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The receptor tyrosine kinase/PI3K/AKT/mammalian target of rapamycin (RTK/PI3K/AKT/mTOR) pathway is frequently altered in cancer, but the underlying mechanism leading to tumorigenesis by activated mTOR remains less clear. Here we show that mTOR is a positive regulator of Notch signaling in mouse and human cells, acting through induction of the(More)
In the central nervous system, tuberous sclerosis complex (TSC) is characterized by a range of lesions including cortical tubers, white matter heterotopias, subependymal nodules, and subependymal giant cell astrocytomas (SEGAs). Recent studies have implicated an important role for the TSC genes TSC1 and TSC2, in a signaling pathway involving the mammalian(More)
Cortical tubers are developmental brain malformations in the tuberous sclerosis complex (TSC) that cause epilepsy and autism in TSC patients whose pathogenesis is uncertain. Tsc2 null murine neuroepithelial progenitor (NEP) cells display persistent growth when growth factors are withdrawn, express GFAP at high levels, and have reduced expression of a set of(More)
Cell growth can be suppressed by stressful environments, but the role of stress pathways in this process is largely unknown. Here we show that a cascade of p38β mitogen-activated protein kinase (MAPK) and p38-regulated/activated kinase (PRAK) plays a role in energy-starvation-induced suppression of mammalian target of rapamycin (mTOR), and that energy(More)
Despite the growing understanding of pdgf signaling, studies of pdgf function have encountered two major obstacles: the functional redundancy of PDGFRalpha and PDGFRbeta in vitro and their distinct roles in vivo. Here we used wild-type mouse embryonic fibroblasts (MEF), MEF null for either PDGFRalpha, beta, or both to dissect PDGF-PDGFR signaling pathways.(More)
Mutations that inactivate either TSC1 or TSC2 cause tuberous sclerosis. We have used immunoblotting and immunohistochemical analysis to see whether there is phosphorylation of p70 S6 kinase, and the ribosomal S6 protein in angiomyolipomas occurring in tuberous scierosis. Hamartin (encoded by TSC1) and S6K was expressed in all samples. Tuberin (TSC2) was(More)
This paper proposes and evaluates a new algorithm on measuring the packet loss burstiness to be applied in ITU E-Model. The algorithm reveals the packet loss burstiness characteristics directly from the packet loss pattern. A new parameter called equivalent random packet loss is obtained based on the burstiness measurement. This new parameter is used in the(More)
region encoded by exon 11 and another in the C-terminal region of the protein. By contrast, BRCA1 colocalizes with, but does not interact directly with hRAD51, suggesting that they may be present within the same multi-protein complex (Mizuta et al. data suggesting that BRCA1 is hyperphosphorylated Genetics and Molecular Biology Program and undergoes altered(More)
The PI3K-Akt-mTOR pathway plays crucial roles in regulating both innate and adaptive immunity. However, the role of TSC1, a critical negative regulator of mTOR, in peripheral T cell homeostasis remains elusive. With T cell-specific Tsc1 conditional knockout (Tsc1 KO) mice, we found that peripheral naïve CD8(+) T cells but not CD4(+) T cells were severely(More)
Traffic incidents are a major source of congestion in Virginia. Secondary incidents comprise a relatively small but important portion of all incidents, and relatively little is known about their occurrence, characteristics, and associated delays. The main objectives of this study were to define secondary incidents, understand and analyze the occurrence and(More)