Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination

scientific article published on 03 March 2014

Activation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination is …
instance of (P31):
scholarly articleQ13442814

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P819ADS bibcode2014PNAS..111E.988Z
P356DOI10.1073/PNAS.1320486111
P932PMC publication ID3964074
P698PubMed publication ID24591601
P5875ResearchGate publication ID260486621

P50authorJavier M Di NoiaQ58227120
Stephen P MethotQ59599651
Anne DurandyQ42348498
P2093author name stringKohsuke Imai
Paul Foster
Mani Larijani
Anne-Marie Patenaude
Heather Fifield
Anil K Eranki
Ramiro E Verdun
Astrid Zahn
Elena M Cortizas
P2860cites workActivation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2)Q24290325
Human CtIP promotes DNA end resectionQ24646062
Activation-induced cytidine deaminase initiates immunoglobulin gene conversion and hypermutation by a common intermediateQ24802780
AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversificationQ28208979
Activation-induced cytidine deaminase induces reproducible DNA breaks at many non-Ig Loci in activated B cellsQ42630118
AID mutant analyses indicate requirement for class-switch-specific cofactorsQ42798287
AID is required for c-myc/IgH chromosome translocations in vivoQ45021537
Differences in the enzymatic efficiency of human and bony fish AID are mediated by a single residue in the C terminus modulating single-stranded DNA bindingQ45167924
AID constrains germinal center size by rendering B cells susceptible to apoptosis.Q45991820
Analysis of class switch recombination and somatic hypermutation in patients affected with autosomal dominant hyper-IgM syndrome type 2.Q46490209
RAG proteins shepherd double-strand breaks to a specific pathway, suppressing error-prone repair, but RAG nicking initiates homologous recombinationQ47765927
Alternative end-joining and classical nonhomologous end-joining pathways repair different types of double-strand breaks during class-switch recombination.Q53085728
Rag mutations reveal robust alternative end joiningQ59098597
Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesisQ28274000
AID is required to initiate Nbs1/gamma-H2AX focus formation and mutations at sites of class switchingQ28366125
Mismatch recognition and uracil excision provide complementary paths to both Ig switching and the A/T-focused phase of somatic mutationQ28586304
53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination.Q29465548
Clinical, immunologic and genetic analysis of 29 patients with autosomal recessive hyper-IgM syndrome due to Activation-Induced Cytidine Deaminase deficiencyQ33359560
Alternative end-joining catalyzes class switch recombination in the absence of both Ku70 and DNA ligase 4.Q33656097
53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombinationQ33794964
The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemiaQ34099472
Programmed cell death pathways in cancer: a review of apoptosis, autophagy and programmed necrosisQ34303405
Regulation of activation-induced deaminase stability and antibody gene diversification by Hsp90.Q34340626
Impaired induction of DNA lesions during immunoglobulin class-switch recombination in humans influences end-joining repairQ34438294
RPA accumulation during class switch recombination represents 5'-3' DNA-end resection during the S-G2/M phase of the cell cycleQ34537165
The AID-induced DNA damage response in chromatinQ34715036
Mechanism and regulation of class switch recombinationQ34764888
The RAG2 C terminus suppresses genomic instability and lymphomagenesisQ35216006
REG-γ associates with and modulates the abundance of nuclear activation-induced deaminaseQ35669089
A structural basis for the biochemical behavior of activation-induced deoxycytidine deaminase class-switch recombination-defective hyper-IgM-2 mutantsQ36201805
CtIP promotes microhomology-mediated alternative end joining during class-switch recombinationQ36316904
AID from bony fish catalyzes class switch recombinationQ36403021
Mechanism of DNA resection during intrachromosomal recombination and immunoglobulin class switchingQ36547669
Pathophysiology of B-cell intrinsic immunoglobulin class switch recombination deficienciesQ36845690
The biochemistry of somatic hypermutationQ37096080
The C-terminal region of activation-induced cytidine deaminase is responsible for a recombination function other than DNA cleavage in class switch recombinationQ37115233
S-S synapsis during class switch recombination is promoted by distantly located transcriptional elements and activation-induced deaminaseQ37164427
A portable hot spot recognition loop transfers sequence preferences from APOBEC family members to activation-induced cytidine deaminase.Q37371679
C-terminal region of activation-induced cytidine deaminase (AID) is required for efficient class switch recombination and gene conversionQ37587676
A DNA break- and phosphorylation-dependent positive feedback loop promotes immunoglobulin class-switch recombination.Q37733531
Classical and alternative end-joining pathways for repair of lymphocyte-specific and general DNA double-strand breaksQ38051860
14-3-3 adaptor proteins recruit AID to 5'-AGCT-3'-rich switch regions for class switch recombination.Q39664674
Antibody class switching mediated by yeast endonuclease-generated DNA breaks.Q40196054
The double-edged sword of activation-induced cytidine deaminase.Q40474265
C-terminal deletion of AID uncouples class switch recombination from somatic hypermutation and gene conversion.Q40627624
AID upmutants isolated using a high-throughput screen highlight the immunity/cancer balance limiting DNA deaminase activityQ40818553
Clonal selection and learning in the antibody systemQ41002744
Active nuclear import and cytoplasmic retention of activation-induced deaminaseQ41792388
AID recruits UNG and Msh2 to Ig switch regions dependent upon the AID C terminus [corrected].Q41870415
AID associates with single-stranded DNA with high affinity and a long complex half-life in a sequence-independent manner.Q42101206
Separation of function between isotype switching and affinity maturation in vivo during acute immune responses and circulating autoantibodies in UNG-deficient miceQ42438365
P433issue11
P407language of work or nameEnglishQ1860
P304page(s)E988-97
P577publication date2014-03-03
P1433published inProceedings of the National Academy of Sciences of the United States of AmericaQ1146531
P1476titleActivation induced deaminase C-terminal domain links DNA breaks to end protection and repair during class switch recombination
P478volume111

