Alok Jha

TL;DR: It is suggested that D PDG1s and DPDG2s developed disorganized actin cytoskeleton as a consequence of disrupted APOL1-miR193a axis, and docking and co-labeling studies suggested an interaction between AP OL1 and CD2AP.

TL;DR: In this paper, the role of K+ efflux in the activation of inflammasomes in APOL1 risk and non-risk milieus was investigated, where alterations in the structural configurations of channels and activation of nucleotide-binding domain were evaluated.

TL;DR: Docking, protein-protein interaction, and immunoprecipitation studies with anti-autophagy related gene (ATG) 14L, anti-UV radiation resistance-associated gene (UVRAG), or Rubicon antibodies suggested the formation of ATG14L complex I and UVRAG complex II in G0- podocytes and theformation of Rubicon complex III in G1- and G2-podocytes.

TL;DR: It is demonstrated that high glucose increases EDA2R expression in kidney cells and that Eda2R induces podocyte apoptosis and dedifferentiation in high glucose milieu partially through enhanced ROS generation.

TL;DR: Interactions between miR193a and YY1/WT1/Sox2/VDR/APOL1 3′ UTR region and transcription factors and their effects on podocytes’ molecular phenotype suggest that down-regulation of miR 193a could be used to enhance the expression of podocyte differentiating markers as a therapeutic strategy.