Basic Information

Enzyme AID
Full Name Activation-induced cytidine deaminase
Location Chr12:8602166..8612970
Ensembl ENSG00000111732
Aliases AICDA;ARP2;CDA2;HIGM2;HEL-S-284

Disease Related Information

Disease Species Regulator Expression/Aberrance Target Target Function Regulation Editing-Level Relationship Correlation Editing Effect Phenotype Editing-Dependent PMID
Gastric Cancer Human NA Increase CDKN2A;CDKN2B CDKN2A: This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported. Helicobacter pylori infection triggers the deletion of tumor suppressor genes CDKN2A and CDKN2B via up-regulating endogenous AID expression in the gastric mucosa. Increased Correlated Positive AID-mediated genotoxic effects occur frequently at the CDKN2b-CDKN2a locus and contribute to malignant transformation of the gastric mucosa. Affect mutations of cancer Yes
Cholangiocarcinoma Human TNF-α; NF-κB Increase TP53;INK4A TP53: This gene encodes a tumor suppressor protein containing transcriptional activation. Aberrant expression of AID in biliary cells results in the generation of somatic mutations in tumor related genes, including p53, c-myc, and the promoter region of the INK4A/p16 sequences. Increased Correlated Positive The proinflammatory cytokine-induced aberrant production of AID may link bile duct inflammation to an enhanced genetic susceptibility to mutagenesis, leading to cholangiocarcinogenesis. Promote genetic susceptibility to mutagenesis Yes
Chronic Hepatitis Human NA Increase virus HBV core protein NA AID is expressed in germinal center B cells and randomly edits C residues to U in the variable region of immunoglobulin gene loci. Increased Causative Negative AID edits HBV DNA and facilitates the mutation of HBV DNA, which may assist the virus to evolve and potentially escape from the immune responses. Promote virus escape from the immune resistance Yes