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  1. Apobec2 deficiency causes mitochondrial defects and mitophagy in skeletal muscle
  2. CTNNBL1 facilitates the association of CWC15 with CDC5L and is required to maintain the abundance of the Prp19 spliceosomal complex
  3. Active RNAP pre-initiation sites are highly mutated by cytidine deaminases in yeast, with AID targeting small RNA genes
  4. Uracil excision by endogenous SMUG1 glycosylase promotes efficient Ig class switching and impacts on A:T substitutions during somatic mutation
  5. Michael S. Neuberger 1953–2013
  6. Structural and mutational analysis reveals that CTNNBL1 binds NLSs in a manner distinct from that of its closest armadillo‐relative, karyopherin α
  7. Active demethylation in mouse zygotes involves cytosine deamination and base excision repair
  8. DNA deaminases induce break-associated mutation showers with implication of APOBEC3B and 3A in breast cancer kataegis
  9. Abstract 611: AID/APOBEC cytidine deaminases can mimic the phenomenon of localized hypermutation in cancer or kataegis .
  10. Deficiency in spliceosome-associated factor CTNNBL1 does not affect ongoing cell cycling but delays exit from quiescence and results in embryonic lethality in mice
  11. The cytoplasmic AID complex
  12. ATMIN Is Required for Maintenance of Genomic Stability and Suppression of B Cell Lymphoma
  13. A High-Throughput Assay for DNA Deaminases
  14. The dependence of Ig class‐switching on the nuclear export sequence of AID likely reflects interaction with factors additional to Crm1 exportin
  15. AID upmutants isolated using a high-throughput screen highlight the immunity/cancer balance limiting DNA deaminase activity
  16. AID and RPA: PKA makes the connection local
  17. Interaction between Antibody-Diversification Enzyme AID and Spliceosome-Associated Factor CTNNBL1
  18. microRNA-155 Regulates the Generation of Immunoglobulin Class-Switched Plasma Cells
  19. SMUG1 is able to excise uracil from immunoglobulin genes: insight into mutation versus repair
  20. Somatic hypermutation at A·T pairs: polymerase error versus dUTP incorporation
  21. The mechanism of somatic hypermutation at A·T pairs remains an open question
  22. Mismatch Recognition and Uracil Excision Provide Complementary Paths to Both Ig Switching and the A/T-Focused Phase of Somatic Mutation
  23. Comparison of the Differential Context-dependence of DNA Deamination by APOBEC Enzymes: Correlation with Mutation Spectra in Vivo
  24. Immunoglobulin Isotype Switching Is Inhibited and Somatic Hypermutation Perturbed in UNG-Deficient Mice
  25. Correlation of somatic hypermutation specificity and A-T base pair substitution errors by DNA polymerase η during copying of a mouse immunoglobulin κ light chain transgene
  26. Epigenetics: Monoallelic Expression in the Immune System
  27. Hot Spot Focusing of Somatic Hypermutation in MSH2-Deficient Mice Suggests Two Stages of Mutational Targeting
  28. Monitoring and interpreting the intrinsic features of somatic hypermutation
  29. The 5′ hypermutation boundary of x chains is independent of local and neighbouring sequences and related to the distance from the initiation of transcription
  30. The targeting of somatic hypermutation
  31. The maturation of the antibody response
  32. The 5′ boundary of somatic hypermutation in a Vχ gene is in the leader intron
  33. Affinity maturation leads to differential expression of multiple copies of a κ light-chain transgene
  34. Concerted evolution of class I genes in the major histocompatibility complex of murine rodents.