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2. Genome-wide screening identifies Polycomb repressive complex 1.3 as an essential regulator of human naïve pluripotent cell reprogramming

7. The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11

9. Minimal genome-wide human CRISPR-Cas9 library

11. Genome‐wide loss‐of‐function genetic screen identifies INSIG2 as the vulnerability of hepatitis B virus‐integrated hepatoma cells

13. Prioritization of cancer therapeutic targets using CRISPR–Cas9 screens

14. Constitutively Active SMAD2/3 Are Broad-Scope Potentiators of Transcription-Factor-Mediated Cellular Reprogramming

17. Agreement between two large pan-cancer CRISPR-Cas9 gene dependency data sets

18. Functional linkage of gene fusions to cancer cell fitness assessed by pharmacological and CRISPR-Cas9 screening

20. RENGE infers gene regulatory networks using time-series single-cell RNA-seq data with CRISPR perturbations

21. ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

22. SRPK1 maintains acute myeloid leukemia through effects on isoform usage of epigenetic regulators including BRD4

25. A Genetic Progression Model of BrafV600E-Induced Intestinal Tumorigenesis Reveals Targets for Therapeutic Intervention

30. PiggyBac Transposon Mutagenesis: A Tool for Cancer Gene Discovery in Mice

31. Pharmacologic characterization of TBP1901, a prodrug form of aglycone curcumin, and CRISPR-Cas9 screen for therapeutic targets of aglycone curcumin

34. Targeted gene correction of α1-antitrypsin deficiency in induced pluripotent stem cells

35. Additional file 1 of Minimal genome-wide human CRISPR-Cas9 library

36. Genome-wide phenotype analysis in ES cells by regulated disruption of Bloom's syndrome gene

37. Measurement of the nuclear concentration of α-ketoglutarate during adipocyte differentiation by using a fluorescence resonance energy transfer-based biosensor with nuclear localization signals

39. Rad54 is dispensable for the ALT pathway

40. KAT7 is a genetic vulnerability of acute myeloid leukemias driven by MLL rearrangements

41. Additional file 1: of Structural rearrangements generate cell-specific, gene-independent CRISPR-Cas9 loss of fitness effects

42. Genetic Vulnerabilities of DNMT3AR882H in Myeloid Malignancies

43. CRISPR-Knockout Screen Identifies Dmap1 as a Regulator of Chemically Induced Reprogramming and Differentiation of Cardiac Progenitors

44. CRISPR-Knockout Screen Identifies Dmap1 as a Regulator of Chemically Induced Reprogramming and Differentiation of Cardiac Progenitors

45. The CADM1tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11

48. Genome-wide and high-density CRISPR-Cas9 screens identify point mutations in PARP1 causing PARP inhibitor resistance

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