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The 159th RIKEN BRC SEMINAR

The Conventional and Non-conventional Roles of Protein N-α-acetyltransferase in Development and Obesity

The 159th RIKEN BRC SEMINAR
Poster(PDF)

Date

Jan 22(Wed.) 2020. 16:00 – 17:30(JST)

Place

Moriwaki Hall (BioResource Research Center Main Building 1F)

The invited lecturer

Dr. Chen-Cheng Lee
Genomics Research Center, Academia Sinica, Taiwan

Summary

Mammalian N-terminal acetyltransferases (Nats) cotranslationally acetylates N-termini (at the α amino group) of 80–90% of human proteins. Despite the prevalence, the biological functions of protein N-terminal acetylation and NATs are still largely unknown.

Importantly, mutation of N-α-acetyltransferase 10 protein (Naa10p) the catalytic subunit of NatA complex is linked to severe developmental defects including mental retardation and infancy death in the human Ogden syndrome. In contrast, overexpression of Naa10p facilitates DNA methyltransferase 1 (DNMT1) to methylate and shut down specific tumor suppressor genes, leading to lung tumorigenesis (J Clinc Invest, 2010).

In the past few years, we have been focusing on Naa10p for studying the biological functions of NatA using traditional and tissue-specific knockout (KO) mice. Here, I will present conventional and non-conventional functions of Naa10p to you by summarizing our previous and recent works. Our results not only link Naa10p mutationassociated human disease to defective DNA methylation and genomic imprinting (Molecular Cell, 2017), but also make inhibition of Naa10p enzymatic activity as a potential strategy for treating obesity (Molecular Cell, 2019; highlighted in Nat Struc Mol Biol).

Contact

Bioresource Engineering Division   
Atsuo Ogura atsuo.ogura@riken.jp

This seminar is intended for students and researchers/ engineers only.
If you are students/researchers outside RIKEN, please show your ID at the gate and get the permit for the entry.