Open AccessJournal Article
14-3-3 proteins: an important regulator of autophagy in diseases.
TLDR
The role of 14-3-3 proteins in the control of autophagy in cancer, neurodegenerative diseases and other pathological conditions is summarized.Abstract:
Autophagy is a cell digestion process that determines cell fate by promoting cell survival or inducing cell death in a cell context-dependent manner. Several classical signaling pathways, such as phosphoinositide-3-kinase and mammalian target of rapamycin, tightly regulate autophagy. 14-3-3 proteins regulate various signaling pathways by phosphorylation-dependent binding with partner proteins. 14-3-3 proteins also regulate autophagy by binding with autophagy-related proteins such as Beclin-1 and hVPS34. This review summarizes the role of 14-3-3 proteins in the control of autophagy in cancer, neurodegenerative diseases and other pathological conditions.read more
Citations
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Characterization of the expression and prognostic value of 14-3-3 isoforms in breast cancer
TL;DR: The findings systematically elucidate the expression and distinct prognostic value of 14-3-3 isoforms in BrCa, which may provide potential therapeutic targets and prognostic biomarkers for BrCa.
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Serum levels of 14-3-3η are associated with increased disease risk, activity and duration of rheumatoid arthritis in Chinese patients.
TL;DR: Wang et al. as discussed by the authors determined the association between serum 14-3-3η expression levels and disease risk, inflammation level and disease duration in Chinese patients with rheumatoid arthritis.
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hucMSC-sEVs-Derived 14-3-3ζ Serves as a Bridge between YAP and Autophagy in Diabetic Kidney Disease
Siqi Yin,Wanzhu Liu,Cheng Ji,Yuan Zhu,Yunjie Shan,Zi-Qin Zhou,Wenya Chen,Leilei Zhang,Zixuan Sun,Wen-Yu Zhou,Hui Qian +10 more
TL;DR: This study provides new strategies for the prevention of DKD and proposes the possibility of hucMSC-sEVs becoming a new treatment for DKD in the future.
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Physiological Consequences of Targeting 14-3-3 and Its Interacting Partners in Neurodegenerative Diseases
Akshatha Ganne,Meenakshisundaram Balasubramaniam,Nirjal Mainali,Paavani Atluri,Robert J. Shmookler Reis,Srinivas Ayyadevara +5 more
TL;DR: In this article , the authors used intra-aggregate crosslinking to identify 14-3-3 interaction partners, all of which were significantly enriched in AD brain aggregates relative to controls.
References
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Noboru Mizushima,Masaaki Komatsu +1 more
TL;DR: It is explored how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease.
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TL;DR: This review summarizes the current knowledge about the molecular machinery of autophagy and the role of the autophagic machinery in eukaryotic development and identifies a set of evolutionarily conserved genes that are essential forAutophagy.
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Sophie Pattingre,Sophie Pattingre,Amina T. Tassa,Xueping Qu,Xueping Qu,Rita Garuti,Xiao Huan Liang,Noboru Mizushima,Milton Packer,Michael D. Schneider,Beth Levine,Beth Levine +11 more
TL;DR: Bcl-2 not only functions as an antiapoptotic protein, but also as an antiautophagy protein via its inhibitory interaction with Beclin 1, which may help maintain autophagy at levels that are compatible with cell survival, rather than cell death.
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Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease.
Brinda Ravikumar,Coralie Vacher,Zdenek Berger,Janet E. Davies,Shouqing Luo,Lourdes Garcia Oroz,Francesco Scaravilli,Douglas F. Easton,Rainer Duden,Cahir J. O'Kane,David C. Rubinsztein +10 more
TL;DR: This work shows that mammalian target of rapamycin (mTOR) is sequestered in polyglutamine aggregates in cell models, transgenic mice and human brains, and provides proof-of-principle for the potential of inducing autophagy to treat Huntington disease.
Journal ArticleDOI
Promotion of tumorigenesis by heterozygous disruption of the beclin 1 autophagy gene
Xueping Qu,Jie Yu,Govind Bhagat,Norihiko Furuya,Hanina Hibshoosh,Andrea B. Troxel,Jeffrey M. Rosen,Eeva-Liisa Eskelinen,Noboru Mizushima,Yoshinori Ohsumi,Giorgio Cattoretti,Beth Levine +11 more
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