J
Jie Qi
Researcher at Scripps Research Institute
Publications - 11
Citations - 369
Jie Qi is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Senescence & Zebrafish. The author has an hindex of 8, co-authored 9 publications receiving 321 citations. Previous affiliations of Jie Qi include Chinese Ministry of Education & Harvard University.
Papers
More filters
Journal ArticleDOI
The identification of zebrafish mutants showing alterations in senescence-associated biomarkers.
Shuji Kishi,Peter E. Bayliss,Junzo Uchiyama,Eriko Koshimizu,Eriko Koshimizu,Jie Qi,Jie Qi,Puru Nanjappa,Shintaro Imamura,Asiful Islam,Donna Neuberg,Adam Amsterdam,Thomas M. Roberts +12 more
TL;DR: In this article, the same authors used the same SA-β-gal assay to screen chemically mutagenized zebrafish, each of which was heterozygous for lesions in multiple genes, under the sensitizing conditions of oxidative stress.
Journal ArticleDOI
Embryonic Senescence and Laminopathies in a Progeroid Zebrafish Model
Eriko Koshimizu,Shintaro Imamura,Jie Qi,Jie Qi,Jamal Toure,Delgado M. Valdez,Christopher E. Carr,Jun-ichi Hanai,Shuji Kishi,Shuji Kishi +9 more
TL;DR: New zebrafish models for a human premature aging disorder are generated and the utility for studying laminopathies is demonstrated, which may provide a new platform for future drug screening as well as genetic analyses aimed at identifying modifier genes that influence not only progeria and laminationopathies but also other age-associated human diseases common in vertebrates.
Journal ArticleDOI
Aberrant Autolysosomal Regulation Is Linked to The Induction of Embryonic Senescence: Differential Roles of Beclin 1 and p53 in Vertebrate Spns1 Deficiency
Tomoyuki Sasaki,Shanshan Lian,Jie Qi,Peter E. Bayliss,Christopher E. Carr,Jennifer L. Johnson,Sujay Guha,Patrick Kobler,Sergio D. Catz,Matthew S. Gill,Kailiang Jia,Daniel J. Klionsky,Shuji Kishi +12 more
TL;DR: Evidence is provided that Spns1 operates during autophagy and senescence differentially with Beclin 1 and p53, and a chemical and genetic blockage of lysosomal acidification and biogenesis mediated by the vacuolar-type H+-ATPase prevents the appearance of the hallmarks caused by the Spns 1 deficiency, irrespective of the basal p53 state.
Journal ArticleDOI
Inhibitory effect of Lycium barbarum polysaccharides on cell apoptosis and senescence is potentially mediated by the p53 signaling pathway
TL;DR: The results demonstrated that the effects of LBPs on cell apoptosis and aging might be mediated by the p53-mediated pathway.
Aberrant Autolysosomal Regulation Is Linked to The Induction of Embryonic Senescence: Differential Roles of Beclin 1 and p53 in Vertebrate Spns1 Deficiency
Tomoyuki Sasaki,Shanshan Lian,Jie Qi,Peter E. Bayliss,Christopher E. Carr,Jennifer L. Johnson,Sujay Guha,Patrick Kobler,Sergio D. Catz,Matthew S. Gill,Kailiang Jia,Daniel J. Klionsky,Shuji Kishi +12 more
TL;DR: In this article, the authors used zebrafish as a genetic model to investigate the role of Spin homolog 1 (Spns1) deficiency in the development of senescence and accelerated aging.