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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.7
- 수록면
- 441 - 449 (9page)
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초록· 키워드
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Proteolysis in eukaryotic cells is mainly mediated by the ubiquitin (Ub)-proteasome system (UPS) and the autophagy-lysosome system (hereafter autophagy). The UPS is a selective proteolytic system in which substrates are recognized and tagged with ubiquitin for processive degradation by the proteasome. Autophagy is a bulk degradative system that uses lysosomal hydrolases to degrade proteins as well as various other cellular constituents. Since the inception of their discoveries, the UPS and autophagy were thought to be independent of each other in components, action mechanisms, and substrate selectivity. Recent studies suggest that cells operate a single proteolytic network comprising of the UPS and autophagy that share notable similarity in many aspects and functionally cooperate with each other to maintain proteostasis. In this review, we discuss the mechanisms underlying the crosstalk and interplay between the UPS and autophagy, with an emphasis on substrate selectivity and compensatory regulation under cellular stresses.
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참고문헌 (88)
참고문헌 신청
Akutsu, M. / 2016 / Ubiquitin chain diversity at a glance / J. Cell Sci 129:875~880
B'Chir, W. / 2013 / The eIF2alpha/ATF4 pathway is essential for stress-induced autophagy gene expression / Nucleic Acids Res 41:7683~7699
Bachmair, A. / 1986 / In vivo half-life of a protein is a function of its amino-terminal residue / Science 234:179~186
Bao, X. / 2017 / Bortezomib induces apoptosis and suppresses cell growth and metastasis by inactivation of Stat3 signaling in chondrosarcoma / Int. J. Oncol 50:477~486
Bates, G. P. / 2015 / Huntington disease / Nat. Rev. Dis. Primers 1:15005
B'Chir, W. / 2013 / The eIF2alpha/ATF4 pathway is essential for stress-induced autophagy gene expression / Nucleic Acids Res 41:7683~7699
Bachmair, A. / 1986 / In vivo half-life of a protein is a function of its amino-terminal residue / Science 234:179~186
Bao, X. / 2017 / Bortezomib induces apoptosis and suppresses cell growth and metastasis by inactivation of Stat3 signaling in chondrosarcoma / Int. J. Oncol 50:477~486
Bates, G. P. / 2015 / Huntington disease / Nat. Rev. Dis. Primers 1:15005
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