D
Dominick G. A. Burton
Researcher at Weizmann Institute of Science
Publications - 19
Citations - 1654
Dominick G. A. Burton is an academic researcher from Weizmann Institute of Science. The author has contributed to research in topics: DNA damage & Senescence. The author has an hindex of 16, co-authored 19 publications receiving 1335 citations. Previous affiliations of Dominick G. A. Burton include University of Miami & University of Surrey.
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Journal ArticleDOI
NKG2D ligands mediate immunosurveillance of senescent cells
Adi Sagiv,Dominick G. A. Burton,Dominick G. A. Burton,Zhana Moshayev,Ezra Vadai,Felix M. Wensveen,Shifra Ben-Dor,Ofra Golani,Bojan Polić,Valery Krizhanovsky +9 more
TL;DR: The results provide new insights into the mechanisms regulating the expression of immune ligands in senescent cells and reveal the importance of NKG2D receptor-ligand interaction in protecting against liver fibrosis.
Journal ArticleDOI
Physiological and pathological consequences of cellular senescence
TL;DR: A perspective on the triggers, mechanisms and physiological as well as pathological consequences of senescent cells is provided.
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Cellular senescence: Immunosurveillance and future immunotherapy.
TL;DR: An overview of the research to date concerning senescence immunosurviellance is provided, including a focused discussion on the mechanisms by which macrophages may recognise senescent cells, and strategies as an alternative to senolytics for the removal ofsenescent cells are discussed.
Journal ArticleDOI
Cellular senescence, ageing and disease
TL;DR: Recent findings which suggest that cellular senescence does contribute to ageing and the development/progression of disease are discussed.
Journal ArticleDOI
Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence.
Priyamvada Rai,Jennifer J. Young,Jennifer J. Young,Dominick G. A. Burton,Maria G. Giribaldi,Tamer T. Onder,Tamer T. Onder,Robert A. Weinberg +7 more
TL;DR: It is demonstrated that overexpression of MTH1 can prevent the oncogenic H-RAS-induced DDR and attendant premature senescence, although it does not affect the observed elevation in ROS levels produced by RAS oncoprotein expression.