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Rapamycin-Induced Abundance Changes in the Proteome of Budding Yeast
Genomics & Informatics ; : 203-207, 2009.
Article in English | WPRIM | ID: wpr-86742
ABSTRACT
The target of rapamycin (TOR) signaling pathway conserved from yeast to human plays critical roles in regulation of eukaryotic cell growth. It has been shown that TOR pathway is involved in several cellular processes, including ribosome biogenesis, nutrient response, autophagy and aging. However, due to the functional diversity of TOR pathway, we do not know yet some key effectors of the pathway. To find unknown effectors of TOR signaling pathway, we took advantage of a green fluorescent protein (GFP)-tagged collection of budding yeast Saccharomyces cerevisiae . We analyzed protein abundance changes by measuring the GFP fluorescence intensity of 4156 GFP-tagged yeast strains under inhibition of TOR pathway. Our proteomic analysis argues that 83 proteins are decreased whereas 32 proteins are increased by treatment of rapamycin, a specific inhibitor of TOR complex 1 (TORC1). We found that, among the 115 proteins that show significant changes in protein abundance under rapamycin treatment, 37 proteins also show expression changes in the mRNA levels by more than 2-fold under the same condition. We suggest that the 115 proteins indentified in this study may be directly or indirectly involved in TOR signaling and can serve as candidates for further investigation of the effectors of TOR pathway.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Ribosomes / Saccharomyces cerevisiae / Autophagy / Yeasts / Organelle Biogenesis / Aging / RNA, Messenger / Proteins / Sirolimus / Proteome Limits: Humans Language: English Journal: Genomics & Informatics Year: 2009 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Ribosomes / Saccharomyces cerevisiae / Autophagy / Yeasts / Organelle Biogenesis / Aging / RNA, Messenger / Proteins / Sirolimus / Proteome Limits: Humans Language: English Journal: Genomics & Informatics Year: 2009 Type: Article