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Symbol FLT1 contributors: mct - updated : 21-09-2016
HGNC name fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability factor receptor)
HGNC id 3763
corresponding disease(s)
Other morbid association(s)
TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
constitutional     --low  
in hemangioma endothelial cells, resulting in VEGF-dependent activation of KDR and downstream signaling pathways
constitutional     --over  
in placentas of preeclampsia and HELLP syndrome
constitutional     --over  
higher expression in severe preeclampsia or eclampsia than in normal pregnancy
constitutional     --over  
in coronary artery disease where cardiac tissue has been subjected to prolonged or chronic hypoxia, increased VEGFR1, thus selecting for non-ischemic in endothelial cells in promoting pro-angiogenic responses including nitric oxide production
constitutional     --low  
loss of expression of FLT1, moderate expression of KDR and high concentration of nitrate associated with aneurysm formation
constitutional     --over  
concentration of FLT1 in severe preeclampsia is higher compared with normal pregnancy
constitutional     --over  
contributes to endothelial injury in in IgA nephropathy (IgAN)
constitutional     --low  
decreased expression of FLT1 in decidua and weaker VEGFA and KDR expression in placental villi and decidua may be associated with early pregnancy loss
constitutional     --low  
decreased significantly in serum of patients with ALS
Variant & Polymorphism
Candidate gene
  • with PLGF, is an effective biomarker in predicting PE (preeclampsia) during the second trimester, before the clinical onset of PE
  • sFLT1 levels may be an effective biomarker to predict the progression of heart failure in patients with coronary artery disease (CAD)
  • elevated levels of FLT1 are associated with adverse outcomes in stable patients with heart failure
  • FLT1 mRNA expression in maternal blood can be used as a marker to predict the development of fetal growth restriction (FGR), long before a clinical diagnosis is made
  • molecular detection of MAML2 rearrangement combined with FLT1 may be of important clinical value for Primary pulmonary mucoepidermoid carcinoma (PMEC)
  • Therapy target
  • in treating neovascular diseases
  • SystemTypeDisorderPubmed
    potential therapy target in conditions where inducing angiogenesis might be benficial (preeclampsia, wound healing, strocke and heart disease)
    therapeutic potential for FLT1-modifying drugs in cancer pain
    disrupting PGF/FLT1 pathway could modulate endothelial-colony-forming cells (ECFCs)-induced tubulogenesis, the cell type responsible for newly formed vessels
  • Flk1 disrupted transgenic mice
  • mdx:Flt-1(+/-) adult mice display a developmentally increased vascular density in skeletal muscle compared with the wild-type and mdx mice (mdx:utrophin(-/-):Flt-1(+/-) mice display improved muscle histology and significantly higher survival rates compared with the mdx:utrophin(-/-) mice, which show more severe muscle phenotypes than the mdx mice)
  • loss of normal foot process structure in mice lacking Flt1 results in massive protein leakage into the urine due to disruption of the glomerular permeability barrier, resulting eventually in kidney failure