D
David O. Ferguson
Researcher at University of Michigan
Publications - 22
Citations - 5759
David O. Ferguson is an academic researcher from University of Michigan. The author has contributed to research in topics: DNA repair & Genome instability. The author has an hindex of 19, co-authored 20 publications receiving 5542 citations. Previous affiliations of David O. Ferguson include Harvard University & Howard Hughes Medical Institute.
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Journal ArticleDOI
Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells
Ömer H. Yilmaz,Riccardo Valdez,Brian K. Theisen,Wei Guo,David O. Ferguson,Hong Wu,Sean J. Morrison +6 more
TL;DR: Mechanistic differences between normal stem cells and cancer stem cells can thus be targeted to depletecancer stem cells without damaging normalstem cells.
Journal ArticleDOI
Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development
Yijie Gao,David O. Ferguson,David O. Ferguson,Wei Xie,John P. Manis,JoAnn Sekiguchi,Karen M. Frank,Jayanta Chaudhuri,James W. Horner,Ronald A. DePinho,Frederick W. Alt +10 more
TL;DR: It is shown that p53-deficiency rescues several aspects of the XRCC4-deficient phenotype, including embryonic lethality, neuronal apoptosis, and impaired cellular proliferation, but there was no significant rescue of impaired V(D)J recombination or lymphocyte development.
Journal ArticleDOI
Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors.
Craig H. Bassing,Heikyung Suh,David O. Ferguson,David O. Ferguson,Katrin F. Chua,John P. Manis,Mark Eckersdorff,Megan Gleason,Rodrick Bronson,Charles Lee,Frederick W. Alt +10 more
TL;DR: H2AX functions as a dosage-dependent suppressor of genomic instability and tumors in mice and maps to a cytogenetic region frequently altered in human cancers, possibly implicating similar functions in man.
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DNA Ligase IV Deficiency in Mice Leads to Defective Neurogenesis and Embryonic Lethality via the p53 Pathway
Karen M. Frank,Norman E. Sharpless,Yijie Gao,JoAnn Sekiguchi,David O. Ferguson,Chengming Zhu,John P. Manis,James W. Horner,Ronald A. DePinho,Frederick W. Alt +9 more
TL;DR: In the context of Lig4 deficiency, embryonic lethality and neuronal apoptosis likely result from a p53-dependent response to unrepaired DNA damage, and neurons apoptosis and lymphocyte developmental defects can be mechanistically dissociated.
Journal ArticleDOI
Unrepaired DNA breaks in p53-deficient cells lead to oncogenic gene amplification subsequent to translocations.
Chengming Zhu,Kevin D. Mills,David O. Ferguson,Charles Lee,John P. Manis,James Fleming,Yijie Gao,Cynthia C. Morton,Frederick W. Alt +8 more
TL;DR: It is shown that pro-B lymphomas in mice deficient for both p53 and nonhomologous end-joining (NHEJ) contain complicons that coamplify c-myc and IgH sequences, suggesting a general model for oncogenic complicon formation.