Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes.
Rajasekhar, Vinagolu K
Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes. [electronic resource] - Molecular cell Oct 2003 - 889-901 p. digital
Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
1097-2765
10.1016/s1097-2765(03)00395-2 doi
Animals
Brain Neoplasms--genetics
Cell Cycle Proteins--metabolism
Cell Transformation, Neoplastic--drug effects
Cluster Analysis
Enzyme Inhibitors--pharmacology
Gene Expression Regulation, Neoplastic--genetics
Glioblastoma--genetics
Humans
Mice
Mice, Transgenic
Oligonucleotide Array Sequence Analysis
Polyribosomes--genetics
Protein Biosynthesis--drug effects
Protein Serine-Threonine Kinases
Proto-Oncogene Proteins--antagonists & inhibitors
Proto-Oncogene Proteins c-akt
RNA, Messenger--analysis
Signal Transduction--drug effects
Tumor Cells, Cultured
ras Proteins--antagonists & inhibitors
Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes. [electronic resource] - Molecular cell Oct 2003 - 889-901 p. digital
Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
1097-2765
10.1016/s1097-2765(03)00395-2 doi
Animals
Brain Neoplasms--genetics
Cell Cycle Proteins--metabolism
Cell Transformation, Neoplastic--drug effects
Cluster Analysis
Enzyme Inhibitors--pharmacology
Gene Expression Regulation, Neoplastic--genetics
Glioblastoma--genetics
Humans
Mice
Mice, Transgenic
Oligonucleotide Array Sequence Analysis
Polyribosomes--genetics
Protein Biosynthesis--drug effects
Protein Serine-Threonine Kinases
Proto-Oncogene Proteins--antagonists & inhibitors
Proto-Oncogene Proteins c-akt
RNA, Messenger--analysis
Signal Transduction--drug effects
Tumor Cells, Cultured
ras Proteins--antagonists & inhibitors