Project description:Investigating transcriptional changes after autophagy induction by rapamycin to compare changes in autophagy-related genes to changes in histone modifications.
Project description:Investigation of differential pre-mRNA splicing in breast cancer cell line MCF-7 treated with rapamycin compared to vehicle DMSO that are overexpressing TRIB3
Project description:Compound CID 3538206 inhibits yeast TORC1 activity and functionally mimic rapamycin. We used microarrays to compare the global gene expression with the treatment of CID 3528206 and rapamycin. BY4741 yeast cells were treated with1% DMSO, 20 uM CID 3528206 and 200 nM rapamycin in duplicate for 3hrs. RNA extracted and labeled to probe yeast gene arrays
Project description:To shed light on the TOR signaling network in crop plants, we investigated the global transcriptome changes in rice suspension cells (cultivar Kitaake) treated with the TOR-specific inhibitor rapamycin.
Project description:Investigation of proteomic changes in HEK 293T cells after 8h of actinomycin D treatment with special focus on RNA modifying enzymes.
Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. Experiment Overall Design: CEM-C1 cells were treated with 10 nM rapamycin or DMSO and harvested for microarray analysis at 24 hours
Project description:The first aim was to identify genes whose transcription is induced by rapamycin feeding in Drosophila larvae. Secondly, the goal was to find out which contribution the transcription factor REPTOR (=CG13624) has to the observed changes in expression. We thus compared gene epxression between rapamycin fed and control fed larvae in wild type larvae and in REPTOR KO larvae. 3 biological replicates from 4 conditions: control larvae plus/miuns rapamycin, KO larvae plus/minus rapamycin; overall 12 samples
Project description:T-47 cells were treated with rapamycin, 3-methyladenine (3MA)-rapamycin and vehicle (DMSO, control) in a time series manner (1, 8, 24 and 48h), Affymetrix Genechip U133 Plus 2.0 array were used to compare the gene expression patterns of rapamycin-treated, 3MA-rapamycin treated versus control cells. All experiments were carried out in triplicates and a total of 24 chips were used. 3MA-Rapamycin treated samples were only limited to 24 h as total RNA for 48h was degraded.