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FLASH GENE
Symbol SLC13A5 contributors: mct - updated : 28-02-2014
HGNC name solute carrier family 13 (sodium-dependent citrate transporter), member 5
HGNC id 23089
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • 11 transmembrane domains
    • conjugated GlycoP
    mono polymer homomer , dimer
    HOMOLOGY
    intraspecies homolog to SLC13A2,SLC13A3
    Homologene
    FAMILY
  • SLC13A transporter family
  • NADC subfamily
    • CATEGORY transport carrier
    SUBCELLULAR LOCALIZATION     plasma membrane
    basic FUNCTION
  • playing an important role in the cellular utilization of citrate in blood for the synthesis of fatty acids and cholesterol (liver) and for the generation of energy (liver and brain)
  • may be facilitating the utilization of circulating citrate for the generation of metabolic energy and for the synthesis of fatty acids and cholesterol
  • tricarboxylate plasma transporter with a preference for citrate
  • primarily a citrate transporter located in the liver and brain, and its activity may regulate metabolic processes
  • CREB-dependent glucagon target gene that is induced in fasting and in type 2 diabetes
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism energetic
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) EIEE25
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    diabetetype 2 
    might be a therapeutic target for the treatment of obesity and type 2 diabetes
    obesity  
    might be a therapeutic target for the treatment of obesity and type 2 diabetes
    ANIMAL & CELL MODELS
  • Nact (also known as Slc13a5)-knockout mice have been found to have increased hepatic mitochondrial biogenesis, higher lipid oxidation and energy expenditure, and reduced lipogenesis, which taken together protect the mice from obesity and insulin resistance
  • mIndy was induced in livers of fasted as well as in high-fat-diet-streptozotocin diabetic rats, in which Creb is constitutively activated. mIndy induction was completely prevented when Creb was depleted in these rats by antisense oligonucleotides