The 159th RIKEN BRC SEMINARBRC SEMINAR 2020年1月22日（水） 16:00～17:30...
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Mammalian N-terminal acetyltransferases (Nats) cotranslationally acetylates N-termini (at the α amino group) of 80~90% of human proteins. Despite the prevalence, the bio- logical functions of protein N-terminal acetylation and NATs are still largely unknown. Importantly, mutation of N-α-acetyltransferase 10 protein (Naa10p) the catalytic sub- unit of NatA complex is linked to severe developmental defects including mental retar- dation 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 summariz- ing our previous and recent works. Our results not only link Naa10p mutation- associated human disease to defective DNA methylation and genomic imprinting 当セミナーは、学生、研究者、技術者を対象としたものです。 理化学研究所以外からご参加の方は、所属する大学または 研究機関が発行する身分証をご持参になり、守衛所にて 入構証をお受け取りください。 The 159th RIKEN BRC SEMINAR 2020年1月22日 （水）16:00～17:30 バイオリソース研究センター BRC棟１階 森脇和郎ホール 連絡先：遺伝工学基盤技術室 小倉 淳郎 [email protected] Dr. Chen-Cheng Lee Genomics Research Center, Academia Sinica, Taiwan The Conventional and Non-conventional Roles of Protein N-α-acetyltransferase in Development and Obesity (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).
Transcript of The 159th RIKEN BRC SEMINARBRC SEMINAR 2020年1月22日（水） 16:00～17:30...
Mammalian N-terminal acetyltransferases (Nats) cotranslationally acetylates N-termini (at the α amino group) of 80~90% of human proteins. Despite the prevalence, the bio-logical functions of protein N-terminal acetylation and NATs are still largely unknown. Importantly, mutation of N-α-acetyltransferase 10 protein (Naa10p) the catalytic sub-unit of NatA complex is linked to severe developmental defects including mental retar-dation 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 summariz-ing our previous and recent works. Our results not only link Naa10p mutation-associated human disease to defective DNA methylation and genomic imprinting
当セミナーは、学生、研究者、技術者を対象としたものです。理化学研究所以外からご参加の方は、所属する大学または研究機関が発行する身分証をご持参になり、守衛所にて入構証をお受け取りください。
The 159th RIKENBRC SEMINAR
2020年1月22日 （水）16:00～17:30バイオリソース研究センター BRC棟１階 森脇和郎ホール
連絡先：遺伝工学基盤技術室 小倉 淳郎 [email protected]
Dr. Chen-Cheng LeeGenomics Research Center, Academia Sinica, Taiwan
The Conventional and Non-conventional Rolesof Protein N-α-acetyltransferasein Development and Obesity
(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).
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