scispace - formally typeset
M

Masataka Sugimoto

Researcher at Nagoya University

Publications -  37
Citations -  2314

Masataka Sugimoto is an academic researcher from Nagoya University. The author has contributed to research in topics: Senescence & Small hairpin RNA. The author has an hindex of 17, co-authored 36 publications receiving 2053 citations. Previous affiliations of Masataka Sugimoto include University of Tsukuba & St. Jude Children's Research Hospital.

Papers
More filters
Journal ArticleDOI

Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence.

TL;DR: A role is demonstrated for the Ets1 and Ets2 transcription factors based on their ability to activate the p16INK4a promoter through an ETS-binding site and their patterns of expression during the lifespan of human diploid fibroblasts.
Journal ArticleDOI

Physical and Functional Interactions of the Arf Tumor Suppressor Protein with Nucleophosmin/B23.

TL;DR: Using tandem-affinity-tagged p19Arf, Arf-associated proteins from mouse NIH 3T3 fibroblasts undergoing cell cycle arrest were purified and linked to nucleolar and ribosomal proteins, including nucleophosmin/B23 (NPM), a protein thought to foster the maturation of preribosomal particles.
Journal ArticleDOI

Nucleolar Arf Tumor Suppressor Inhibits Ribosomal RNA Processing

TL;DR: It is shown that p19(Arf) inhibits production of ribosomal RNA, retarding processing of 47/45S and 32S precursors and preventing the proliferation of cells lacking Mdm2 and p53, albeit less efficiently.
Journal ArticleDOI

Senolysis by glutaminolysis inhibition ameliorates various age-associated disorders.

TL;DR: In this article, the authors identified glutaminase 1 (GLS1) as an essential gene for the survival of human senescent cells and showed that inhibition of GLS1-dependent glutaminolysis in aged mice eliminated the cells specifically and ameliorated age-associated organ dysfunction.
Journal ArticleDOI

Elimination of p19 ARF -expressing cells enhances pulmonary function in mice

TL;DR: It is demonstrated that pulmonary function in 12-month-old mice was reversibly restored by the elimination of p19ARF-expressing cells, indicating that the aging-associated decline in lung function was, at least partly, attributed to p19arF and was recovered by eliminating p19 ARF- expressing cells.