Flt1

**FLT1 (Fms-like tyrosine kinase 1)**

FLT1, or Fms-like tyrosine kinase 1, is a receptor tyrosine kinase encoded by the *VEGFR1* gene, located on the short arm of chromosome 13 in humans. It belongs to the vascular endothelial growth factor (VEGF) receptor family and plays a critical role in vascular development, angiogenesis, and hematopoiesis. FLT1 is primarily expressed on endothelial cells, monocytes, and certain immune cells, though its function varies depending on its ligand binding state.

FLT1 functions as a decoy receptor for VEGF-A, binding to it without activating downstream signaling pathways. This binding inhibits the pro-angiogenic effects of VEGF-A by preventing it from interacting with more active VEGF receptor 2 (VEGFR2). As a result, FLT1 modulates vascular permeability, immune cell migration, and placental development. In contrast, when FLT1 lacks VEGF-A binding, it can signal through alternative pathways, influencing cell survival and inflammation.

FLT1 is also involved in the regulation of hematopoietic stem cells and the response to hypoxia. Dysregulation of FLT1 has been implicated in various pathological conditions, including placental insufficiency during pregnancy, certain cancers (such as breast and ovarian cancer), and chronic inflammatory diseases. Additionally, FLT1 has been explored as a potential therapeutic target in conditions where excessive angiogenesis is detrimental, such as in certain types of tumors.

Research into FLT1 continues to expand, particularly in understanding its role in disease mechanisms and developing targeted therapies. Its dual role as both a signaling receptor and a VEGF-A trap makes it a key focus in vascular biology and therapeutic interventions.