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FLASH GENE
Symbol FABP4 contributors: mct/npt - updated : 17-06-2016
HGNC name fatty acid binding protein 4, adipocyte
HGNC id 3559
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
4 - 838 15 132 - Cabre (2008)
EXPRESSION
Type widely
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Cardiovascularheart   highly Homo sapiens
Endocrineparathyroid   highly
Urinarybladder   highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Connectiveadipose  highly
Muscularstriatumcardiacmyocardium  Homo sapiens
cells
SystemCellPubmedSpeciesStageRna symbol
Lymphoid/Immunemacrophage Homo sapiens
Muscularmyocyte Homo sapiens
not specificadipocyte Homo sapiens
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • repeated structure with topology beta barrel and remarkable structural signature
  • a consensus alignment for the binding site as F-Acidic-Acidic-YMKX2GVG (Smith 2008)
  • an helix-turn-helix domain being a site for homodimerization
  • mono polymer homomer , dimer
    HOMOLOGY
    Homologene
    FAMILY
  • lipocalin, calycin family
  • cytoplasmic fatty acid-binding protein (FABP) multigene family
  • CATEGORY adaptor , regulatory , transport carrier
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,cytosolic
    intracellular,nucleus
    basic FUNCTION
  • fatty acid-binding protein 4, involved in lipid transport protein in adipocytes
  • with hormone-sensitive lipase (LIPE), form a physical complex that affects basal and hormone-stimulated adipocyte fatty acid efflux ((Smith 2008)
  • having a role as a fatty acid sensor affecting cellular metabolism via protein-protein interactions (Thompson 2009)
  • fatty acid carrier solubilizing and enabling diffusion of fatty acids throughout the aqueous cellular environment (Thompson 2009)
  • mechanistic linkage between FABP4 and impaired endothelial function in diabetes, which leads to an increased cardiovascular risk.
  • is an adipokine linking adipocytes to hepatic glucose production
  • FABP4/5 is potentially novel targets for the modulation of energy homeostasis
  • cytoplasmic fatty acid chaperone expressed primarily in adipocytes and myeloid cells and implicated in the development of insulin resistance and atherosclerosis
  • might promote human prostate cancer cell progression by binding with fatty acids
  • is functionally expressed in endometrial epithelium and is necessary for maintaining the cell function of epithelial cells of endometrium
  • mediates apoptosis via endoplasmic reticulum stress in mesangial cells of diabetic nephropathy
  • adipose tissue-secreted adipokine that is involved in the regulation of energetic metabolism and inflammation
  • plays an important role in regulating heart function under pressure overload
  • FABP4 over-expression in cardiomyocytes can aggravate the development of cardiac hypertrophy through the activation of ERK signal pathway
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS coagulation/hemostasis , cellular trafficking transport
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • binds both long chain fatty acid and retinoic acid
  • two lipogenic genes encoding DGAT2 and FABP4 were induced in ELOVL2-overexpressing cells, whereas no such effect was seen on the fatty acid synthase (FASN) gene
  • interaction with LIPE (hormone-sensitive lipase) requires that a fatty acid be bound to FABP4 and the association is considered to be regulatory, serving as a potential negative feedback loop regulating lipid hydrolysis (Smith 2008)
  • interacts with JAK2 in a fatty acid-dependent manner, through the helix-turn-helix domain (Thompson 2009)
  • suppression of PPARG by FABP4 in visceral fat may explain the reported role of FABP4 in the development of obesity-related morbidities, including insulin resistance, diabetes, and atherosclerosis
  • FABP4 induction by VEGFA was reduced by blockade of DLL4 binding to NOTCH1 or inhibition of NOTCH1 signal transduction
  • exogenous FABP4 interacts with plasma membrane proteins, specifically KRT1
  • PATZ1 acted as a potent transcriptional corepressor of FABP4, an essential convergence point for angiogenic and metabolic signaling pathways in endothelial cells (ECs)
  • cell & other
    REGULATION
    induced by NOTCH1 (is directly induced by NOTCH1 and stimulation of NOTCH1 signaling with human recombinant DLL4 led to FABP4 induction, independently of VEGFA)
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    elevation of circulating FABP4 may contribute to left ventricular (LV) diastolic dysfunction
    tumoral     --over  
    in bone metastasis samples from prostate cancer patients
    constitutional     --over  
    before the clinical onset of preeclampsia, and this increase occurs independently of maternal body mass index
    Susceptibility to type 2 diabetes, hypertriglyceridemia, and cardiovascular disease
    Variant & Polymorphism other T-87C polymorphism having lower serum triglyceride levels and significantly reduced risk for coronary heart disease and type 2 diabetes
    Candidate gene clinical biomarker for atherogenic dyslipidemia, independent of obesity and insulin resistance, in type 2 diabetic subjects
    Marker
  • significantly associated with ischemic stroke and may serve as a useful prognostic indicator for early mortality
  • may potentially serve as a novel biomarker for the prediction of gestational diabetes mellitus
  • FABP4 in leucocytes is a potential and easy accessible biomarker of atherosclerosis which could be of future clinical relevance
  • Therapy target
    SystemTypeDisorderPubmed
    diabete  
    neutralizing secreted FABP4 may represent an effective therapeutic strategy against diabetes
    ANIMAL & CELL MODELS
  • mice deficient for both FABP4 and FABP5 (FABP4/5 DKO mice) exhibited defective uptake of fatty acid (FA) with compensatory up-regulation of glucose consumption in these tissues during fasting