Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.5.4.5 extracted from

  • Meyers, G.; Ng, Y.S.; Bannock, J.M.; Lavoie, A.; Walter, J.E.; Notarangelo, L.D.; Kilic, S.S.; Aksu, G.; Debre, M.; Rieux-Laucat, F.; Conley, M.E.; Cunningham-Rundles, C.; Durandy, A.; Meffre, E.
    Activation-induced cytidine deaminase (AID) is required for B-cell tolerance in humans (2011), Proc. Natl. Acad. Sci. USA, 108, 11554-11559.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining

Source Tissue

Source Tissue Comment Organism Textmining

General Information

General Information Comment Organism
malfunction patients with hyper-IgM syndromes who are deficient in activation-induced cytidine deaminase, which is required for class switch recombination and somatic hypermutation, are prone to develop autoimmune diseases. Defective peripheral B-cell tolerance checkpoint occurs in AID-deficient patients, overview Homo sapiens
physiological function AID is required for the establishment of both central and peripheral B-cell tolerance Homo sapiens