The University of Osaka · 의학
타케시 노다 교수의 연구실은 세포 자가분해 과정인 아귀토파지의 분자 기전과 그 조절 메커니즘을 중심으로 연구를 진행하고 있습니다. 특히, 토르(Tor) 키나제가 아귀토파지 유도를 억제하는 핵심 조절자임을 밝혀내었으며, 맛물기반의 PI3-kinase 복합체와 Atg14L 단백질이 아귀토파지 소포 형성에 어떻게 관여하는지 규명하고 있습니다. 또한, 영양 상태에 따라 세포 내 단백질 수송 경로가 어떻게 전환되는지에 대한 기전 연구를 통해 세포의 대사 적응 메커니즘을 탐구하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Autophagy is a bulk protein degradation process that is induced by starvation. The control mechanism for induction of autophagy is not well understood. We found that Tor, a phosphatidylinositol kinase homologue, is involved in the control of autophagy in the yeast, Saccharomyces cerevisiae. When rapamycin, an inhibitor of Tor function, is added, autophagy is induced even in cells growing in nutrient-rich medium. A temperature-sensitive tor mutant also leads to induction of autophagy at a nonperm
Autophagy is a catabolic process that allows cells to digest their cytoplasmic constituents via autophagosome formation and lysosomal degradation. Recently, an autophagy-specific phosphatidylinositol 3-kinase (PI3-kinase) complex, consisting of hVps34, hVps15, Beclin-1, and Atg14L, has been identified in mammalian cells. Atg14L is specific to this autophagy complex and localizes to the endoplasmic reticulum (ER). Knockdown of Atg14L leads to the disappearance of the DFCP1-positive omegasome, whi
In nutrient-rich, vegetative conditions, the yeast Saccharomyces cerevisiae transports a resident protease, aminopeptidase I (API), to the vacuole by the cytoplasm to vacuole targeting (Cvt) pathway, thus contributing to the degradative capacity of this organelle. When cells subsequently encounter starvation conditions, the machinery that recruited precursor API (prAPI) also sequesters bulk cytosol for delivery, breakdown, and recycling in the vacuole by the autophagy pathway. Each of these over
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