Disrupted control of origin activation compromises genome integrity upon destabilization of Polε and dysfunction of the TRP53-CDKN1A/P21 axis

[1]  V. D’Angiolella,et al.  E2F1: Cause and Consequence of DNA Replication Stress , 2021, Frontiers in Molecular Biosciences.

[2]  S. Boulton,et al.  Spotlight on the Replisome: Aetiology of DNA Replication-Associated Genetic Diseases. , 2020, Trends in genetics : TIG.

[3]  Chun-long Chen,et al.  DNA polymerase α interacts with H3-H4 and facilitates the transfer of parental histones to lagging strands , 2020, Science Advances.

[4]  S. Mirarab,et al.  Sequence Analysis , 2020, Encyclopedia of Bioinformatics and Computational Biology.

[5]  Junjie Chen,et al.  CRISPR/CAS9-based DNA damage response screens reveal gene-drug interactions. , 2020, DNA repair.

[6]  G. Leone,et al.  The broken cycle: E2F dysfunction in cancer , 2019, Nature Reviews Cancer.

[7]  D. Durocher,et al.  A consensus set of genetic vulnerabilities to ATR inhibition , 2019, bioRxiv.

[8]  Martin A. M. Reijns,et al.  DNA Polymerase Epsilon Deficiency Causes IMAGe Syndrome with Variable Immunodeficiency , 2018, American journal of human genetics.

[9]  S. Boulton,et al.  POLE3-POLE4 Is a Histone H3-H4 Chaperone that Maintains Chromatin Integrity during DNA Replication , 2018, Molecular cell.

[10]  M. Aladjem,et al.  Dual Roles of Poly(dA:dT) Tracts in Replication Initiation and Fork Collapse , 2018, Cell.

[11]  J. Bartek,et al.  High speed of fork progression induces DNA replication stress and genomic instability , 2018, Nature.

[12]  G. Stamp,et al.  Polε Instability Drives Replication Stress, Abnormal Development, and Tumorigenesis , 2018, Molecular cell.

[13]  M. Murphy,et al.  p53 orchestrates DNA replication restart homeostasis by suppressing mutagenic RAD52 and POLθ pathways , 2018, eLife.

[14]  T. Halazonetis,et al.  Intragenic origins due to short G1 phases underlie oncogene-induced DNA replication stress , 2018, Nature.

[15]  R. Chatterjee,et al.  p53 gain‐of‐function mutations increase Cdc7‐dependent replication initiation , 2017, EMBO reports.

[16]  A. Nicolas,et al.  The impact of replication stress on replication dynamics and DNA damage in vertebrate cells , 2017, Nature Reviews Genetics.

[17]  P. Zegerman,et al.  Chk1 Inhibition of the Replication Factor Drf1 Guarantees Cell-Cycle Elongation at the Xenopus laevis Mid-blastula Transition , 2017, Developmental cell.

[18]  T. Kunkel,et al.  Eukaryotic DNA Replication Fork. , 2017, Annual review of biochemistry.

[19]  S. Grossman,et al.  Mutant p53 establishes targetable tumor dependency by promoting unscheduled replication , 2017, The Journal of clinical investigation.

[20]  J. Casanova,et al.  Inherited GINS1 deficiency underlies growth retardation along with neutropenia and NK cell deficiency , 2017, The Journal of clinical investigation.

[21]  M. Fischer,et al.  Census and evaluation of p53 target genes , 2017, Oncogene.

[22]  C. Prives,et al.  Transcriptional Regulation by Wild-Type and Cancer-Related Mutant Forms of p53. , 2017, Cold Spring Harbor perspectives in medicine.

[23]  M. Dobbelstein,et al.  p53 Activity Results in DNA Replication Fork Processivity. , 2016, Cell reports.

[24]  V. Gottifredi,et al.  Cyclin Kinase-independent role of p21CDKN1A in the promotion of nascent DNA elongation in unstressed cells , 2016, eLife.

[25]  H. Pospiech,et al.  DNA damage tolerance pathway involving DNA polymerase ι and the tumor suppressor p53 regulates DNA replication fork progression , 2016, Proceedings of the National Academy of Sciences.

[26]  S. Bell,et al.  Chromosome Duplication in Saccharomyces cerevisiae , 2016, Genetics.

[27]  C. F. Cheok,et al.  p53 Maintains Genomic Stability by Preventing Interference between Transcription and Replication. , 2016, Cell reports.

[28]  J. Casanova,et al.  A novel mutation in the POLE2 gene causing combined immunodeficiency. , 2016, The Journal of allergy and clinical immunology.

