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    FADS3 fatty acid desaturase 3 [ Homo sapiens (human) ]

    Gene ID: 3995, updated on 12-Sep-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Placental expression of Fatty Acid Desaturases 1, 2 and 3 in selected pregnancy pathologies.

    Placental expression of Fatty Acid Desaturases 1, 2 and 3 in selected pregnancy pathologies.
    Bobiński R, Mazurek U, Zmarzly N, Ulman-Włodarz I, Dutka M, Pizon M, Pollok-Waksmańska W, Pielesz A, Hajduga M, Zimmer K, Bujok J, Pająk C, Ilczak T.

    03/21/2023
    Overexpression of fatty acid desaturase 3 predicts poor prognosis in head and neck squamous cell carcinoma.

    Overexpression of fatty acid desaturase 3 predicts poor prognosis in head and neck squamous cell carcinoma.
    Su K, Wang Y, Gu H, Ma L, Xuan G., Free PMC Article

    01/14/2023
    FADS3 is a Delta14Z sphingoid base desaturase that contributes to gender differences in the human plasma sphingolipidome.

    FADS3 is a Δ14Z sphingoid base desaturase that contributes to gender differences in the human plasma sphingolipidome.
    Karsai G, Lone M, Kutalik Z, Brenna JT, Li H, Pan D, von Eckardstein A, Hornemann T., Free PMC Article

    10/24/2020
    Biosynthesis of the anti-lipid-microdomain sphingoid base 4,14-sphingadiene by the ceramide desaturase FADS3.

    Biosynthesis of the anti-lipid-microdomain sphingoid base 4,14-sphingadiene by the ceramide desaturase FADS3.
    Jojima K, Edagawa M, Sawai M, Ohno Y, Kihara A.

    10/10/2020
    Data demonstrated that the rs1000778-G allele in the FADS3 gene is related to increased risk for coronary artery disease in the northern Chinese Han population.

    Association of the FADS gene cluster with coronary artery disease and plasma lipid concentrations in the northern Chinese Han population.
    Wu Y, Zeng L, Chen X, Xu Y, Ye L, Qin L, Chen L, Xie L.

    12/16/2017
    pairwise comparison showed that individuals major homozygous for the SNP rs1000778 in the FADS3 gene had lower concentrations of a-linolenic acid and linoleic acid in their breast milk

    Association of polyunsaturated fatty acids in breast milk with fatty acid desaturase gene polymorphisms among Chinese lactating mothers.
    Ding Z, Liu GL, Li X, Chen XY, Wu YX, Cui CC, Zhang X, Yang G, Xie L.

    08/5/2017
    Minor allele homozygotes and heterozygotes of rs174455 in FADS3 gene had lower levels of 22:5 omega-3, 20:4 omega-6, and Delta5desaturase activity in patients with type 2 diabetes mellitus.

    Genetic variants in desaturase gene, erythrocyte fatty acids, and risk for type 2 diabetes in Chinese Hans.
    Huang T, Sun J, Chen Y, Xie H, Xu D, Huang J, Li D.

    02/14/2015
    Data suggest that FADS3 alternative transcripts/splicing are up-regulated in liver by dietary docosahexaenoic/arachidonic acids by peroxisome proliferator-activated receptor gamma (PPARg)-dependent mechanism unrelated to other desaturases (FADS1/2).

    Dietary long-chain polyunsaturated fatty acids upregulate expression of FADS3 transcripts.
    Reardon HT, Hsieh AT, Park WJ, Kothapalli KS, Anthony JC, Nathanielsz PW, Brenna JT., Free PMC Article

    07/6/2013
    genetic association study in maternal/child dyads in England: Data suggest that SNPs in FADS3 (and in FADS1/FADS2) influence fetal fatty acid metabolism; both maternal and child FADS genotypes/haplotypes influence cord plasma long-chain fatty acids.

    Umbilical cord PUFA are determined by maternal and child fatty acid desaturase (FADS) genetic variants in the Avon Longitudinal Study of Parents and Children (ALSPAC).
    Lattka E, Koletzko B, Zeilinger S, Hibbeln JR, Klopp N, Ring SM, Steer CD., Free PMC Article

    06/1/2013
    it is highly likely that a gene product of FADS3 has desaturating activity.

    Genetic variation in polyunsaturated fatty acid metabolism and its potential relevance for human development and health.
    Glaser C, Lattka E, Rzehak P, Steer C, Koletzko B., Free PMC Article

    05/14/2011
    Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)

    Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study.
    Bailey SD, Xie C, Do R, Montpetit A, Diaz R, Mohan V, Keavney B, Yusuf S, Gerstein HC, Engert JC, Anand S, DREAM investigators., Free PMC Article

    09/15/2010
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (4) articles

    FADS gene polymorphisms in Koreans: association with ω6 polyunsaturated fatty acids in serum phospholipids, lipid peroxides, and coronary artery disease.
    Kwak JH, Paik JK, Kim OY, Jang Y, Lee SH, Ordovas JM, Lee JH.

