Flk1null

Flk1null refers to an organism or cell line carrying a null mutation of the Flk1 gene, also known as Vegfr2 or Kdr in mice. Flk1 encodes a receptor tyrosine kinase that binds vascular endothelial growth factor (VEGF) and mediates signaling essential for blood vessel formation. In mice, Flk1 is often described as Flk1/VEGFR2 and is expressed in mesodermal progenitors that give rise to endothelial cells and vascular structures.

In development, Flk1 signaling promotes endothelial differentiation, proliferation, and survival, guiding the formation of the primitive vascular network and the developing circulatory system. The Flk1 pathway acts early in vasculogenesis and contributes to later angiogenic processes that shape the established vasculature.

Flk1null embryos exhibit early embryonic lethality due to severe vascular defects. They typically die around embryonic day 8.5 (E8.5) because the yolk sac vessels fail to form a functional network, and the embryo cannot sustain proper circulation. Associated defects include disorganized yolk sac vasculature and impaired formation of major vascular beds, reflecting the indispensable role of VEGF–Flk1 signaling in early vascular development and hematopoiesis.

Because Flk1 is essential for early vascular development, Flk1null alleles are usually studied with conditional knockout approaches or in combination with other genetic backgrounds to explore later roles in angiogenesis, tissue regeneration, or disease models. Flk1/VEGFR2 remains a central focus in vascular biology and in therapeutic strategies targeting pathological angiogenesis.