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Huong Huynh
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Journal Articles
Yingchun Wang, Eric Vachon, Jinyi Zhang, Vera Cherepanov, Joshua Kruger, Jun Li, Kan Saito, Patrick Shannon, Nunzio Bottini, Huong Huynh, Heyu Ni, Hong Yang, Colin McKerlie, Sue Quaggin, Zhizhuang Joe Zhao, Philip A. Marsden, Tomas Mustelin, Katherine A. Siminovitch, Gregory P. Downey
Journal:
Journal of Experimental Medicine
Journal of Experimental Medicine (2005) 202 (11): 1587–1597.
Published: 05 December 2005
Abstract
MEG2, a protein tyrosine phosphatase with a unique NH 2 -terminal lipid-binding domain, binds to and is modulated by the polyphosphoinositides PI (4,5) P 2 and PI (3,4,5) P 3 . Recent data implicate MEG2 in vesicle fusion events in leukocytes. Through the genesis of Meg2-deficient mice, we demonstrate that Meg2 − / − embryos manifest hemorrhages, neural tube defects including exencephaly and meningomyeloceles, cerebral infarctions, abnormal bone development, and >90% late embryonic lethality. T lymphocytes and platelets isolated from recombination activating gene 2 − / − mice transplanted with Meg2 − / − embryonic liver–derived hematopoietic progenitor cells showed profound defects in activation that, in T lymphocytes, was attributable to impaired interleukin 2 secretion. Ultrastructural analysis of these lymphocytes revealed near complete absence of mature secretory vesicles. Taken together, these observations suggest that MEG2-mediated modulation of secretory vesicle genesis and function plays an essential role in neural tube, vascular, and bone development as well as activation of mature platelets and lymphocytes.