Related references
Note: Only part of the references are listed.Mechanism and regulation of class switch recombination
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JOURNAL OF EXPERIMENTAL MEDICINE (2007)
Activation-induced cytidine deaminase-dependent DNA breaks in class switch recombination occur during G1 phase of the cell cycle and depend upon mismatch repair
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IgH class switching and translocations use a robust non-classical end-joining pathway
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NATURE (2007)
DNA polymerase β is able to repair breaks in switch regions and plays an inhibitory role during immunoglobulin class switch recombination
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JOURNAL OF EXPERIMENTAL MEDICINE (2007)
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Antibody class switching mediated by yeast endonuclease-generated DNA breaks
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Regulation of reactive oxygen species by Atm is essential for proper response to DNA double-strand breaks in lymphocytes
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The in vivo pattern of AID targeting to immunoglobulin switch regions deduced from mutation spectra in msh2-/- ung-/- mice
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AID in somatic hypermutation and class switch recombination
S Longerich et al.
CURRENT OPINION IN IMMUNOLOGY (2006)
Inducible DNA breaks in Ig S regions are dependent on AID and UNG
CE Schrader et al.
JOURNAL OF EXPERIMENTAL MEDICINE (2005)
Staggered AID-dependent DNA double strand breaks are the predominant DNA lesions targeted to Sμ in Ig class switch recombination
JS Rush et al.
INTERNATIONAL IMMUNOLOGY (2004)
DNA substrate length and surrounding sequence affect the activation-induced deaminase activity at cytidine
KF Yu et al.
JOURNAL OF BIOLOGICAL CHEMISTRY (2004)
Growth retardation and dyslymphopoiesis accompanied by G2/M arrest in APEX2-null mice
Y Ide et al.
BLOOD (2004)
Biochemical analysis of hypermutational targeting by wild type and mutant activation-induced cytidine deaminase
R Bransteitter et al.
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The generation of antibody diversity through somatic hypermutation and class switch recombination
ZQ Li et al.
GENES & DEVELOPMENT (2004)
Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells
K Ito et al.
NATURE (2004)
Mutations occur in the Ig Sμ region but rarely in Sγ regions prior to class switch recombination
CE Schrader et al.
EMBO JOURNAL (2003)
Human uracil-DNA glycosylase deficiency associated with profoundly impaired immunoglobulin class-switch recombination
K Imai et al.
NATURE IMMUNOLOGY (2003)
The block in immunoglobulin class switch recombination caused by activation-induced cytidine deaminase deficiency occurs prior to the generation of DNA double strand breaks in switch μ region
N Catalan et al.
JOURNAL OF IMMUNOLOGY (2003)
Processive AID-catalysed cytosine deamination on single-stranded DNA simulates somatic hypermutation
P Pham et al.
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Transcription-targeted DNA deamination by the AID antibody diversification enzyme
J Chaudhuri et al.
NATURE (2003)
Activation-induced cytidine deaminase deaminates deoxycytidine on single-stranded DNA but requires the action of RNase
R Bransteitter et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2003)
Immunoglobulin isotype switching is inhibited and somatic hypermutation perturbed in UNG-deficient mice
C Rada et al.
CURRENT BIOLOGY (2002)
Altering the pathway of immunoglobulin hypermutation by inhibiting uracil-DNA glycosylase
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AID mutates E-coli suggesting a DNA deamination mechanism for antibody diversification
SK Petersen-Mahrt et al.
NATURE (2002)
Determinants in nuclease specificity of Ape1 and Ape2, human homologues of Escherichia coli exonuclease III
MZ Hadi et al.
JOURNAL OF MOLECULAR BIOLOGY (2002)
Activation-induced deaminase (AID)-directed hypermutation in the immunoglobulin Sμ region:: Implication of AID involvement in a common step of class switch recombination and somatic hypermutation
H Nagaoka et al.
JOURNAL OF EXPERIMENTAL MEDICINE (2002)
AID is required to initiate Nbs1/γ-H2AX focus formation and mutations at sites of class switching
S Petersen et al.
NATURE (2001)
Human APE2 protein is mostly localized in the nuclei and to some extent in the mitochondria, while nuclear APE2 is partly associated with proliferating cell nuclear antigen
D Tsuchimoto et al.
NUCLEIC ACIDS RESEARCH (2001)
Mice reconstituted with DNA polymerase β-deficient fetal liver cells are able to mount a T cell-dependent immune response and mutate their Ig genes normally
G Esposito et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2000)
Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2)
P Revy et al.
CELL (2000)
Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme
M Muramatsu et al.
CELL (2000)