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  4. FADS3 Antibody

FADS3 Antibody

  • 中文名稱：
    FADS3兔多克隆抗體
  • 貨號：
    CSB-PA007961GA01HU
  • 規格：
    ￥3,900
  • 其他：

產品詳情

  • Uniprot No.：
  • 基因名：
    FADS3
  • 別名：
    FADS3; CYB5RP; Fatty acid desaturase 3; Delta(13 fatty acid desaturase; Delta(13 desaturase
  • 宿主：
    Rabbit
  • 反應種屬：
    Human,Mouse,Rat
  • 免疫原：
    Human FADS3
  • 免疫原種屬：
    Homo sapiens (Human)
  • 抗體亞型：
    IgG
  • 純化方式：
    Antigen Affinity purified
  • 濃度：
    It differs from different batches. Please contact us to confirm it.
  • 保存緩沖液：
    PBS with 0.1% Sodium Azide, 50% Glycerol, pH 7.3. -20°C, Avoid freeze / thaw cycles.
  • 產品提供形式：
    Liquid
  • 應用范圍：
    ELISA,WB
  • Protocols：
  • 儲存條件：
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 貨期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
  • 用途：
    For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

  • 功能：
    Mammals have different sphingoid bases that differ in their length and/or pattern of desaturation and hydroxyl groups. The predominant sphingoid base in mammalian ceramides is sphing-4-enine (sphingosine or SPH) which has a trans desaturation at carbon 4. FADS3 is a ceramide desaturase that introduces a cis double bond between carbon 14 and carbon 15 of the SPH-containing ceramides, producing sphinga-4,14-dienine-containing ceramides (SPD ceramides). SPD ceramides occur widely in mammalian tissues and cells. Due to their unusual structure containing a cis double bond, SPD ceramides may have an opposite, negative role in lipid microdomain formation relative to conventional ceramides. FADS3 also acts as a methyl-end fatty acyl coenzyme A (CoA) desaturase that introduces a cis double bond between the preexisting double bond and the terminal methyl group of the fatty acyl chain. Desaturates (11E)-octadecenoate (trans-vaccenoate, the predominant trans fatty acid in human milk) at carbon 13 to generate (11E,13Z)-octadecadienoate (also known as conjugated linoleic acid 11E,13Z-CLA).
  • 基因功能參考文獻：
    1. 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. PMID: 28237083
    2. 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 PMID: 27269715
    3. 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. PMID: 24985009
    4. 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). PMID: 22398025
    5. 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. PMID: 22877655
    6. it is highly likely that a gene product of FADS3 has desaturating activity. PMID: 21366865
    7. FADS3 does exist under multiple protein isoforms depending on the mammalian tissues. PMID: 19752397
    8. USF1 and FADS3 are causal candidate genes for the Mexican familial combined hyperlipidemia. PMID: 19750004

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  • 亞細胞定位：
    Endoplasmic reticulum membrane; Multi-pass membrane protein.
  • 蛋白家族：
    Fatty acid desaturase type 1 family
  • 組織特異性：
    Highly expressed in various organs and tissues including liver, kidney, brain, lung, pancreas, testis, ovary and skeletal muscle (at protein level).
  • 數據庫鏈接：

    HGNC: 3576

    OMIM: 606150

    KEGG: hsa:3995

    STRING: 9606.ENSP00000278829

    UniGene: Hs.21765



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