially estrogen) metabolism, benzoapyrene toxification (forming (+)-benzoapyrene-7,8-dihydrodiol-9,10-epoxide)||3 subfamilies, 3 genes, 1 pseudogene||CYP1A1, CYP1A2, CYP1B1|
|CYP2||drug and steroid metabolism||13 subfamilies, 16 genes, 16 pseudogenes||CYP2A6, CYP2A7, CYP2A13, CYP2B6, CYP2C8, CYP2C9, CYP2C18, CYP2C19, CYP2D6, CYP2E1, CYP2F1, CYP2J2, CYP2R1, CYP2S1, CYP2U1, CYP2W1|
|CYP3||drug and steroid (including testosterone) metabolism||1 subfamily, 4 genes, 2 pseudogenes||CYP3A4, CYP3A5, CYP3A7, CYP3A43|
|CYP4||arachidonic acid or fatty acid metabolism||6 subfamilies, 12 genes, 10 pseudogenes||CYP4A11, CYP4A22, CYP4B1, CYP4F2, CYP4F3, CYP4F8, CYP4F11, CYP4F12, CYP4F22, CYP4V2, CYP4X1, CYP4Z1|
|CYP5||thromboxane A2 synthase||1 subfamily, 1 gene||CYP5A1|
|CYP7||bile acid biosynthesis 7-alpha hydroxylase of steroid nucleus||2 subfamilies, 2 genes||CYP7A1, CYP7B1|
|CYP8||varied||2 subfamilies, 2 genes||CYP8A1 (prostacyclin synthase), CYP8B1 (bile acid biosynthesis)|
|CYP11||steroid biosynthesis||2 subfamilies, 3 genes||CYP11A1, CYP11B1, CYP11B2|
|CYP17||steroid biosynthesis, 17-alpha hydroxylase||1 subfamily, 1 gene||CYP17A1|
|CYP19||steroid biosynthesis: aromatase synthesizes estrogen||1 subfamily, 1 gene||CYP19A1|
|CYP20||unknown function||1 subfamily, 1 gene||CYP20A1|
|CYP21||steroid biosynthesis||2 subfamilies, 1 gene, 1 pseudogene||CYP21A2|
|CYP24||vitamin D degradation||1 subfamily, 1 gene||CYP24A1|
|CYP26||retinoic acid hydroxylase||3 subfamilies, 3 genes||CYP26A1, CYP26B1, CYP26C1|
|CYP27||varied||3 subfamilies, 3 genes||CYP27A1 (bile acid biosynthesis), CYP27B1 (vitamin D3 1-alpha hydroxylase, activates vitamin D3), CYP27C1 (unknown function)|
|CYP39||7-alpha hydroxylation of 24-hydroxycholesterol||1 subfamily, 1 gene||CYP39A1|
|CYP46||cholesterol 24-hydroxylase||1 subfamily, 1 gene||CYP46A1|
|CYP51||cholesterol biosynthesis||1 subfamily, 1 gene, 3 pseudogenes||CYP51A1 (lanosterol 14-alpha demethylase)|
Omega-3 reduces problems due to CYP2E1 – Aug 2017
Omega-3 Polyunsaturated Fatty Acids Normalize the Functions of Mitochondria, Pro- and Antioxidant Enzymes of, and Cytochrome P450 2E1 Expression after Isoproterenol-Induced Myocardial Injury
International Journal of Physiology and Pathophysiology, DOI: 10.1615/IntJPhysPathophys.v8.i2.40 , pages 131-139
We studied the effect of dietary ω-3 polyunsaturated fatty acids (ω-3 PUFA) on the subsarcolemmal and interfibrillar mitochondrial fractions of rat myocardium, changes in expression of cytochrome P450 (CYP2E1), and the activity of pro-antioxidant enzymes after isoproterenol-induced myocardial injury. It has been found that ω-3 PUFA (Epadol 0.1 ml/100 g for 4 weeks) significantly reduces the swelling of the subsarcolemmal and interfibrillar mitochondrial fractions by 65.52% and 54.84%, respectively, indicating a decrease in damage to the mitochondrial function during isoproterenol-induced injury (two daily subcutaneous injections of isoproterenol at the dose of 60 mg/kg). In case of isoproterenol-induced myocardial injury, the use of ω-3 PUFAs prevents a decrease in the activity of antioxidant enzymes, namely catalase and superoxide dismutase (2.65 and 7.1 times, respectively). We have revealed that the development of oxidative stress after isoproterenol-induced myocardial injury can be triggered by a significant increase in the expression of cytochrome P450 2E1 (73.3%), and applying of ω-3 PUFAs prevents such changes.