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논문 기본 정보

자료유형
학술저널
저자정보
김상균 (Harvard University) John Blenis (Harvard Medical School Boston) Gwen R. Buel (Harvard Medical School)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제35권 제6호
발행연도
2013.6
수록면
463 - 473 (11page)
DOI
10.1007/s10059-013-0138-2

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The mammalian target of rapamycin (mTOR) is an evolu-tionally conserved kinase which exists in two distinct structural and functional complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). Of the two complexes, mTORC1 couples nutrient abundance to cell growth and proliferation by sensing and integrating a variety of inputs arising from amino acids, cellular stresses, energy status, and growth factors. Defects in mTORC1 regulation are implicated in the development of many metabolic diseases, including cancer and diabetes. Over the past decade, significant advances have been made in deciphering the complexity of the signaling processes contributing to mTORC1 regulation and function, but the mechanistic details are still not fully understood. In particular, how amino acid availability is sensed by cells and signals to mTORC1 remains unclear. In this review, we discuss the current understanding of nutrient-dependent control of mTORC1 signaling and will focus on the key components involved in amino acid signaling to mTORC1.

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