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Loss of lamin B receptor is necessary to induce cellular senescence

Biochemical journal, 2017-01, Vol.474 (2), p.281-300

2017

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Two New Faces of Amifostine: Protector from DNA Damage in Normal Cells and Inhibitor of DNA Repair in Cancer Cells

Journal of medicinal chemistry, 2016-04, Vol.59 (7), p.3003-3017

2016

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Changes in Cryopreserved Cell Nuclei Serve as Indicators of Processes during Freezing and Thawing

Langmuir, 2019-06, Vol.35 (23), p.7496-7508

2019

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Chromatin architecture changes and DNA replication fork collapse are critical features in cryopreserved cells that are differentially controlled by cryoprotectants

Scientific reports, 2018-10, Vol.8 (1), p.14694-18, Article 14694

2018

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HMGB1 and HMGB2 Cell-specifically Down-regulate the p53- and p73-dependent Sequence-specific Transactivation from the Human Bax Gene Promoter

The Journal of biological chemistry, 2002-03, Vol.277 (9), p.7157-7164

2002

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Incorporation of Low Concentrations of Gold Nanoparticles: Complex Effects on Radiation Response and Fate of Cancer Cells

Pharmaceutics, 2022-01, Vol.14 (1), p.166

2022

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Recruitment of 53BP1 Proteins for DNA Repair and Persistence of Repair Clusters Differ for Cell Types as Detected by Single Molecule Localization Microscopy

International journal of molecular sciences, 2018-11, Vol.19 (12), p.3713

2018

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Distinct cellular responses to replication stress leading to apoptosis or senescence

FEBS open bio, 2019-05, Vol.9 (5), p.870-890

2019

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Granulocyte maturation determines ability to release chromatin NETs and loss of DNA damage response; these properties are absent in immature AML granulocytes

Biochimica et biophysica acta, 2013-03, Vol.1833 (3), p.767-779

2013

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Heterochromatinization associated with cell differentiation as a model to study DNA double strand break induction and repair in the context of higher-order chromatin structure

Applied radiation and isotopes, 2014-01, Vol.83, p.177-185

2014

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Function of chromatin structure and dynamics in DNA damage, repair and misrepair: γ-rays and protons in action

Applied radiation and isotopes, 2014-01, Vol.83, p.128-136

2014

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Determining Omics spatiotemporal dimensions using exciting new nanoscopy techniques to assess complex cell responses to DNA damage: part A--radiomics

Critical reviews in eukaryotic gene expression, 2014, Vol.24 (3), p.205

2014

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Determining Omics spatiotemporal dimensions using exciting new nanoscopy techniques to assess complex cell responses to DNA damage: part B--structuromics

Critical reviews in eukaryotic gene expression, 2014, Vol.24 (3), p.225

2014

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Accumulation of DNA Damage and Cell Death after Fractionated Irradiation

Radiation research, 2011-06, Vol.175 (6), p.708-718

2011

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Single-molecule localization microscopy as a promising tool for γH2AX/53BP1 foci exploration

The European physical journal. D, Atomic, molecular, and optical physics, 2018-09, Vol.72 (9), p.1-11, Article 158

2018

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Critical defects in cryopreserved cell nuclei: dna structure changes

Cryobiology, 2018-12, Vol.85, p.135-135

2018

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γH2AX/53BP1 foci as a potential pre-treatment marker of HNSCC tumors radiosensitivity – preliminary methodological study and discussion

The European physical journal. D, Atomic, molecular, and optical physics, 2017-09, Vol.71 (9), p.1-7, Article 241

2017

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DNA repair in head and neck tumor cells and possibilities of its monitoring to estimate individual tumor radioresistance and selection of optimal primary treatment

Časopis lékařů českých, 2020, Vol.159 (7-8), p.268

2020

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HMGB1 interacts with human topoisomerase IIalpha and stimulates its catalytic activity

Nucleic acids research, 2007, Vol.35 (15), p.5001

2007

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Freezing processes in cryoprotective solutions of Me2SO, trehalose and antifreeze protein ApAFP752 and their impact on chromatin condition of cryopreserved cells

Cryobiology, 2015-12, Vol.71 (3), p.561-561

2015

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Primary and secondary clustering of DSB repair foci and repair kinetics compared for gamma -rays, protons of different energies and high-LET super(20)Ne ions

