FLT4

(redirected from VEGFR3)

FLT4

A gene on chromosome 5q35.3 that encodes a tyrosine kinase receptor for vascular endothelial growth factors (VEGF) C and D, which appear to play a role in lymphangiogenesis and maintenance of the lymphatic endothelium.

Molecular pathology
FLT4 mutations cause hereditary lymphedema type IA.
References in periodicals archive ?
Discovered and developed in house by Eisai, LENVIMA is an orally administered kinase inhibitor with a novel binding mode that selectively inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors (VEGFR1, VEGFR2 and VEGFR3) and fibroblast growth factor (FGF) receptors (FGFR1, FGFR2, FGFR3 and FGFR4) in addition to other pathway-related RTKs (including the platelet-derived growth factor (PDGF) receptor PDGFRalpha; KIT; and RET) involved in tumor angiogenesis, tumor progression and modification of tumor immunity.
Lenvima, discovered and developed by Eisai, is a kinase inhibitor that inhibits the kinase activities of vascular endothelial growth factor receptors VEGFR1, VEGFR2, and VEGFR3.
LENVIMA is a kinase inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR) and VEGFR3 (FLT4).
NK cell depletion in a transgenic model reduced macrophage numbers in the cornea as well as mRNA expression of VEGF-A, VEGF-C, and VEGFR3 while in a laser-induced corneal neovascularisation model, NK cell depletion leads to a reduction of neovascularisation while significantly downregulating IFN-[gamma] and VEGFs in the choroid [92].
Anti-VEGF-A treatment reduced both blood and lymphatic vascular densities, decreased VEGFR3 expression in LECs [106], and reduced metastasis in a breast cancer model [109].
Schulte et al., "Ccbe1 regulates Vegfc-mediated induction of Vegfr3 signaling during embryonic lymphangiogenesis," Development, vol.
(8) Coamplification of the FMS-like tyrosine kinase 4 (FLT4) gene encoding the vascular endothelial growth factor receptor 3 (VEGFR3), in association with MYC amplification, was found by Guo et al (10) in 25% of secondary angiosarcomas but not in other radiation-associated, atypical vascular lesions.
Correlations between absorbances associated with the serum levels of autoantibodies to VEGFR3 from the indirect ELISA and AST (Figure 2(a)), ALT (Figure 2(b)), TB (Figure 2(c)), and the relative fibrotic area (Figure 2(d)) were performed.
Congenital Hereditary Lymphedema Caused by a Mutation That Inactivates VEGFR3 Tyrosine Kinase.
Fruquintinib is designed to selectively inhibit VEGF receptors, namely VEGFR1, VEGFR2 and VEGFR3. Angiogenesis is an important mechanism in tumour pathogenesis, and inhibition of VEGF- mediated angiogenesis has been important in the treatment of a variety of cancers.