The Yeast Role in Medical Applications 2018
DOI: 10.5772/intechopen.70784
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TOR Signaling in Budding Yeast

Abstract: TOR (Target of Rapamycin) is a Ser/Thr kinase that was originally identified by genetic screening using the budding yeast Saccharomyces cerevisiae. The TOR protein forms two structurally and functionally distinct complexes (TOR complex 1, TORC1, and TOR complex 2, TORC2). TORC1 is involved in various cellular activities, such as cell growth, ribosome biogenesis, translation initiation, metabolism, stress response, aging, and autophagy. TORC2 is involved in actin organization, sphingolipid biogenesis, and endoc… Show more

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Cited by 7 publications
(4 citation statements)
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“…These observations indicate a role of the HOG MAPK pathway in fungal-bacteria interactions. Furthermore, the TOR kinase targeted by rifamycin functions upstream from MAP kinase cascades in S. cerevisiae and filamentous fungi (Loewith and Hall 2011;Inoue and Nomura 2018), suggesting indirect inhibition of fungal MAPKs by antibiotics produced by bacteria.…”
Section: Interactions With Bacteriamentioning
confidence: 99%
“…These observations indicate a role of the HOG MAPK pathway in fungal-bacteria interactions. Furthermore, the TOR kinase targeted by rifamycin functions upstream from MAP kinase cascades in S. cerevisiae and filamentous fungi (Loewith and Hall 2011;Inoue and Nomura 2018), suggesting indirect inhibition of fungal MAPKs by antibiotics produced by bacteria.…”
Section: Interactions With Bacteriamentioning
confidence: 99%
“…The S. cerevisiae TOR pathway senses nitrogen-availability and is involved in several important cellular activities including ribosome biosynthesis and growth promotion [48,54,180].…”
Section: The Tor Pathwaymentioning
confidence: 99%
“… 46 However, rapamycin acts by binding rapamycin binding protein, Fpr1 in yeast and the Fpr1‐rapamycin complex directly binds to TORC1 to inactivate it, thereby bypassing any SEA complex inhibition. 47 , 48 Surprisingly, Atg13 remained phosphorylated in vps501 Δ sea1 Δ cells, regardless of nitrogen starvation or rapamycin treatment, indicating autophagy induction is defective in these mutants, (Figure 5C,D ). Moreover, this suggests the vacuolar pool of TORC1 is not accessible to the Fpr1‐rapamycin inhibition in vps501 Δ sea1 Δ cells, likely resulting in a broad TORC1 signaling defect independent of autophagy induction.…”
Section: Resultsmentioning
confidence: 95%
“…46 However, rapamycin acts by binding rapamycin binding protein, Fpr1 in yeast and the Fpr1-rapamycin complex directly binds to TORC1 to inactivate it, thereby bypassing any SEA complex inhibition. 47,48 Surprisingly, Atg13 remained phosphorylated in vps501Δsea1Δ cells, regardless of nitrogen starvation or rapamycin treatment, indicating autophagy induction is defective in these mutants, (Figure 5C,D).…”
Section: The Torc1 Complex and Induction Of Autophagy Are Defective I...mentioning
confidence: 97%