Journal of radiation research, 2014-03, Vol.55, p.i79-i80

2014

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Primary and secondary clustering of DSB repair foci and repair kinetics compared for γ-rays, protons of different energies and high-LET 20Ne ions

Journal of radiation research, 2014-03, Vol.55 (Suppl 1), p.i79-i80

2014

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Primary and secondary clustering of DSB repair foci and repair kinetics compared for [gamma]-rays, protons of different energies and high-LET [sup.20]Ne ions

Journal of radiation research, 2014-03, Vol.55, p.88

2014

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Primary and secondary clustering of DSB repair foci and repair kinetics compared for -rays, protons of different energies and high-LET 20Ne ions

Journal of radiation research, 2014-03, Vol.55 (suppl_1), p.i79-i80

2014

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Chromatin differentiation of white blood cells decreases DSB damage induction, prevents functional assembly of repair foci, but has no influence on protrusion of heterochromatic DSBs into the low-dense chromatin

Journal of radiation research, 2014-03, Vol.55 (suppl_1), p.i81-i82

2014

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Loss of lamin B receptor is necessary to induce cellular senescence

Two New Faces of Amifostine: Protector from DNA Damage in Normal Cells and Inhibitor of DNA Repair in Cancer Cells

Changes in Cryopreserved Cell Nuclei Serve as Indicators of Processes during Freezing and Thawing

Chromatin architecture changes and DNA replication fork collapse are critical features in cryopreserved cells that are differentially controlled by cryoprotectants

HMGB1 and HMGB2 Cell-specifically Down-regulate the p53- and p73-dependent Sequence-specific Transactivation from the Human Bax Gene Promoter

Incorporation of Low Concentrations of Gold Nanoparticles: Complex Effects on Radiation Response and Fate of Cancer Cells

Recruitment of 53BP1 Proteins for DNA Repair and Persistence of Repair Clusters Differ for Cell Types as Detected by Single Molecule Localization Microscopy

Distinct cellular responses to replication stress leading to apoptosis or senescence

Granulocyte maturation determines ability to release chromatin NETs and loss of DNA damage response; these properties are absent in immature AML granulocytes

Heterochromatinization associated with cell differentiation as a model to study DNA double strand break induction and repair in the context of higher-order chromatin structure

Function of chromatin structure and dynamics in DNA damage, repair and misrepair: γ-rays and protons in action

Determining Omics spatiotemporal dimensions using exciting new nanoscopy techniques to assess complex cell responses to DNA damage: part A--radiomics

Determining Omics spatiotemporal dimensions using exciting new nanoscopy techniques to assess complex cell responses to DNA damage: part B--structuromics

Accumulation of DNA Damage and Cell Death after Fractionated Irradiation

Single-molecule localization microscopy as a promising tool for γH2AX/53BP1 foci exploration

Critical defects in cryopreserved cell nuclei: dna structure changes

γH2AX/53BP1 foci as a potential pre-treatment marker of HNSCC tumors radiosensitivity – preliminary methodological study and discussion

DNA repair in head and neck tumor cells and possibilities of its monitoring to estimate individual tumor radioresistance and selection of optimal primary treatment

HMGB1 interacts with human topoisomerase IIalpha and stimulates its catalytic activity

Freezing processes in cryoprotective solutions of Me2SO, trehalose and antifreeze protein ApAFP752 and their impact on chromatin condition of cryopreserved cells

Primary and secondary clustering of DSB repair foci and repair kinetics compared for gamma -rays, protons of different energies and high-LET super(20)Ne ions

Primary and secondary clustering of DSB repair foci and repair kinetics compared for γ-rays, protons of different energies and high-LET 20Ne ions

Primary and secondary clustering of DSB repair foci and repair kinetics compared for [gamma]-rays, protons of different energies and high-LET [sup.20]Ne ions

Primary and secondary clustering of DSB repair foci and repair kinetics compared for -rays, protons of different energies and high-LET 20Ne ions

Chromatin differentiation of white blood cells decreases DSB damage induction, prevents functional assembly of repair foci, but has no influence on protrusion of heterochromatic DSBs into the low-dense chromatin

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