Search Results - "SCHEIDENHELM, Danielle K"

High-grade glioma formation results from postnatal pten loss or mutant epidermal growth factor receptor expression in a transgenic mouse glioma model by QINGXIA WEI, CLARKE, Laura, PUREV, Enkhtsetseg, LAVOIE, Jean-Francois, BAJENARU, M. Livia, SHANNON, Patrick, HERLYN, Dorothee, KAPLAN, David, HENKELMAN, R. Mark, GUTMANN, David H, GUHA, Abhijit, SCHEIDENHELM, Danielle K, BAOPING QIAN, TONG, Amanda, SABHA, Nesrin, KARIM, Zia, BOCK, Nicholas A, RETI, Robert, SWOBODA, Rolf

“…High-grade gliomas are devastating brain tumors associated with a mean survival of <50 weeks. Two of the most common genetic changes observed in these tumors…”
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Akt-Dependent Cell Size Regulation by the Adhesion Molecule on Glia Occurs Independently of Phosphatidylinositol 3-Kinase and Rheb Signaling by Scheidenhelm, Danielle K., Cresswell, Jennifer, Haipek, Carrie A., Fleming, Timothy P., Mercer, Robert W., Gutmann, David H.

“…Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley…”
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Mouse Models of Tuberous Sclerosis Complex by Scheidenhelm, Danielle K., Gutmann, David H.

“…The most devastating complications of tuberous sclerosis complex affect the central nervous system and include epilepsy, mental retardation, autism, and glial…”
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TSC1 sets the rate of ribosome export and protein synthesis through nucleophosmin translation by PELLETIER, Corey L, MAGGI, Leonard B, BRADY, Suzanne N, SCHEIDENHELM, Danielle K, GUTMANN, David H, WEBER, Jason D

“…Nucleophosmin (B23) is a nucleolar phosphoprotein that has been implicated in numerous cellular processes. In particular, nucleophosmin interacts with…”
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Loss of tuberous sclerosis complex 1 (Tsc1) expression results in increased Rheb/S6K pathway signaling important for astrocyte cell size regulation by Uhlmann, Erik J., Li, Wen, Scheidenhelm, Danielle K., Gau, Chia-Ling, Tamanoi, Fuyuhiko, Gutmann, David H.

“…Individuals with tuberous sclerosis complex (TSC) develop central nervous system abnormalities that may reflect astrocyte dysfunction. In an effort to model…”
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