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Science 3 January 1997:
Vol. 275. no. 5296, pp. 27 - 28
DOI: 10.1126/science.275.5296.27
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Research News

Carol Featherstone

For many years, immunologists have puzzled over how a single gene mutation can cause the diverse symptoms of Wiskott-Aldrich syndrome, a rare hereditary disease characterized by symptoms ranging from a severely compromised immune system to bleeding and cancer. Recent studies of WASp, protein produced by the gene at fault in WAS, are helping to solve that mystery, and at the same time are pointing to some intriguing new connections between the cell's internal communication pathways.

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Congenital Disorders of Platelet Signal Transduction.
A. K. Rao and J. Gabbeta (2000)
Arterioscler Thromb Vasc Biol 20, 285-289
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The Human WASP-interacting Protein, WIP, Activates the Cell Polarity Pathway in Yeast.
G. Vaduva, N. Martinez-Quiles, I. M. Anton, N. C. Martin, R. S. Geha, A. K. Hopper, and N. Ramesh (1999)
J. Biol. Chem. 274, 17103-17108
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Cdc42: An Essential Rho-Type GTPase Controlling Eukaryotic Cell Polarity.
D. I. Johnson (1999)
Microbiol. Mol. Biol. Rev. 63, 54-105
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WIP, a protein associated with Wiskott-Aldrich syndrome protein, induces actin polymerization and redistribution in lymphoid cells.
N. Ramesh, I. M. Anton, J. H. Hartwig, and R. S. Geha (1997)
PNAS 94, 14671-14676
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Defective Actin Reorganization and Polymerization of Wiskott-Aldrich T Cells in Response to CD3-Mediated Stimulation.
M. D. Gallego, M. Santamaria, J. Pena, and I. J. Molina (1997)
Blood 90, 3089-3097
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In Vitro Reconstitution of Cortical Actin Assembly Sites in Budding Yeast.
T. Lechler and R. Li (1997)
J. Cell Biol. 138, 95-103
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