Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.
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Summary
Results suggest that AID may be involved in regulation or catalysis of the DNA modification step of both class switching and somatic hypermutation in CH12F3-2 B lymphoma.
- Type
- article
- Published
- 2000-09-01
- Cited by
- 3,617
- References
- 86
- Access
- Open access
- OpenAlex
- https://openalex.org/W2165608602
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:17606942
Keywords
Cytidine deaminase, Somatic hypermutation, Biology, Activation-induced (cytidine) deaminase, RNA editing
References
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- Secondary genomic rearrangement events in pre‐B cells: VHDJH replacement by a LINE‐1 sequence and directed class switching.
- Specificity of immunoglobulin heavy chain switch correlates with activity of germline heavy chain genes prior to switching.
- Quantitation of immunoglobulin mu-gamma 1 heavy chain switch region recombination by a digestion-circularization polymerase chain reaction method.
- Circular DNA is a product of the immunoglobulin class switch rearrangement
- Molecular cloning of an apolipoprotein B messenger RNA editing protein.
- Molecular mechanism of immunoglobulin class switch recombination.
- Somatic hypermutation of immunoglobulin genes is linked to transcription initiation.
- CD40 ligand mutations in X-linked immunodeficiency with hyper-IgM
- RAG-2-deficient blastocyst complementation: an assay of gene function in lymphocyte development.
- Unique and unprecedented recombination mechanisms in class switching.
- Frequent occurrence of deletions and duplications during somatic hypermutation: implications for oncogene translocations and heavy chain disease.
- Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).
- Switch circular DNA formed in cytokine-treated mouse splenocytes: evidence for intramolecular DNA deletion in immunoglobulin class switching.
Cited by
- Chronic lymphocytic leukaemia: clinical translations of biological features.
- Multiple Biochemical Activities of NM23/NDP Kinase in Gene Regulation
- Cis and trans-acting elements in somatic hypermutation
- The proto-oncogene c-myc in terminal B lymphocyte differentiation its role in plasma cell and memory B cell generation
- The repair and signaling responses to DNA double-strand breaks.
- Immunoglobulin Somatic Hypermutation: Double-Strand DNA Breaks, AID and Error-Prone DNA Repair
- Quantitative Regulation of Class Switch Recombination by Switch Region Transcription
- Blimp-1 orchestrates plasma cell differentiation by extinguishing the mature B cell gene expression program.
- Differential expression of NAT1 translational repressor during development of bovine intramuscular adipocytes.
- Aberrant somatic hypermutation in multiple subtypes of AIDS-associated non-Hodgkin lymphoma.
- Gene-targeted mice lacking the Ung uracil-DNA glycosylase develop B-cell lymphomas
- Molecular Pathogenesis of Non-Hodgkin's Lymphoma: the Role of Bcl-6
- XPF/ERCC4 and ERCC1: their products and biological roles.
- Histone deacetylase inhibitor Trichostatin A reduces anti-DNA autoantibody production and represses IgH gene transcription.
- AID to overcome the limitations of genomic information
- RING-H2 Protein WSSV249 from White Spot Syndrome Virus Sequesters a Shrimp Ubiquitin-Conjugating Enzyme, PvUbc, for Viral Pathogenesis
- T-independent type II immune responses generate memory B cells
- Mutagenesis at methylated CpG sequences.
- Somatic hypermutation and VH gene usage in hairy cell leukaemia
- B cell development and its deregulation to transformed states at the pre-B cell receptor-expressing pre-BII cell stage.
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