Published in PLoS Comput Biol on May 28, 2015
A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms. BMC Syst Biol (2016) 1.41
Modelling the molecular mechanisms of ageing. Biosci Rep (2017) 0.75
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature (2005) 19.13
The DNA-damage response in human biology and disease. Nature (2009) 17.86
Cellular senescence: when bad things happen to good cells. Nat Rev Mol Cell Biol (2007) 16.55
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell (2005) 12.73
Signaling to p53: breaking the MDM2-p53 circuit. Cell (1998) 8.63
The Systems Biology Graphical Notation. Nat Biotechnol (2009) 8.53
Dynamics of the p53-Mdm2 feedback loop in individual cells. Nat Genet (2004) 8.30
ATM and DNA-PK function redundantly to phosphorylate H2AX after exposure to ionizing radiation. Cancer Res (2004) 6.38
Aging, cellular senescence, and cancer. Annu Rev Physiol (2012) 5.08
Lost in transcription: p21 repression, mechanisms, and consequences. Cancer Res (2005) 4.60
Oscillations and variability in the p53 system. Mol Syst Biol (2006) 4.59
gammaH2AX and MDC1: anchoring the DNA-damage-response machinery to broken chromosomes. DNA Repair (Amst) (2006) 4.36
Generation of oscillations by the p53-Mdm2 feedback loop: a theoretical and experimental study. Proc Natl Acad Sci U S A (2000) 3.74
Rule-based modeling of biochemical systems with BioNetGen. Methods Mol Biol (2009) 3.47
BioNetGen: software for rule-based modeling of signal transduction based on the interactions of molecular domains. Bioinformatics (2004) 3.32
p53 dynamics control cell fate. Science (2012) 3.30
Feedback between p21 and reactive oxygen production is necessary for cell senescence. Mol Syst Biol (2010) 3.27
Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation. Nat Cell Biol (2012) 3.03
Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nat Commun (2012) 2.90
DNA ligase III as a candidate component of backup pathways of nonhomologous end joining. Cancer Res (2005) 2.73
Differential roles for cyclin-dependent kinase inhibitors p21 and p16 in the mechanisms of senescence and differentiation in human fibroblasts. Mol Cell Biol (1999) 2.64
Basal dynamics of p53 reveal transcriptionally attenuated pulses in cycling cells. Cell (2010) 2.40
DNA damage checkpoints in stem cells, ageing and cancer. Nat Rev Mol Cell Biol (2012) 2.39
A plausible model for the digital response of p53 to DNA damage. Proc Natl Acad Sci U S A (2005) 2.32
Efficient modeling, simulation and coarse-graining of biological complexity with NFsim. Nat Methods (2010) 2.24
Stimulus-dependent dynamics of p53 in single cells. Mol Syst Biol (2011) 2.02
Radiation-induced cell death mechanisms. Tumour Biol (2010) 2.02
Quantitative live cell imaging reveals a gradual shift between DNA repair mechanisms and a maximal use of HR in mid S phase. Mol Cell (2012) 1.91
H2AX is required for cell cycle arrest via the p53/p21 pathway. Mol Cell Biol (2009) 1.36
Regulation of the cellular DNA double-strand break response. Biochem Cell Biol (2007) 1.31
Backup pathways of NHEJ in cells of higher eukaryotes: cell cycle dependence. Radiother Oncol (2009) 1.28
Senescence evasion by MCF-7 human breast tumor-initiating cells. Breast Cancer Res (2010) 1.19
Fourier analysis and systems identification of the p53 feedback loop. Proc Natl Acad Sci U S A (2010) 1.19
Regulation of tissue- and stimulus-specific cell fate decisions by p53 in vivo. J Pathol (2010) 1.15
Biochemical kinetics model of DSB repair and induction of gamma-H2AX foci by non-homologous end joining. Radiat Res (2008) 1.11
The ATM signaling network in development and disease. Front Genet (2013) 1.09
Changes in the level and distribution of Ku proteins during cellular senescence. DNA Repair (Amst) (2007) 1.08
Poly(ADP-Ribose) polymerase-1 and DNA-dependent protein kinase have equivalent roles in double strand break repair following ionizing radiation. Int J Radiat Oncol Biol Phys (2009) 1.08
Gamma radiation induces senescence in human adult mesenchymal stem cells from bone marrow and periodontal ligaments. Int J Radiat Biol (2012) 1.07
Kinetic analysis of the Ku-DNA binding activity reveals a redox-dependent alteration in protein structure that stimulates dissociation of the Ku-DNA complex. J Biol Chem (2006) 1.07
DNA damage strength modulates a bimodal switch of p53 dynamics for cell-fate control. BMC Biol (2013) 1.06
PARP inhibition sensitizes to low dose-rate radiation TMPRSS2-ERG fusion gene-expressing and PTEN-deficient prostate cancer cells. PLoS One (2013) 1.06
Roles and mechanisms of cellular senescence in regulation of tissue homeostasis. Cancer Sci (2013) 1.02
An accelerated senescence response to radiation in wild-type p53 glioblastoma multiforme cells. J Neurosurg (2006) 0.98
Induction of accelerated senescence by gamma radiation in human solid tumor-derived cell lines expressing wild-type TP53. Radiat Res (2005) 0.96
Accumulation of DNA double-strand breaks in normal tissues after fractionated irradiation. Int J Radiat Oncol Biol Phys (2010) 0.96
Quantitative model of cell cycle arrest and cellular senescence in primary human fibroblasts. PLoS One (2012) 0.88
The non-homologous end-joining (NHEJ) pathway for the repair of DNA double-strand breaks: I. A mathematical model. Radiat Res (2013) 0.87
Computational experiments reveal the efficacy of targeting CDK2 and CKIs for significantly lowering cellular senescence bar for potential cancer treatment. Biosystems (2012) 0.85
A stochastic model of DNA fragments rejoining. PLoS One (2012) 0.83
Modeling the basal dynamics of p53 system. PLoS One (2011) 0.83
Ionizing radiation induces microhomology-mediated end joining in trans in yeast and mammalian cells. Radiat Res (2009) 0.81
Down-regulation of Ku autoantigen, DNA-dependent protein kinase, and poly(ADP-ribose) polymerase during cellular senescence. Biochem Biophys Res Commun (1997) 0.81
Systems modelling of NHEJ reveals the importance of redox regulation of Ku70/80 in the dynamics of dna damage foci. PLoS One (2013) 0.80
Poly (ADP-ribose) polymerase inhibitors in cancer treatment. Am J Clin Oncol (2014) 0.78