MutSα and MutSβ as size-dependent cellular determinants for prime editing in human embryonic stem cells

[1]  Christopher D. Heinen,et al.  Loss of mismatch repair promotes a direct selective advantage in human stem cells , 2022, Stem cell reports.

[2]  L. Studer,et al.  Transient inhibition of p53 enhances prime editing and cytosine base-editing efficiencies in human pluripotent stem cells , 2022, Nature Communications.

[3]  Graham T Dempsey,et al.  Homozygous might be hemizygous: CRISPR/Cas9 editing in iPSCs results in detrimental on-target defects that escape standard quality controls , 2022, Stem cell reports.

[4]  Luke A. Gilbert,et al.  Highly efficient generation of isogenic pluripotent stem cell models using prime editing , 2022, bioRxiv.

[5]  S. Moon,et al.  Multiple isogenic GNE-myopathy modeling with mutation specific phenotypes from human pluripotent stem cells by base editors. , 2022, Biomaterials.

[6]  S. Bae,et al.  High expression of uracil DNA glycosylase determines C to T substitution in human pluripotent stem cells , 2021, Molecular therapy. Nucleic acids.

[7]  David R. Liu,et al.  Enhanced prime editing systems by manipulating cellular determinants of editing outcomes , 2021, Cell.

[8]  J. Loizou,et al.  Prime editing efficiency and fidelity are enhanced in the absence of mismatch repair , 2021, bioRxiv.

[9]  Simon P. Shen,et al.  Engineered pegRNAs improve prime editing efficiency , 2021, Nature Biotechnology.

[10]  S. Bae,et al.  Comprehensive analysis of prime editing outcomes in human embryonic stem cells , 2021, bioRxiv.

[11]  S. Bae,et al.  Safe scarless cassette-free selection of genome-edited human pluripotent stem cells using temporary drug resistance. , 2020, Biomaterials.

[12]  L. Lai,et al.  Large-Fragment Deletions Induced by Cas9 Cleavage while Not in the BEs System , 2020, Molecular therapy. Nucleic acids.

[13]  F. Buchholz,et al.  Efficient Generation and Correction of Mutations in Human iPS Cells Utilizing mRNAs of CRISPR Base Editors and Prime Editors , 2020, Genes.

[14]  Oana M. Enache,et al.  Cas9 activates the p53 pathway and selects for p53-inactivating mutations , 2020, Nature Genetics.

[15]  P. Reddy,et al.  DNA repair fidelity in stem cell maintenance, health, and disease. , 2020, Biochimica et biophysica acta. Molecular basis of disease.

[16]  Gregory A. Newby,et al.  Search-and-replace genome editing without double-strand breaks or donor DNA , 2019, Nature.

[17]  P. Sakhuja,et al.  Microsatellite instability in mismatch repair and tumor suppressor genes and their expression profiling provide important targets for the development of biomarkers in gastric cancer. , 2019, Gene.

[18]  Wankyu Kim,et al.  Structure-Activity Relationship Analysis of YM155 for Inducing Selective Cell Death of Human Pluripotent Stem Cells , 2019, Front. Chem..

[19]  H. Nakauchi,et al.  Highly Efficient and Marker-free Genome Editing of Human Pluripotent Stem Cells by CRISPR-Cas9 RNP and AAV6 Donor-Mediated Homologous Recombination. , 2019, Cell stem cell.

[20]  G. Cullot,et al.  CRISPR-Cas9 genome editing induces megabase-scale chromosomal truncations , 2019, Nature Communications.

[21]  G. Daley,et al.  Induced pluripotent stem cells in disease modelling and drug discovery , 2019, Nature reviews genetics.

[22]  David R. Liu,et al.  Base editing: precision chemistry on the genome and transcriptome of living cells , 2018, Nature Reviews Genetics.

[23]  A. Bradley,et al.  Repair of double-strand breaks induced by CRISPR–Cas9 leads to large deletions and complex rearrangements , 2018, Nature Biotechnology.

