C
Cristina Rada
Researcher at Laboratory of Molecular Biology
Publications - 61
Citations - 5941
Cristina Rada is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Somatic hypermutation & Cytidine deaminase. The author has an hindex of 36, co-authored 60 publications receiving 5640 citations. Previous affiliations of Cristina Rada include Medical Research Council.
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Journal ArticleDOI
microRNA-155 Regulates the Generation of Immunoglobulin Class-Switched Plasma Cells
Elena Vigorito,Kerry L. Perks,Cei Abreu-Goodger,Sam F Bunting,Zou Xiang,Susan Kohlhaas,Partha Pratim Das,Eric A. Miska,Antony Rodriguez,Allan Bradley,Kenneth G. C. Smith,Cristina Rada,Anton J. Enright,Kai-Michael Toellner,Ian C. M. MacLennan,Martin R Turner +15 more
TL;DR: The intrinsic requirement for miR-155 is shown in B cell responses to thymus-dependent and -independent antigens and implicate post-transcriptional regulation of gene expression for establishing the terminal differentiation program of B cells.
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Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice
Cristina Rada,Gareth T. Williams,Hilde Nilsen,Deborah E. Barnes,Tomas L Lindahl,Michael S. Neuberger +5 more
TL;DR: The results provide strong support for the DNA deamination model for antibody diversification with respect to class-switching as well as hypermutation and suggest that UNG is the major mouse DNA glycosylase responsible for processing the programmed dU/dG lesions within the immunoglobulin locus.
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Mismatch Recognition and Uracil Excision Provide Complementary Paths to Both Ig Switching and the A/T-Focused Phase of Somatic Mutation
TL;DR: While antibody diversification is perturbed by single deficiency in either UNG or MSH2, combined UNG/MSH2 deficiency leads to a total ablation both of switch recombination and of IgV hypermutation at dA:dT pairs.
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Hot spot focusing of somatic hypermutation in MSH2-deficient mice suggests two stages of mutational targeting.
TL;DR: It is suggested that MSH2 (or factors dependent upon it) plays a role in the mechanism of mutation fixation is indicated by a strikingly increased focusing of the mutations on intrinsic hot spots, and two phases to hypermutation targeting are proposed.
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DNA deaminases induce break-associated mutation showers with implication of APOBEC3B and 3A in breast cancer kataegis.
Benjamin Taylor,Serena Nik-Zainal,Yee Ling Wu,Lucy Stebbings,Keiran Raine,Peter J. Campbell,Cristina Rada,Michael R. Stratton,Michael S. Neuberger +8 more
TL;DR: It is shown kataegis can result from AID/APOBEC-catalysed cytidine deamination in the vicinity of DNA breaks, likely through action on single-stranded DNA exposed during resection.