A disease gene for autosomal hyper-IgM syndrome: More genes associated with more immunodeficiencies

Clinical Immunology

Volumn 97, Issue 3, 2000, Pages 191-192

  Puck, Jennifer M ^a  

^a NATIONAL HUMAN GENOME RESEARCH INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

IMMUNOGLOBULIN M; TUMOR NECROSIS FACTOR;

AUTOSOMAL DISORDER; EDITORIAL; GENETIC LINKAGE; GENOTYPE; HUMAN; HYPERIMMUNOGLOBULINEMIA; IMMUNE DEFICIENCY; MULTIGENE FAMILY; NOMENCLATURE; PREVALENCE; PRIORITY JOURNAL;

EID: 0033664967     PISSN: 15216616     EISSN: None     Source Type: Journal    
DOI: 10.1006/clim.2000.4973     Document Type: Editorial

References (7)

1. Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2)
2. Mutations in AID in patients with hyper IgM syndrome
3. Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells
4. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme
5. Hematopoietic stem-cell transplantation for the treatment of severe combined immunodeficiency