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:Investigation of proteomic changes in HEK 293T cells after 8h of actinomycin D treatment with special focus on RNA modifying enzymes.
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: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:In order to study the impact of rapamycin on AD-MSC under inflammatory or resting conditions, primary human Adipose-derived Mesenchymal Stromal Cells (AD-MSC) at passage 1 were plated at 1.5x10^4 in MEM-alpha, 5% Human Platelet Lysate, 1% Penicillin-Streptomycin and allowed to stand for 24h. The next day, AD-MSC were stimulated for 2 days (or not) with 20ng/mL IFN-gamma in presence of 10nM rapamycin (from 10.000X stock in DMSO) or DMSO (at 1:10000 dilution) as vehicle control. After 2 days, media were removed and RNA were extracted using RNeasy kit from QIAGEN with an on-column DNAse I digestion as manufacturer's instructions. RNA intergrity number were estimated on Agilent Bioanalyzer and were all above 9 before sequencing. Libraries and RNA sequencing were performed by the Beijing Genomics Institute (BGI)
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