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cites work (P2860)
Q52723490A licensing step links AID to transcription elongation for mutagenesis in B cells.
Q41995688AID Biology: A pathological and clinical perspective
Q57292354AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice
Q36304376Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance
Q40090064Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites
Q35768862Cell Cycle Regulates Nuclear Stability of AID and Determines the Cellular Response to AID.
Q38982117Chromatin reader Brd4 functions in Ig class switching as a repair complex adaptor of nonhomologous end-joining
Q35289306Consecutive interactions with HSP90 and eEF1A underlie a functional maturation and storage pathway of AID in the cytoplasm.
Q90057553Current insights into the mechanism of mammalian immunoglobulin class switch recombination
Q37395827Decreased somatic hypermutation induces an impaired peripheral B cell tolerance checkpoint
Q47404983Depletion of recombination-specific cofactors by the C-terminal mutant of the activation-induced cytidine deaminase causes the dominant negative effect on class switch recombination
Q36710679Functional requirements of AID's higher order structures and their interaction with RNA-binding proteins
Q35590309Identification of DNA cleavage- and recombination-specific hnRNP cofactors for activation-induced cytidine deaminase
Q27001131IgH chain class switch recombination: mechanism and regulation
Q40926418Increased serum IgM, immunodeficiency, and autoimmunity: A clinical series
Q35744148Individual substitution mutations in the AID C terminus that ablate IgH class switch recombination
Q48256770Main steps in DNA double-strand break repair: an introduction to homologous recombination and related processes.
Q42837072Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching
Q40093841Molecular characterization of AID-mediated reduction of hepatitis B virus transcripts
Q39077274RNA Exosome and Non-coding RNA-Coupled Mechanisms in AID-Mediated Genomic Alterations
Q36955793The SAGA Deubiquitination Module Promotes DNA Repair and Class Switch Recombination through ATM and DNAPK-Mediated γH2AX Formation.
Q55491385Transient AID expression for in situ mutagenesis with improved cellular fitness.
Q37346703UNG protects B cells from AID-induced telomere loss.

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