COTL1 Antibody

During the development of the mammalian cortex, neurons generated by neuronal progenitors migrate to reach their final destinations in the cortical plate. This migration is regulated by filamentous-actin (F-actin), and Cotl1 modulates F-actin dynamics . Cotl1 binds to F-actin and inhibits the de-polymerization of Cofilin-mediated F-actin . Mutations in Cotl1, such as Lys 75 and Arg 73, can significantly impact its ability to bind F-actin . Overexpression of Cotl1 has been shown to inhibit neuronal migration and increase the length of neuronal leading processes .

Cotl1 also plays a significant role in platelet biology. It integrates signaling critical for shear-dependent thrombus formation in mouse platelets . Cotl1 deficiency in platelets affects their aggregate formation on collagen and adhesion to immobilized von Willebrand factor at high shear rates . This deficiency also impacts the biomechanical properties of platelets, leading to increased deformability at high shear rates . Additionally, Cotl1 is involved in the biosynthesis of pro-inflammatory leukotrienes (LT) in granulocytes .

Research on Cotl1 has provided valuable insights into its role in various cellular processes. For instance, studies have shown that overexpression of Cotl1 can inhibit the proliferation and mitotic activity of neuronal progenitors . In the context of platelet function, Cotl1 deficiency has been linked to prolonged tail bleeding times and protection from occlusive arterial thrombus formation .