Navjotsingh Pabla

TL;DR: It is proposed that Cdkl5 is a stress-responsive kinase that promotes renal injury in part through phosphorylation-dependent suppression of pro-survival transcription regulator Sox9, and kinome-wide screening approaches reveal a pathogenic role of CDKL5 kinase in acute kidney injury, which is dependent on suppression of a SOX9-associated transcriptional network.

TL;DR: It is proposed that better experimental models are required to elucidate the differential contributions of various processes in intracellular drug accumulation and the role of membrane‐trafficking in drug transport remains underappreciated and unexplored.

TL;DR: It is reported that the VHL protein (pVHL) may be a substrate of Nek1, and non-phosphorylable pVHL reconstituted in VHL-deficient cells induces more stable cilia than wild-type VHL during serum stimulation and Nocodazole treatment.

TL;DR: It is reported that loss of Nek1 results in severe proliferation defect due to a delay in S-phase of the cell cycle, and Nek1 may facilitate S- phase progression by interacting with Ku80 and regulating chromatin loading of replication factors.

TL;DR: The role of Rb1 is delineated in AKI and the pharmacological basis of the renal protective effects of ribociclib during cisplatin nephrotoxicity is illustrated, which is likely dependent on the maintenance of R b1 in a hypo-phosphorylated and functionally active form under stress conditions.