Tsutomu Suzuki

Professor

University of Tokyo

Japan

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Tsutomu Suzuki is a Professor at the University of Tokyo, specializing in the biogenesis and modification of tRNA and its implications for human health and diseases. His recent research includes examining the mechanisms of initiator tRNA selection and mitochondrial mRNA translation, as well as studying the effects of post-transcriptional modifications on mitochondrial pathology. He also investigates the structural characteristics of tRNAs and their interactions within translation systems.

Articles (20)

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2025

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2021

Collaborators (16)

Kenjyo Miyauchi

The Univeristy of Tokyo

JAPAN

Tsutomu Suzuki

Research Interests

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Articles (20)

Biogenesis and roles of tRNA queuosine modification and its glycosylated derivatives in human health and diseases

Selection of initiator tRNA and start codon by mammalian mitochondrial initiation factor 3 in leaderless mRNA translation

An anticodon-sensing T-boxzyme generates the elongator nonproteinogenic aminoacyl-tRNA in situ of a custom-made translation system for incorporation

Functional redundancy of ubiquitin-like sulfur-carrier proteins facilitates flexible, efficient sulfur utilization in the primordial archaeon Thermococcus kodakarensis

Near-identical macromolecules spontaneously partition into concentric circles

Toxic Small Alarmone Synthetase FaRel2 inhibits translation by pyrophosphorylating tRNAGly and tRNAThr

Post-transcriptional methylation of mitochondrial-tRNA differentially contributes to mitochondrial pathology

Human DUS1L catalyzes dihydrouridine modification at tRNA positions 16/17, and DUS1L overexpression perturbs translation

Substrate specificity of Mycobacterium tuberculosis tRNA terminal nucleotidyltransferase toxin MenT3

Structural insights into the decoding capability of isoleucine tRNAs with lysidine and agmatidine

Mitochondrial haplotype mutation alleviates respiratory defect of MELAS by restoring taurine modification in tRNA with 3243A &gt; G mutation

Restoration of mitochondrial function through activation of hypomodified tRNAs with pathogenic mutations associated with mitochondrial diseases

Mechanistic insights into tRNA cleavage by a contact-dependent growth inhibitor protein and translation factors

Regulation of A-to-I RNA editing and stop codon recoding to control selenoprotein expression during skeletal myogenesis

m 6 A modification of HSATIII lncRNAs regulates temperature‐dependent splicing

m 6 A‐mediated alternative splicing coupled with nonsense‐mediated mRNA decay regulates SAM synthetase homeostasis

The expanding world of tRNA modifications and their disease relevance

A single m6A modification in U6 snRNA diversifies exon sequence at the 5’ splice site

Loss of Ftsj1 perturbs codon-specific translation efficiency in the brain and is associated with X-linked intellectual disability

N6-methyladenosine (m6A) is an endogenous A3 adenosine receptor ligand

Collaborators (16)

Kenjyo Miyauchi

Takeshi Uchiumi

Tetsuro Hirose

Fumiki Katsuoka

kensuke ishiguro

Joseph A Piccirilli

Hiroaki Suga

Kozo Tomita

Shinichiro Akichika

Miho Yanagisawa

Becky Carlyle

Shinsuke Fujiwara

Fan-Yan Wei

Sharmin Hasan

Yutaka Suzuki

Shintaro Iwasaki

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Mitochondrial haplotype mutation alleviates respiratory defect of MELAS by restoring taurine modification in tRNA with 3243A > G mutation