scholarly journals Fluorescently-labelled CPD and 6-4PP photolyases: new tools for live-cell DNA damage quantification and laser-assisted repair

2019 ◽  
Vol 47 (7) ◽  
pp. 3536-3549 ◽  
Author(s):  
Barbara Steurer ◽  
Yasemin Turkyilmaz ◽  
Marvin van Toorn ◽  
Wessel van Leeuwen ◽  
Paula Escudero-Ferruz ◽  
...  
Keyword(s):  
Dna Damage ◽  
Live Cell ◽  
Damage Quantification

Development of computational model for cell dose and DNA damage quantification of multicellular system

2019 ◽  
Vol 95 (11) ◽  
pp. 1484-1497 ◽  
Author(s):  
Ruirui Liu ◽  
Tianyu Zhao ◽  
Maciej H. Swat ◽  
Francisco J. Reynoso ◽  
Kathryn A. Higley
Keyword(s):  
Dna Damage ◽  
Computational Model ◽  
Cell Dose ◽  
Damage Quantification ◽  
Multicellular System

scholarly journals Photosensitized one-electron oxidation of DNA

2005 ◽  
Vol 77 (6) ◽  
pp. 963-975 ◽  
Author(s):  
Kiyohiko Kawai ◽  
Tetsuro Majima
Keyword(s):  
Dna Damage ◽  
High Performance ◽  
Transient Absorption ◽  
Basic Mechanism ◽  
Absorption Measurement ◽  
Mechanistic Study ◽  
Hole Transfer ◽  
Damage Quantification ◽  
Oxidation Of Dna ◽  
Kinetics Of

Photosensitized one-electron oxidation of DNA has attracted much interest because it causes oxidative damage which leads to mutation, and because it is involved in the basic mechanism of photodynamic therapy. In the present article, we describe the mechanistic study of photosensitized DNA damage, especially addressing the kinetics of hole transfer by adenine(A)-hopping and its effect on the DNA damage. The combination of the transient absorption measurement and DNA damage quantification by high-performance liquid chromatography clearly demonstrate that the yield of the DNA damage correlates well with the lifetime of the charge-separated state caused by A-hopping, showing that hole transfer helps DNA damage. These findings led us to propose a new method to accomplish the efficient DNA damage using a combination of two-color, two-laser irradiation.

scholarly journals LORD-Q: a long-run real-time PCR-based DNA-damage quantification method for nuclear and mitochondrial genome analysis

2013 ◽  
Vol 42 (6) ◽  
pp. e41-e41 ◽  
Author(s):  
Simon Lehle ◽  
Dominic G. Hildebrand ◽  
Britta Merz ◽  
Peter N. Malak ◽  
Michael S. Becker ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Genome ◽  
Real Time ◽  
Genome Analysis ◽  
Real Time Pcr ◽  
Quantification Method ◽  
Damage Quantification ◽  
Long Run

scholarly journals Simultaneous quantification of DNA damage and mitochondrial copy number by long-run DNA-damage quantification (LORD-Q)

Oncotarget ◽  
2017 ◽  
Vol 8 (68) ◽  
pp. 112417-112425 ◽  
Author(s):  
Benjamin Dannenmann ◽  
Simon Lehle ◽  
Sebastian Lorscheid ◽  
Stephan M. Huber ◽  
Frank Essmann ◽  
...  
Keyword(s):  
Dna Damage ◽  
Copy Number ◽  
Simultaneous Quantification ◽  
Damage Quantification ◽  
Long Run ◽  
Mitochondrial Copy Number

scholarly journals Persistence and Dynamics of DNA Damage Signal Amplification Determined by Microcolony Formation and Live-cell Imaging

2011 ◽  
Vol 52 (6) ◽  
pp. 766-774 ◽  
Author(s):  
Yasuyoshi OKA ◽  
Motohiro YAMAUCHI ◽  
Masatoshi SUZUKI ◽  
Shunichi YAMASHITA ◽  
Keiji SUZUKI
Keyword(s):  
Dna Damage ◽  
Signal Amplification ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Live Cell

scholarly journals Micropatterned comet assay enables high throughput and sensitive DNA damage quantification

Mutagenesis ◽  
2014 ◽  
Vol 30 (1) ◽  
pp. 11-19 ◽  
Author(s):  
J. Ge ◽  
D. N. Chow ◽  
J. L. Fessler ◽  
D. M. Weingeist ◽  
D. K. Wood ◽  
...  
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
High Throughput ◽  
Damage Quantification

CBIO-17. A NOVEL ROLE FOR ATR KINASE DETERMINES GLIOBLASTOMA TUMOUR CELL INVASION

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi30-vi30
Author(s):  
ross carruthers ◽  
Sarah Derby ◽  
Karen Strathdee ◽  
Anthony Chalmers ◽  
Jim Norman ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Live Cell ◽  
Tumour Cell Invasion ◽  
Atr Kinase

Abstract BACKGROUND: Widespread contamination of the brain with malignant cells is a predominant feature of glioblastoma (GBM) and fatal brainstem infiltration is frequently observed at autopsy. Whilst radiotherapy improves survival, irradiation increases GBM cell invasion, resulting in sublethal dose to cells migrating outside the irradiated volume. Tumour cell invasion should be a therapeutic priority if survival is to be improved. The responsible molecular mechanisms are key to improving outcomes but remain enigmatic. Ataxia telangiectasia and rad3-related (ATR) is a DNA damage response (DDR) kinase involved in DNA replication stress (RS) response and is an established therapeutic target for GBM. In this study we demonstrate a novel role for ATR kinase in facilitating malignant cell invasion. METHODS AND RESULTS: Invading margins of human GBM samples demonstrated increased pATR expression relative to core. Live cell imaging demonstrated a reduction in cell velocity following ATR inhibition (ATRi; VE822) or ATR siRNA, and a retraction defect was evident in vitro. Extensive cytoplasmic vacuolation occurred following ATRi or siRNA which were single walled structures on electron microscopy which could engulf high molecular weight dextran, suggesting blockade of macropinosome processing. Live cell imaging with GFP-integrin α5 and integrin recycling assays showed integrin sequestration within macropinosomes and reduced integrin internalisation respectively. Interrogation of a published ‘ATR interactome’ revealed ATR targets with functions in endocytic vesicle trafficking. Intravital in vivo imaging of murine xenograft tumours confirmed vacuolation and dextran uptake following ATRi, whilst a further study demonstrated reduced invading tumour cells following ATRi in intracranial xenografts. CONCLUSION: We demonstrate a novel role for ATR in facilitating macropinocytic vesicle trafficking and integrin internalisation. ATRi results in a profound motility defect in vitro and in vivo. ATR inhibitors are entering early phase trials as radiation sensitisers and we propose that therapeutic benefit will extend beyond DNA damage potentiation.

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