T
Tokio Sano
Researcher at Scripps Research Institute
Publications - 4
Citations - 1709
Tokio Sano is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: DNA damage & Senescence. The author has an hindex of 3, co-authored 4 publications receiving 1008 citations. Previous affiliations of Tokio Sano include Scripps Health.
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Journal ArticleDOI
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs
Yi-Yi Zhu,Tamara Tchkonia,Tamar Pirtskhalava,Adam C. Gower,Husheng Ding,Nino Giorgadze,Allyson K. Palmer,Yuji Ikeno,Yuji Ikeno,Gene B. Hubbard,Gene B. Hubbard,Marc E. Lenburg,Steven P. O'Hara,Nicholas F. LaRusso,Jordan D. Miller,Carolyn M Roos,Grace C Verzosa,Nathan K. LeBrasseur,Jonathan D. Wren,Joshua N. Farr,Sundeep Khosla,Michael B. Stout,Sara J. McGowan,Heike Fuhrmann-Stroissnigg,Aditi U. Gurkar,Jing-jing Zhao,Debora Colangelo,Akaitz Dorronsoro,Yuan Yuan Ling,Amira S. Barghouthy,Diana C. Navarro,Tokio Sano,Paul D. Robbins,Laura J. Niedernhofer,James L. Kirkland +34 more
TL;DR: The results demonstrate the feasibility of selectively ablating senescent cells and the efficacy of senolytics for alleviating symptoms of frailty and extending healthspan.
Journal ArticleDOI
An aged immune system drives senescence and ageing of solid organs.
Matthew J. Yousefzadeh,Rafael R. Flores,Yi Zhu,Zoe C. Schmiechen,Robert W. Brooks,Christy E. Trussoni,Yuxiang Cui,Luise A. Angelini,Kyoo a. Lee,Sara J. McGowan,Adam L. Burrack,Dong Wang,Qing Dong,Aiping Lu,Tokio Sano,Ryan D. O’Kelly,Collin A. McGuckian,Jonathan I. Kato,Michael P. Bank,Erin A. Wade,Smitha P. S. Pillai,Jenna Klug,Warren C. Ladiges,Christin E. Burd,Sara E. Lewis,Nicholas F. LaRusso,Nam Vo,Yinsheng Wang,Eric E. Kelley,Johnny Huard,Ingunn M. Stromnes,Paul D. Robbins,Laura J. Niedernhofer +32 more
TL;DR: In this paper, the contribution of immune system ageing to organism ageing was defined by selectively deleting Ercc1, which encodes a crucial DNA repair protein, in mouse haematopoietic cells to increase the burden of endogenous DNA damage and thereby senescence.
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ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging.
Jing Zhao,Jing Zhao,Jing Zhao,Lei Zhang,Lei Zhang,Aiping Lu,Yingchao Han,Debora Colangelo,Debora Colangelo,Christina Bukata,Alex C. Scibetta,Matthew J. Yousefzadeh,Matthew J. Yousefzadeh,Xuesen Li,Aditi U. Gurkar,Sara J. McGowan,Sara J. McGowan,Luise Angelini,Luise Angelini,Ryan D. O’Kelly,Ryan D. O’Kelly,Hongshuai Li,Lana Corbo,Tokio Sano,Heather Nick,Enrico Pola,Smitha P.S. Pilla,Warren C. Ladiges,Nam Vo,Johnny Huard,Laura J. Niedernhofer,Laura J. Niedernhofer,Paul D. Robbins,Paul D. Robbins +33 more
TL;DR: It is demonstrated that the ATM kinase is a major mediator of DNA damage-induced, NF-κB-mediated cellular senescence, stem cell dysfunction and aging and thus represents a therapeutic target to slow the progression of aging.
Journal ArticleDOI
Increased insulin sensitivity and diminished pancreatic beta-cell function in DNA repair deficient Ercc1 d/- mice
Ana P. Huerta Guevara,Sara J. McGowan,Melissa Kazantzis,Tania Rozgaja Stallons,Tokio Sano,Niels L. Mulder,Angelika Jurdzinski,Theo H. van Dijk,Bart J. L. Eggen,Johan W. Jonker,Laura J. Niedernhofer,Janine K. Kruit +11 more
TL;DR: In this article, the authors used mice deficient for the DNA excision-repair gene Ercc1 to study the impact of persistent endogenous DNA damage accumulation on energy metabolism, glucose homeostasis and beta-cell function.