RGD Reference Report - DNA damage: a trigger of innate immunity but a requirement for adaptive immune homeostasis. - Rat Genome Database

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DNA damage: a trigger of innate immunity but a requirement for adaptive immune homeostasis.

Authors: Xu, Y 
Citation: Xu Y Nat Rev Immunol. 2006 Apr;6(4):261-70.
RGD ID: 1578504
Pubmed: PMID:16498454   (View Abstract at PubMed)
DOI: DOI:10.1038/nri1804   (Journal Full-text)

Chromosome breakage is frequently associated with viral infection and cellular transformation, but it is also required for two processes that are crucial for the development and function of adaptive immunity: V(D)J recombination and class-switch recombination. The cellular responses that result from this type of DNA damage, which are mostly activated by the protein kinase ataxia-telangiectasia mutated (ATM), lead to cell-cycle arrest at several checkpoints and efficient DNA repair. This Review focuses on the important roles of these DNA-damage responses in the activation of innate immunity and the targeting of the innate immune response to infected or transformed cells, as well as in the development and function of adaptive immunity.

Molecular Pathway Annotations    Click to see Annotation Detail View

RGD Manual Annotations

Objects Annotated

Genes (Rattus norvegicus)
Atm  (ATM serine/threonine kinase)
Brca1  (BRCA1, DNA repair associated)
Mre11  (MRE11 homolog, double strand break repair nuclease)
Nbn  (nibrin)
Rad50  (RAD50 double strand break repair protein)

Genes (Mus musculus)
Atm  (ataxia telangiectasia mutated)
Brca1  (breast cancer 1, early onset)
Mre11a  (MRE11A homolog A, double strand break repair nuclease)
Nbn  (nibrin)
Rad50  (RAD50 double strand break repair protein)

Genes (Homo sapiens)
BRCA1  (BRCA1 DNA repair associated)
MRE11  (MRE11 homolog, double strand break repair nuclease)
RAD50  (RAD50 double strand break repair protein)


Additional Information