Impaired Ig class switch in mice deficient for the X-linked lymphoproliferative disease gene Sap
Author:
Affiliation:
1. From the International Agency for Research on Cancer, Lyon, France; the Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University, New York, NY; and the Unité INSERM 429, Hôpital Necker-Enfants Malades, Paris, France.
Abstract
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Link
http://ashpublications.org/blood/article-pdf/106/6/2069/1635104/zh801805002069.pdf
Reference49 articles.
1. Purtilo DT, Cassel CK, Yang JP, Harper R. X-linked recessive progressive combined variable immunodeficiency (Duncan's disease). Lancet.1975;1: 935-940.
2. Seemayer TA, Gross TG, Egeler RM, et al. X-linked lymphoproliferative disease: twenty-five years after the discovery. Pediatr Res.1995;38: 471-478.
3. Coffey AJ, Brooksbank RA, Brandau O, et al. Host response to EBV infection in X-linked lymphoproliferative disease results from mutations in an SH2-domain encoding gene. Nat Genet.1998;20: 129-135.
4. Nichols KE, Harkin DP, Levitz S, et al. Inactivating mutations in an SH2 domain-encoding gene in X-linked lymphoproliferative syndrome. Proc Natl Acad Sci U S A.1998;95: 13765-13770.
5. Sayos J, Wu C, Morra M, et al. The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM. Nature.1998;395: 462-469.
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