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词条 CYP26B1
释义

  1. See also

  2. References

  3. External links

  4. Further reading

{{Infobox_gene}}Cytochrome P450 26B1 is a protein that in humans is encoded by the CYP26B1 gene.[1][2]

This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases that catalyze many reactions involved in drug metabolism and the synthesis of cholesterol, steroids and other lipids. The enzyme encoded by this gene is involved in the specific inactivation of all-trans-retinoic acid to hydroxylated forms, such as 4-oxo-, 4-OH-, and 18-OH-all-trans-retinoic acid.[2]

In a developing mouse embryo, CYP26B1 is expressed in the distal tip of the forming limb bud with an abundance in the apical ectodermal ridge. In a knockout mouse model, mice manifest with severe limb malformations and die after birth due to respiratory distress.[3] However, if the expression of CYP26B1 is conditionally deleted only prior to E9.5, the limbs are not as severely truncated and more digits are visible. Research suggests that this differenece is attributable to the timing of chrondroblast differentiation.[4]

CYP26B1 has been shown to be over-expressed in colorectal cancer cells compared to normal colonic epithelium. CYP26B1 expression was also independently prognostic in patients with colorectal cancer and strong expression was associated with a poorer outcome.[5]

In a genome-wide study, CCHCR1, TCN2, TNXB, LTA, FASN, and CYP26B1 were identified as loci associated with a risk for developing esophageal squamous cell carcinoma. Of these loci, CYP26B1 exhibited the highest effect size. Moreover, the CYP26B1 locus was found to have two alleles with differing capacities to catabolize all-trans retinoic acid, a chemotherapeutic agent. When the allele with the higher catabolic capacity, rs138478634-GA, was overexpressed, cell proliferation was significantly enhanced in comparison to the other allele, rs138478634-GG. Additionally, research is suggestive of a lifestyle interaction where individuals with the risk allele who partake in smoking or drinking present with an odd-ratio over 2-fold higher than smokers or drinkers without the variant or individuals who refrain.[6]

See also

  • Cytochrome P450 oxidoreductase deficiency

References

1. ^{{cite journal | author = Nelson DR | title = A second CYP26 P450 in humans and zebrafish: CYP26B1 | journal = Arch Biochem Biophys | volume = 371 | issue = 2 | pages = 345–7 |date=Dec 1999 | pmid = 10545224 | pmc = | doi = 10.1006/abbi.1999.1438 }}
2. ^1 {{cite web | title = Entrez Gene: CYP26B1 cytochrome P450, family 26, subfamily B, polypeptide 1| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=56603| accessdate = }}
3. ^{{cite journal | vauthors=Yashiro K, Zhao X, Uehara M, Yamshita K, Nishijima M, Nishino J, Saijoh Y, Sakai Y, Hamada H |title=Regulation of retinoic acid distribution is required for proximodistal patterning and outgrowth of the developing mouse limb |journal=Dev. Cell |volume=6 |issue= 3 |pages= 411–22 |year= 2004 |pmid= 15030763}}
4. ^{{cite journal | vauthors=Dranse HJ, Sampaio AV, Petkovich M, Underhill TM |title=Genetic deletion of Cyp26b1 negatively impacts limb skeletogenesis by inhibiting chondrogenesis |journal=J. Cell Sci. |volume=124 |issue= 16 |pages= 2723–34 |year= 2011 |pmid= 21807937 |doi= 10.1242/jcs.084699}}
5. ^{{cite journal|last=Brown|first=Gordon|author2=Beatriz Cash |author3=Daniela Blihoghe |author4=Petronella Johansson |author5=Ayham Alnabulsi |author6=Graeme Murray |title=The Expression and Prognostic Significance of Retinoic Acid Metabolising Enzymes in Colorectal Cancer|journal=PLOS ONE|date=2014-03-07|doi=10.1371/journal.pone.0090776|url=http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0090776#ack |pmid=24608339 |pmc=3946526 |volume=9 |pages=e90776}}
6. ^{{cite journal | vauthors=Chang J, Zhong R, Tian J, Li J, Zhai K, Ke J, Lou J, Chan W, Zhu B, Shen N, Zhang Y, Gong Y, Yang Y, Zou D, Peng X, Zhang Z, Zhang X, Huang K, Wu T, Wu C, Miao X, Lin D |title=Exome-wide analyses identify low-frequency variant in CYP26B1 and additional coding variants associated with esophageal squamous cell carcinoma |journal=Nat. Genet. |volume=50 |issue= 3 |pages= 338–43 |year= 2018 |pmid= 29379198 |doi= 10.1038/s41588-018-0045-8}}

External links

  • {{UCSC gene info|CYP26B1}}

Further reading

{{refbegin | 2}}
  • {{cite journal | vauthors=Rat E, Billaut-Laden I, Allorge D |title=Evidence for a functional genetic polymorphism of the human retinoic acid-metabolizing enzyme CYP26A1, an enzyme that may be involved in spina bifida |journal=Birth Defects Res. Part a Clin. Mol. Teratol. |volume=76 |issue= 6 |pages= 491–8 |year= 2006 |pmid= 16933217 |doi= 10.1002/bdra.20275 |display-authors=etal}}
  • {{cite journal | vauthors=Bowles J, Knight D, Smith C |title=Retinoid signaling determines germ cell fate in mice |journal=Science |volume=312 |issue= 5773 |pages= 596–600 |year= 2006 |pmid= 16574820 |doi= 10.1126/science.1125691 |display-authors=etal}}
  • {{cite journal | vauthors=Hillier LW, Graves TA, Fulton RS |title=Generation and annotation of the DNA sequences of human chromosomes 2 and 4 |journal=Nature |volume=434 |issue= 7034 |pages= 724–31 |year= 2005 |pmid= 15815621 |doi= 10.1038/nature03466 |display-authors=etal}}
  • {{cite journal | vauthors=Gerhard DS, Wagner L, Feingold EA |title=The Status, Quality, and Expansion of the NIH Full-Length cDNA Project: The Mammalian Gene Collection (MGC) |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 | pmc=528928 |display-authors=etal}}
  • {{cite journal | vauthors=Strausberg RL, Feingold EA, Grouse LH |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899–903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 | pmc=139241 |display-authors=etal}}
  • {{cite journal | vauthors=Trofimova-Griffin ME, Juchau MR |title=Developmental expression of cytochrome CYP26B1 (P450RAI-2) in human cephalic tissues |journal=Brain Res. Dev. Brain Res. |volume=136 |issue= 2 |pages= 175–8 |year= 2002 |pmid= 12101034 |doi=10.1016/S0165-3806(02)00305-X }}
  • {{cite journal | vauthors=Abu-Abed S, MacLean G, Fraulob V |title=Differential expression of the retinoic acid-metabolizing enzymes CYP26A1 and CYP26B1 during murine organogenesis |journal=Mech. Dev. |volume=110 |issue= 1–2 |pages= 173–7 |year= 2002 |pmid= 11744378 |doi=10.1016/S0925-4773(01)00572-X |display-authors=etal}}
  • {{cite journal | vauthors=White JA, Ramshaw H, Taimi M |title=Identification of the human cytochrome P450, P450RAI-2, which is predominantly expressed in the adult cerebellum and is responsible for all-trans-retinoic acid metabolism |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=97 |issue= 12 |pages= 6403–8 |year= 2000 |pmid= 10823918 |doi= 10.1073/pnas.120161397 | pmc=18615 |display-authors=etal}}
{{refend}}{{Cytochrome P450}}{{gene-2-stub}}
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