    Genetic loci associated with lipid concentrations and cardiovascular risk factors in the Korean population.
    Park MH, Kim N, Lee JY, Park HY.

    FADS genetic variants and omega-6 polyunsaturated fatty acid metabolism in a homogeneous island population.
    Mathias RA, Vergara C, Gao L, Rafaels N, Hand T, Campbell M, Bickel C, Ivester P, Sergeant S, Barnes KC, Chilton FH.

    Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip.
    Talmud PJ, Drenos F, Shah S, Shah T, Palmen J, Verzilli C, Gaunt TR, Pallas J, Lovering R, Li K, Casas JP, Sofat R, Kumari M, Rodriguez S, Johnson T, Newhouse SJ, Dominiczak A, Samani NJ, Caulfield M, Sever P, Stanton A, Shields DC, Padmanabhan S, Melander O, Hastie C, Delles C, Ebrahim S, Marmot MG, Smith GD, Lawlor DA, Munroe PB, Day IN, Kivimaki M, Whittaker J, Humphries SE, Hingorani AD, ASCOT investigators, NORDIL investigators, BRIGHT Consortium.

    09/15/2010
    FADS3 does exist under multiple protein isoforms depending on the mammalian tissues.

    The fatty acid desaturase 3 gene encodes for different FADS3 protein isoforms in mammalian tissues.
    Pédrono F, Blanchard H, Kloareg M, D'andréa S, Daval S, Rioux V, Legrand P., Free PMC Article

    05/10/2010
    USF1 and FADS3 are causal candidate genes for the Mexican familial combined hyperlipidemia.

    A systems genetics approach implicates USF1, FADS3, and other causal candidate genes for familial combined hyperlipidemia.
    Plaisier CL, Horvath S, Huertas-Vazquez A, Cruz-Bautista I, Herrera MF, Tusie-Luna T, Aguilar-Salinas C, Pajukanta P., Free PMC Article

    01/21/2010
    Observational study and genome-wide association study of gene-disease association. (HuGE Navigator)See all PubMed (3) articles

    Genome-wide association study of plasma polyunsaturated fatty acids in the InCHIANTI Study.
    Tanaka T, Shen J, Abecasis GR, Kisialiou A, Ordovas JM, Guralnik JM, Singleton A, Bandinelli S, Cherubini A, Arnett D, Tsai MY, Ferrucci L.

    Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts.
    Aulchenko YS, Ripatti S, Lindqvist I, Boomsma D, Heid IM, Pramstaller PP, Penninx BW, Janssens AC, Wilson JF, Spector T, Martin NG, Pedersen NL, Kyvik KO, Kaprio J, Hofman A, Freimer NB, Jarvelin MR, Gyllensten U, Campbell H, Rudan I, Johansson A, Marroni F, Hayward C, Vitart V, Jonasson I, Pattaro C, Wright A, Hastie N, Pichler I, Hicks AA, Falchi M, Willemsen G, Hottenga JJ, de Geus EJ, Montgomery GW, Whitfield J, Magnusson P, Saharinen J, Perola M, Silander K, Isaacs A, Sijbrands EJ, Uitterlinden AG, Witteman JC, Oostra BA, Elliott P, Ruokonen A, Sabatti C, Gieger C, Meitinger T, Kronenberg F, Döring A, Wichmann HE, Smit JH, McCarthy MI, van Duijn CM, Peltonen L, ENGAGE Consortium.

    Common variants at 30 loci contribute to polygenic dyslipidemia.
    Kathiresan S, Willer CJ, Peloso GM, Demissie S, Musunuru K, Schadt EE, Kaplan L, Bennett D, Li Y, Tanaka T, Voight BF, Bonnycastle LL, Jackson AU, Crawford G, Surti A, Guiducci C, Burtt NP, Parish S, Clarke R, Zelenika D, Kubalanza KA, Morken MA, Scott LJ, Stringham HM, Galan P, Swift AJ, Kuusisto J, Bergman RN, Sundvall J, Laakso M, Ferrucci L, Scheet P, Sanna S, Uda M, Yang Q, Lunetta KL, Dupuis J, de Bakker PI, O'Donnell CJ, Chambers JC, Kooner JS, Hercberg S, Meneton P, Lakatta EG, Scuteri A, Schlessinger D, Tuomilehto J, Collins FS, Groop L, Altshuler D, Collins R, Lathrop GM, Melander O, Salomaa V, Peltonen L, Orho-Melander M, Ordovas JM, Boehnke M, Abecasis GR, Mohlke KL, Cupples LA.

    01/11/2009
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