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4. Bi-allelic TTI1 variants cause an autosomal-recessive neurodevelopmental disorder with microcephaly

5. Genome-scale clustered regularly interspaced short palindromic repeats screen identifies nucleotide metabolism as an actionable therapeutic vulnerability in diffuse large B-cell lymphoma

6. Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy

7. Impaired protein hydroxylase activity causes replication stress and developmental abnormalities in humans

8. E3 ligases: a ubiquitous link between DNA repair, DNA replication and human disease.

11. Bi-allelic MCM10 variants associated with immune dysfunction and cardiomyopathy cause telomere shortening

12. Germline RBBP8 variants associated with early-onset breast cancer compromise replication fork stability

13. RNF8 ubiquitylation of XRN2 facilitates R-loop resolution and restrains genomic instability in BRCA1 mutant cells

14. RECON syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1

16. Isomerization of BRCA1–BARD1 promotes replication fork protection

19. USP7 inhibition alters homologous recombination repair and targets CLL cells independently of ATM/p53 functional status

20. Warsaw Breakage Syndrome associated DDX11 helicase resolves G-quadruplex structures to support sister chromatid cohesion

22. Chromosome instability syndromes

23. Identification of Adenovirus E1B-55K Interaction Partners through a Common Binding Motif.

25. Actin nucleators safeguard replication forks by limiting nascent strand degradation

28. Data from Cancer-Associated SF3B1 Mutations Confer a BRCA-Like Cellular Phenotype and Synthetic Lethality to PARP Inhibitors

29. Supplementary Table from Cancer-Associated SF3B1 Mutations Confer a BRCA-Like Cellular Phenotype and Synthetic Lethality to PARP Inhibitors

30. Figure S1 to S7 from MYBL2 Supports DNA Double Strand Break Repair in Hematopoietic Stem Cells

31. Supplementary Data from Cancer-Associated SF3B1 Mutations Confer a BRCA-Like Cellular Phenotype and Synthetic Lethality to PARP Inhibitors

32. Table S1 from MYBL2 Supports DNA Double Strand Break Repair in Hematopoietic Stem Cells

33. Data from MYBL2 Supports DNA Double Strand Break Repair in Hematopoietic Stem Cells

34. Excessive transcription-replication conflicts are a vulnerability of BRCA1-mutant cancers

35. RNF8 ubiquitylation of XRN2 facilitates R-loop resolution and restrains genomic instability in BRCA1 mutant cells

36. Excessive transcription-replication conflicts are a vulnerability of BRCA1-mutant cancers

37. Mutations in DONSON disrupt replication fork stability and cause microcephalic dwarfism

39. Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy

40. H3K4 methylation by SETD1A/BOD1L facilitates RIF1-dependent NHEJ

41. Cancer-Associated SF3B1 Mutations Confer a BRCA-Like Cellular Phenotype and Synthetic Lethality to PARP Inhibitors

46. ATRX proximal protein associations boast roles beyond histone deposition

50. A Degenerate PCNA-Interacting Peptide (DPIP) box targets RNF168 to replicating DNA to limit 53BP1 signaling

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