[24]  Gregory McAllister,et al.  p53 inhibits CRISPR–Cas9 engineering in human pluripotent stem cells , 2018, Nature Medicine.

[25]  Na Young Choi,et al.  Optimization of episomal reprogramming for generation of human induced pluripotent stem cells from fibroblasts , 2018, Animal cells and systems.

[26]  Nicole M. Gaudelli,et al.  Programmable base editing of A•T to G•C in genomic DNA without DNA cleavage , 2017, Nature.

[27]  R. Handsaker,et al.  Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations , 2017, Nature.

[28]  Jing Xu,et al.  Efficient precise knockin with a double cut HDR donor after CRISPR/Cas9-mediated double-stranded DNA cleavage , 2017, Genome Biology.

[29]  David R. Liu,et al.  Programmable editing of a target base in genomic DNA without double-stranded DNA cleavage , 2016, Nature.

[30]  S. Moon,et al.  A porous membrane-mediated isolation of mesenchymal stem cells from human embryonic stem cells. , 2015, Tissue engineering. Part C, Methods.

[31]  Christopher D. Heinen,et al.  Human Pluripotent Stem Cells Have a Novel Mismatch Repair-dependent Damage Response* , 2014, The Journal of Biological Chemistry.

[32]  G. Bepler,et al.  HDAC6 deacetylates and ubiquitinates MSH2 to maintain proper levels of MutSα. , 2014, Molecular cell.

[33]  Jeffry D. Sander,et al.  CRISPR-Cas systems for editing, regulating and targeting genomes , 2014, Nature Biotechnology.

[34]  A. Letai,et al.  High mitochondrial priming sensitizes hESCs to DNA-damage-induced apoptosis. , 2013, Cell stem cell.

[35]  S. Moon,et al.  Inhibition of pluripotent stem cell-derived teratoma formation by small molecules , 2013, Proceedings of the National Academy of Sciences.

[36]  K. Musunuru Genome editing of human pluripotent stem cells to generate human cellular disease models , 2013, Disease Models & Mechanisms.

[37]  K. Eggan,et al.  Modeling human disease with pluripotent stem cells: from genome association to function. , 2013, Cell stem cell.

[38]  James E. DiCarlo,et al.  RNA-Guided Human Genome Engineering via Cas9 , 2013, Science.

[39]  Wei Yang,et al.  Mechanism of mismatch recognition revealed by human MutSβ bound to unpaired DNA loops , 2011, Nature Structural &Molecular Biology.

[40]  P. Glazer,et al.  Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6. , 2006, Carcinogenesis.

[41]  D. Averbeck,et al.  Cadmium: cellular effects, modifications of biomolecules, modulation of DNA repair and genotoxic consequences (a review). , 2006, Biochimie.

[42]  J. Jiricny The multifaceted mismatch-repair system , 2006, Nature Reviews Molecular Cell Biology.

[43]  H. Flores-Rozas,et al.  Cadmium inhibits mismatch repair by blocking the ATPase activity of the MSH2–MSH6 complex , 2005, Nucleic acids research.

[44]  R. Dahiya,et al.  DNA mismatch repair enzyme activity and gene expression in prostate cancer. , 2001, Biochemical and biophysical research communications.

[45]  L. Ricciardiello,et al.  Steady-state Regulation of the Human DNA Mismatch Repair System* , 2000, The Journal of Biological Chemistry.

[46]  M. Radman,et al.  HNPCC-like cancer predisposition in mice through simultaneous loss of Msh3 and Msh6 mismatch-repair protein functions , 1999, Nature Genetics.

[47]  P. Modrich,et al.  Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells. , 1995, Science.

[48]  J. Jiricny,et al.  GTBP, a 160-kilodalton protein essential for mismatch-binding activity in human cells. , 1995, Science.

[49]  N. Benvenisty,et al.  Quality control Genome maintenance in pluripotent stem cells , 2014 .

[50]  L. Beese,et al.  Structure of the human MutSalpha DNA lesion recognition complex. , 2007, Molecular cell.