| CYP4Z1 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Identifiers | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Aliases | CYP4Z1, CYP4A20, cytochrome P450 family 4 subfamily Z member 1 | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | HomoloGene: 138446 GeneCards: CYP4Z1 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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| Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
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CYP4Z1 (cytochrome P450, family 4, subfamily Z, polypeptide 1) is a protein that in humans is encoded by the CYP4Z1 gene.[3]
Function
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 gene is part of a cluster of cytochrome P450 genes on chromosome 1p33.[4]
Clinical significance
CYP4Z1 is overexpressed in breast cancer cells.[3] It has also been demonstrated that the expression of the CYP4Z1 gene is upregulated by activated glucocorticoid and progesterone receptors.[5] The overexpression of CYP4Z1 is associated with the breast cancer cells' increased production of 20-Hydroxyeicosatetraenoic acid (20-HETE); it is hypothesized that CYP4Z1 metabolizes arachidonic acid to 20-HETE and that this overproduction is responsible for increasing the growth and spread of breast cancer cells in human breast cancer.[6][7] CPZ4Z1 is likewise overexpressed in ovarian cancer cells.[7] These studies also suggest that CYP4Z1 will be a valuable marker to distinguish between benign and malignant breast and ovarian growths in humans and/or the prognoses of malignant growths in these tissues.
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000186160 - Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ a b Rieger MA, Ebner R, Bell DR, Kiessling A, Rohayem J, Schmitz M, Temme A, Rieber EP, Weigle B (April 2004). "Identification of a novel mammary-restricted cytochrome P450, CYP4Z1, with overexpression in breast carcinoma". Cancer Res. 64 (7): 2357–64. doi:10.1158/0008-5472.CAN-03-0849. PMID 15059886.
- ^
This article incorporates public domain material from "Entrez Gene: CYP4Z1". Reference Sequence collection. National Center for Biotechnology Information.
- ^ Savas U, Hsu MH, Griffin KJ, Bell DR, Johnson EF (April 2005). "Conditional regulation of the human CYP4X1 and CYP4Z1 genes". Arch. Biochem. Biophys. 436 (2): 377–85. doi:10.1016/j.abb.2005.02.022. PMID 15797250.
- ^ Yu W, Chai H, Li Y, Zhao H, Xie X, Zheng H, Wang C, Wang X, Yang G, Cai X, Falck JR, Yang J (Oct 2012). "Increased expression of CYP4Z1 promotes tumor angiogenesis and growth in human breast cancer". Toxicology and Applied Pharmacology. 264 (1): 73–83. doi:10.1016/j.taap.2012.07.019. PMC 3439529. PMID 22841774.
- ^ a b Zheng L, Li X, Gu Y, Lv X, Xi T (Feb 2015). "The 3'UTR of the pseudogene CYP4Z2P promotes tumor angiogenesis in breast cancer by acting as a ceRNA for CYP4Z1". Breast Cancer Research and Treatment. 150 (1): 105–18. doi:10.1007/s10549-015-3298-2. PMID 25701119. S2CID 11952881.
Further reading
- Zöllner A, Dragan CA, Pistorius D, Müller R, Bode HB, Peters FT, Maurer HH, Bureik M (Apr 2009). "Human CYP4Z1 catalyzes the in-chain hydroxylation of lauric acid and myristic acid". Biological Chemistry. 390 (4): 313–7. doi:10.1515/BC.2009.030. PMID 19090726. S2CID 13454640.
- Nelson DR, Zeldin DC, Hoffman SM, Maltais LJ, Wain HM, Nebert DW (Jan 2004). "Comparison of cytochrome P450 (CYP) genes from the mouse and human genomes, including nomenclature recommendations for genes, pseudogenes and alternative-splice variants". Pharmacogenetics. 14 (1): 1–18. doi:10.1097/00008571-200401000-00001. PMID 15128046.
- Simpson AE (Mar 1997). "The cytochrome P450 4 (CYP4) family". General Pharmacology. 28 (3): 351–9. doi:10.1016/S0306-3623(96)00246-7. PMID 9068972.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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This page was last edited on 15 December 2023, at 04:51