Laurie E. Lenox

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Acute anemia initiates a systemic response that results in the rapid mobilization and differentiation of erythroid progenitors in the adult spleen. The flexed-tail (f) mutant mice exhibit normal steady-state erythropoiesis but are unable to rapidly respond to acute erythropoietic stress. Here, we show that f/f mutant mice have a mutation in Madh5. Our(More)
OBJECTIVE In mice, homeostatic erythropoiesis occurs primarily in the bone marrow. However, in response to acute anemia, bone morphogenetic proteins 4 (BMP-4)-dependent stress erythropoiesis occurs in the adult spleen. BMP-4 can also regulate stress erythropoiesis in the fetal liver. In humans, erythropoiesis occurs in the bone marrow. However, in certain(More)
BACKGROUND Lymphocyte cytosolic protein 2, also known as Src homology 2 domain-containing leukocyte phosphoprotein of 76 kilodaltons (SLP-76), is an essential adaptor molecule in myeloid cells, where it regulates FcepsilonRI-induced mast cell (MC) and FcgammaR- and integrin-induced neutrophil (polymorphonuclear leukocyte [PMN]) functions. SLP-76 contains 3(More)
The Src homology 2 domain-containing leukocyte phosphoprotein of 76 kDa (SLP-76) is an adaptor molecule critical for immunoreceptor and integrin signaling in multiple hemopoietic lineages. We showed previously that SLP-76 is required for neutrophil function in vitro, including integrin-induced adhesion and production of reactive oxygen intermediates, and to(More)
Recent work has identified a growing body of evidence that subtle changes in noncoding sequences can result in significant pathology. These mutations, which would have been called silent polymorphisms in the past, affect gene transcription and mRNA splicing and lead to drastic changes in gene expression. Previous work from our lab has characterized the(More)
SLP-76 (Src homology 2 domain-containing leukocyte phosphoprotein of 76 kDa) organizes signaling from immunoreceptors, including the platelet collagen receptor, the pre-TCR, and the TCR, and is required for T cell development. In this study we examine a mouse in which wild-type SLP-76 is replaced with a mutant constitutively targeted to the cell membrane.(More)
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