ArticleProceedings of the National Academy of Sciences of the United States of America2000
The X-linked lymphoproliferative syndrome gene product SH2D1A associates with p62dok (Dok1) and activates NF-kappa B.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 60 citations in OpenAlex.
- G9a controls plasma cell differentiation through FOXO1 and ETS1 binding site regulatory networks.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Wiskott-Aldrich syndrome protein interacts and inhibits diacylglycerol kinase alpha promoting IL-2 induction.Frontiers in immunology · 2023Article
- Diacylglycerol Kinase alpha in X Linked Lymphoproliferative Disease Type 1.International journal of molecular sciences · 2021Review
- Quantitative genetics in the study of virus-induced disease.Advances in virus research · 2014Review
- Cutaneous human papillomavirus type 38 E7 regulates actin cytoskeleton structure for increasing cell proliferation through CK2 and the eukaryotic elongation factor 1A.Journal of virology · 2011Article
- Review
- A nuclear export signal and phosphorylation regulate Dok1 subcellular localization and functions.Molecular and cellular biology · 2006Article
- IkappaB kinase beta phosphorylates Dok1 serines in response to TNF, IL-1, or gamma radiation.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Wild-type p53 activates SAP expression in lymphoid cells.Oncogene · 2004Article
- Article
- DOK4 and DOK5: new Dok-related genes expressed in human T cells.Genes and immunity · 2003Article
- The dual-function CD150 receptor subfamily: the viral attraction.Nature immunology · 2003Review
- X-linked lymphoproliferative disease: genetic lesions and clinical consequences.Current allergy and asthma reports · 2002Review
- A "three-pronged" binding mechanism for the SAP/SH2D1A SH2 domain: structural basis and relevance to the XLP syndrome.The EMBO journal · 2002Article
- Structural basis for the interaction of the free SH2 domain EAT-2 with SLAM receptors in hematopoietic cells.The EMBO journal · 2001Article
- Inhibition of the motility and growth of B16F10 mouse melanoma cells by dominant negative mutants of Dok-1.Molecular and cellular biology · 2001Article
- Altered lymphocyte responses and cytokine production in mice deficient in the X-linked lymphoproliferative disease gene SH2D1A/DSHP/SAP.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The X-linked lymphoproliferative syndrome (XLP) is a genetic disorder in which affected males have a morbid or fatal response to Epstein-Barr virus infection. The XLP deficiency has been mapped to a gene encoding a 128-residue protein, SH2D1A, which is comprised principally of a Src homology 2 (SH2) domain. We now report that SH2D1A associates with Dok1, a protein that interacts with Ras-GAP, Csk, and Nck. An SH2D1A SH2 domain mutant that has been identified in XLP does not associate with Dok1, in accord with the hypothesis that this interaction is linked to XLP. The association of SH2D1A with Dok1 also depends on phosphorylation of Dok1 Y(449) in the sequence ALYSQVQK. Further, overexpression of SH2D1A is found to activate NF-kappaB in 293T cells. NF-kappaB activation by SH2D1A does not depend on the wild-type SH2 domain and is inhibited by a dominant-negative IkappaB kinase beta. Thus, SH2D1A can affect multiple intracellular signaling pathways that are potentially important in the normal effective host response to Epstein-Barr virus infection.
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