[29]  Gavin D. Grant,et al.  Sequential replication-coupled destruction at G1/S ensures genome stability , 2015, Genes & development.

[30]  M. Méchali,et al.  DNA replication origin activation in space and time , 2015, Nature Reviews Molecular Cell Biology.

[31]  Thanos D Halazonetis,et al.  DNA replication stress as a hallmark of cancer. , 2015, Annual review of pathology.

[32]  W. Huber,et al.  Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2 , 2014, Genome Biology.

[33]  A. Fischer,et al.  Polymerase ε1 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature (“FILS syndrome”) , 2012, The Journal of experimental medicine.

[34]  J. Casanova,et al.  Partial MCM4 deficiency in patients with growth retardation, adrenal insufficiency, and natural killer cell deficiency. , 2012, The Journal of clinical investigation.

[35]  L. Metherell,et al.  MCM4 mutation causes adrenal failure, short stature, and natural killer cell deficiency in humans. , 2012, The Journal of clinical investigation.

[36]  A. Donaldson,et al.  Limiting replication initiation factors execute the temporal programme of origin firing in budding yeast , 2011, The EMBO journal.

[37]  Colin N. Dewey,et al.  RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome , 2011, BMC Bioinformatics.

[38]  James R Bischoff,et al.  A cell-based screen identifies ATR inhibitors with synthetic lethal properties for cancer-associated mutations , 2011, Nature Structural &Molecular Biology.

[39]  B. Kerem,et al.  Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development , 2011, Cell.

[40]  M. Savio,et al.  Multiple roles of the cell cycle inhibitor p21(CDKN1A) in the DNA damage response. , 2010, Mutation research.

[41]  F. Mulero,et al.  A mouse model of ATR-Seckel shows embryonic replicative stress and accelerated aging , 2009, Nature Genetics.

[42]  Anindya Dutta,et al.  p21 in cancer: intricate networks and multiple activities , 2009, Nature Reviews Cancer.

[43]  Ernest Martinez,et al.  Human ATAC Is a GCN5/PCAF-containing Acetylase Complex with a Novel NC2-like Histone Fold Module That Interacts with the TATA-binding Protein* , 2008, Journal of Biological Chemistry.

[44]  Anindya Dutta,et al.  PCNA-dependent regulation of p21 ubiquitylation and degradation via the CRL4Cdt2 ubiquitin ligase complex. , 2008, Genes & development.

[45]  A. Isacchi,et al.  A Cdc7 kinase inhibitor restricts initiation of DNA replication and has antitumor activity. , 2008, Nature chemical biology.

[46]  H. Maki,et al.  Double-stranded DNA Binding, an Unusual Property of DNA Polymerase ϵ, Promotes Epigenetic Silencing in Saccharomyces cerevisiae*♦ , 2006, Journal of Biological Chemistry.

[47]  R. Mantovani,et al.  The Pole3 bidirectional unit is regulated by MYC and E2Fs. , 2006, Gene.

[48]  J. Mesirov,et al.  From the Cover: Gene set enrichment analysis: A knowledge-based approach for interpreting genome-wide expression profiles , 2005 .

[49]  H. Pospiech,et al.  Structural organization and splice variants of the POLE1 gene encoding the catalytic subunit of human DNA polymerase e , 1999 .

[50]  Bernard Ducommun,et al.  p21 binding to PCNA causes G1 and G2 cell cycle arrest in p53-deficient cells , 1998, Oncogene.

[51]  B. Howard,et al.  WAF1 retards S-phase progression primarily by inhibition of cyclin-dependent kinases , 1997, Molecular and cellular biology.

[52]  M. Nakanishi,et al.  The C-terminal Region of p21 Is Involved in Proliferating Cell Nuclear Antigen Binding but Does Not Appear to Be Required for Growth Inhibition (*) , 1995, The Journal of Biological Chemistry.

[53]  M. Kirschner,et al.  Separate domains of p21 involved in the inhibition of Cdk kinase and PCNA , 1995, Nature.

[54]  G. Hannon,et al.  The p21 inhibitor of cyclin-dependent kinases controls DNA replication by interaction with PCNA , 1994, Nature.

[55]  David Beach,et al.  p21 is a universal inhibitor of cyclin kinases , 1993, Nature.

[56]  S. Elledge,et al.  The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases , 1993, Cell.

[57]  L. Donehower,et al.  Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours , 1992, Nature.

[58]  C. Harris,et al.  p53: traffic cop at the crossroads of DNA repair and recombination , 2005, Nature Reviews Molecular Cell Biology.

[59]  A. Sivachenko,et al.  BIOINFORMATICS APPLICATIONS NOTE , 2022 .