CDKAL1 dysfunction impairs lysine codon translation in podocytes and accelerates chronic kidney disease
Hiroko Nagata·Kazuhito Tomizawa·Fan‐Yan Wei·Ryosuke Yamamura·Sumio Ohtsuki·Hideaki Jinnouchi·Masataka Adachi·Hitoshi Nakazato·Korin Sakakida·yu nagayoshi·Takeshi Chujo·Hiroko Ijima·Hideki Yokoi·Koki Matsushita·Yuki Adachi·Yukie Takahashi·Kayo Nishiguchi·Takeshi Masuda·Takaichi Fukuda·Hitomi Kaneko·Kimitoshi Nakamura·Yutaka Kakizoe
Cdk5 regulatory subunit-associated protein 1-like 1 (Cdkal1) encodes a tRNA-modifying enzyme responsible for thiomethylation generating 2-methylthio-N<sup>6</sup>-threonylcarbamoyladenosine (ms<sup>2</sup>t<sup>6</sup>A) in the anticodon loop of tRNA<sup>Lys</sup><sub>UUU</sub>. Genome-wide association studies have identified CDKAL1 variants as risk factors for type 2 diabetes mellitus (DM) and chronic kidney disease (CKD), but whether CKD arises independently of diabetes has remained elusive. H