2013 Fiscal Year Final Research Report
pathophysiological analysis of autophagic substrate Nbr1.
Project/Area Number |
24790332
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Pathological medical chemistry
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Research Institution | Tokyo Metropolitan Institute of Medical Science |
Principal Investigator |
SOU Yu-shin 公益財団法人東京都医学総合研究所, 生体分子先端研究分野, 研究員 (60576221)
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Keywords | オートファジー / Nbr1 |
Research Abstract |
To investigate a physiology of the Nbr1 metabolism, accumulation of Nbr1 and the affect to the liver, we created liver specific Atg7 and Nbr1-double deficient mice, and performed biochemical and morphological analysis.In liver specific Nbr1 knockout mice, the abnormality is not recognized. Simultaneous loss of Atg7 and Nbr1 in the liver cause hepatomegaly and liver dysfunction. It is shown that Loss of Nbr1 has few impacts on liver pathology in Atg7-deficient livers. Further analysis is needed to clarify the pathophysiological role of Nbr1 in Atg7-p62 double knockout tissues.
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Research Products
(5 results)
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[Journal Article] Phosphorylation of p62 activates the Keap1 - Nrf2 pathway during selective autophagy2014
Author(s)
①Ichimura Y, Waguri S, Sou YS, Kageyama S, Hasegawa J, Ishimura R, Saito T, Yang Y, Kouno T, Fukutomi T, Hoshii T, Hirao A, Takagi K, Mizushima T, Motohashi H, Lee MS, Yoshimori T, Tanaka K, Yamamoto M, Komatsu M
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Journal Title
Mol Cell
Volume: 51
Pages: 618-31
Peer Reviewed
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