Cancer is the most leading cause of deaths worldwide. Despite present understanding and experimental advancements, the morbidity and mortality still remain high. Dok2 have been visualized as a key player in multiple biological processes as inflammation, differentiation, cellular migration and even as an important marker for tumor progression. Recent reports have vividly discussed the regulatory aspects and prognostic aspects of Dok2. Here, we sought to summarize the recent shreds of evidence of Dok2 involvement in carcinogenesis. Dok2 represents an attractive marker for cancer progression and represents a valuable therapeutic target.

Glomerular filtration apparatus (GFA) regulates the glomerular permselectivity and ultrafiltration of urine. Podocytes are specialized cells and a key component of the GFA. The mechanism by which the integrity of the GFA is compromised and manifest in proteinuria during ischemic stroke remains enigmatic. Hypoxia is a determining factor in the pathophysiology of ischemia. We investigated the mechanism of ischemic-hypoxia induced proteinuria in a middle cerebral artery occlusion (MCAO) model. Ischemic hypoxia resulted in the accumulation of HIF1α in the glomerular podocytes that resulted in the increased expression of ZEB2. ZEB2, in turn, induced TRPC6 (transient receptor potential cation channel, subfamily C, member 6), which has increased selectivity for calcium.Elevated expression of TRPC6 elicited increased calcium influx and aberrant activation of focal adhesion kinase (FAK) in podocytes. FAK activation resulted in the stress fibers reorganization and podocyte foot process effacement. Our study suggests overactive HIF1α/ZEB2 axis during ischemichypoxia induces intracellular calcium levels via TRPC6 and consequently altered podocyte integrity and permselectivity.3 Introduction: