KDR

(redirected from Flk-1)
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KDR

A gene on chromosome 4q11-q12 that encodes a vascular endothelial growth factor receptor known as kinase insert domain receptor, which is a type-III receptor tyrosine kinase. KDR is the main mediator of VEGF-induced endothelial proliferation, survival, migration, tubular morphogenesis and sprouting.

Molecular pathology
KDR mutations have been linked to infantile capillary haemangiomas.
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Semiquantification of CREB and Flk-1 by immunofluorescence was conducted with ImageJ (version 1.50i software; ImageJ, National Institutes of Health, Bethesda, MD, USA).
The aim of this study was to investigate the expression pattern of VEGF and flk-1 in three components (luminal epithelium, glandular epithelium and stroma) of human endometrium during different phases of menstrual cycle using tissue microarray (TMA) analysis.
VEGF binds two highly related receptor tyrosine kinases, Fit-1 and Flk-1. Flt1 expression is up-regulated by hypoxia.
Chappell et al., "The VEGF receptor Flt-1 spatially modulates Flk-1 signaling and blood vessel branching," Journal of Cell Biology, vol.
EPC levels in the blood were measured by counting events positive for endothelial (Flk-1) and stem cell (Sca-1) antigens using flow cytometry (Figure 2A).
Foetal liver kinase 1 (FLK-1) (also known as KDR) is an RTK that has been identified in primitive and more mature haematopoietic cells as well as in a wide variety of nonhaematopoietic tissues [24].
Higher expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 (Flk-1) and metalloproteinase-9 (MMP-9) in a rat model of peritoneal endometriosis is similar to cancer diseases.
The growth of new blood vessels can be stimulated by cascades of events within the cell - known as pathways - the most notable of which centers around the three proteins Flt-1, Flk-1 and VEGF.
Expression of vascular endothelial growth factor and Flk-1 in developing and glucocorticoid-treated mouse lung.
Flk-1 is one of the VEGF receptors, a main mediator of the angiogenic and permeability-enhancing effects of VEGF, and is activated in a phosphorylated form (17).
Additionally, mesoderm (FLK-1) and hemangioblast marker (FLK-1/VE-Cad) were analyzed by flow cytometry.