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87 |
Vitamin D-binding protein interacts with Aβ and suppresses Aβ-mediated pathology. Moon M, Song H, Hong HJ, Nam DW, Cha MY, Oh MS, Yu J, Ryu H, Mook-Jung I. Cell Death Differ. 2013 Apr;20(4):630-8. |
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86 |
Effect of conjugated linoleic acid, μ-calpain inhibitor, on pathogenesis of Alzheimer's disease. Lee E, Eom JE, Kim HL, Baek KH, Jun KY, Kim HJ, Lee M, Mook-Jung I, Kwon Y.Biochim Biophys Acta. 2013 Apr;1831(4):709-18. |
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85 |
Jin SM, Cho HJ, Kim YW, Hwang JY, Mook-Jung I. Aβ-induced Ca(2+) influx regulates astrocytic BACE1 expression via calcineurin/NFAT4 signals. Biochem Biophys Res Commun. 2012 Aug 31;425(3):649-55. |
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84 |
Son SM, Song H, Byun J, Park KS, Jang HC, Park YJ, Mook-Jung I. Accumulation of autophagosomes contributes to enhanced amyloidogenic APP processing under insulin-resistant conditions. Autophagy. 2012 Aug 29;8(12).
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83 |
Kook SY, Hong HS, Moon M, Ha CM, Chang SH, Mook-Jung I. Aβ1-42-RAGE interaction disrupts tight junctions of the blood brain barrier via Ca2+-calcineurin signaling. J neurosci. 2012. |
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82 |
Kim KH, Moon M, Yu SB, Mook-Jung I. Kim JI. RNASeq analysis of frontal cortex and cerebellum from 5XFAD mice at early stage of disease pathology. Journal of Alzheimer’s disease. In press. (Co-correspondance)
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81 |
Kim C, Choi H, Jung ES, Lee W, Oh S, Jeon NL, Mook-Jung I. HDAC6 inhibitor blocks amyloid beta-induced impairment of mitochondrial transport in hippocampal neurons. PLoS One. 2012;7(8):e42983. |
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80 |
Cha MY, Han SH, Son SM, Hong HS, Choi YS, Byun J, Mook-Jung I. Mitochondria-specific accumulation of amyloid beta induces mitochondrial dysfunction leading to apoptotic cell death. PLoS One. |
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79 |
Son SM, Song H, Byun J, Park KS, Jang HC, Park YJ, Mook-Jung I. (2012) Altered APP processing in the diabetic condition is mediated by autophagosome accumulation. Diabetes. 2012 Dec;61(12):3126-38. |
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78 |
Lee SH, Kim KR, Ryu SY, Son SM, Hong HS, Mook-Jung I, Lee SH, Ho WK. Impaired short-term plasticity caused by mitochondrial dysfunction in dentate granule cells is the earilist synpatic deficit in a mouse model of Alzhiemer's disease. J. Neuroscience. |
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