Activation-Induced Cytidine Deaminase (AID) Deficiency Causes the Autosomal Recessive Form of the Hyper-IgM Syndrome (HIGM2)
Top Cited Papers
- 1 September 2000
- Vol. 102 (5) , 565-575
- https://doi.org/10.1016/s0092-8674(00)00079-9
Abstract
No abstract availableKeywords
This publication has 74 references indexed in Scilit:
- Normal CD40-mediated activation of monocytes and dendritic cells from patients with hyper-IgM syndrome due to a CD40 pathway defect in B cellsEuropean Journal of Immunology, 1998
- Class Switching in B Cells Lacking 3′ Immunoglobulin Heavy Chain EnhancersThe Journal of Experimental Medicine, 1998
- Germinal Center Founder Cells Display Propensity for Apoptosis before Onset of Somatic MutationThe Journal of Experimental Medicine, 1997
- Identification of TRAF6, a Novel Tumor Necrosis Factor Receptor-associated Factor Protein That Mediates Signaling from an Amino-terminal Domain of the CD40 Cytoplasmic RegionPublished by Elsevier ,1996
- The SCID but Not the RAG-2 Gene Product Is Required for Sμ–Sε Heavy Chain Class SwitchingImmunity, 1996
- Within Germinal Centers, Isotype Switching of Immunoglobulin Genes Occurs after the Onset of Somatic MutationImmunity, 1996
- Somatic Hypermutation of Immunoglobulin Genes Is Linked to Transcription InitiationImmunity, 1996
- A novel member of the TRAF family of putative signal transducing proteins binds to the cytosolic domain of CD40FEBS Letters, 1995
- The CD40 ligand, gp39, is defective in activated T cells from patients with X-linked hyper-IgM syndromeCell, 1993
- Immunoenzymatic labeling of monoclonal antibodies using immune complexes of alkaline phosphatase and monoclonal anti-alkaline phosphatase (APAAP complexes).Journal of Histochemistry & Cytochemistry, 1984