Keita Uchida

Oxidized EGCG redirects α-synuclein aggregation through shear-selected interactions

This study shows that oxidized EGCG, not unoxidized EGCG, binds α-synuclein, inhibits fibrillation, and remodels fibrils, with shear flow affecting these interactions.

ROR2 drives right ventricular heart failure via disruption of proteostasis

This study identifies ROR2 as a driver of right ventricular failure by disrupting proteostasis, showing that modulating ROR2 can rescue structural and functional deficits in cardiomyocytes.

Cardiac microtubules mediate transverse (t)-tubule growth and homeostasis

This study shows that cardiac microtubules regulate t-tubule formation and maintenance through BIN1-CLIP-170 and dynein mechanisms, impacting Ca handling and contractile function.

Translatable electrophysiological and behavioral abnormalities in a humanized model of SYNGAP1-disorder

The paper develops humanized mouse models for SYNGAP1 and STXBP1 disorders, showing similar electrophysiological and behavioral abnormalities in mice and patients, and demonstrates the efficacy of antisense oligonucleotides in modulating SYNGAP1 expression.

Dual Translational Control in Cardiomyocytes by Heterogeneous mTORC1 and Hypertrophic ERK Activation

This study identifies heterogeneous mTORC1 activity and a novel ERK-dependent pathway driving 4EBP1 phosphorylation in cardiomyocytes during hypertrophy, revealing dual translational control mechanisms.

Active transport of tRNAs facilitates distributed protein synthesis

This study identifies active transport of tRNAs via endolysosomal vesicles in large cells, showing that LeuRS facilitates this process and its disruption impairs protein synthesis and cell size.

Microtubule forces drive nuclear damage in LMNA cardiomyopathy

This study shows that microtubule forces, not the LINC complex, drive nuclear damage in LMNA cardiomyopathy and that disrupting microtubules can rescue cardiac function.

Transcriptional, post-transcriptional, and post-translational mechanisms rewrite the tubulin code during cardiac hypertrophy and failure

The paper investigates how the tubulin code is rewritten during cardiac hypertrophy and failure through transcriptional, autoregulatory, and post-translational mechanisms.