2023/02/05 更新

写真a

ヤマシタ シュンイチ
山下 俊一
YAMASHITA Shun-ichi
所属
教育研究院 医歯学系 医学系列 助教
医歯学総合研究科 生体機能調節医学専攻 腎科学 助教
職名
助教
外部リンク

学位

  • 博士(農学) ( 2007年5月   京都大学 )

  • 修士(農芸化学) ( 2003年3月   東京農業大学 )

研究キーワード

  • マイトファジー

  • ミトコンドリア

  • ペルオキシソーム

  • Pexophagy

  • Autophagy

  • ペキソファジー

  • オートファジー

研究分野

  • ライフサイエンス / 細胞生物学

経歴(researchmap)

  • 米カリフォルニア工科大学   Division of Biology and Biological Engineering   客員研究員

    2018年10月 - 2019年10月

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  • 新潟大学   大学院医歯学総合研究科機能制御学分野   助教

    2016年7月 - 現在

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  • 新潟大学   大学院医歯学総合研究科機能制御学分野   特任助教

    2014年1月 - 2016年6月

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  • 九州大学   大学院理学研究院生物科学部門   学術研究員

    2013年4月 - 2013年12月

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  • 九州大学   大学院理学研究院生物科学部門   日本学術振興会特別研究員PD

    2010年4月 - 2013年3月

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  • 九州大学   大学院理学研究院生物科学部門   学術研究員

    2008年5月 - 2010年3月

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  • 京都大学   大学院農学研究科応用生命科学専攻   博士研究員

    2007年7月 - 2008年4月

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▶ 全件表示

経歴

  • 新潟大学   医歯学総合研究科 生体機能調節医学専攻 腎科学   助教

    2015年7月 - 現在

  • 新潟大学   医歯学総合研究科   特任助教

    2014年4月 - 2015年6月

学歴

  • 京都大学   農学研究科   応用生命科学専攻

    2003年4月 - 2007年6月

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  • 東京農業大学   農学研究科   農芸化学専攻

    2001年4月 - 2003年3月

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    国名: 日本国

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  • 東京農業大学   農学部   農芸化学科

    1997年4月 - 2001年3月

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    国名: 日本国

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所属学協会

 

論文

  • A new beta cell-specific mitophagy reporter mouse shows that metabolic stress leads to accumulation of dysfunctional mitochondria despite increased mitophagy

    Kyota Aoyagi, Shun-ichi Yamashita, Yoshihiro Akimoto, Chiyono Nishiwaki, Yoko Nakamichi, Haruhide Udagawa, Manabu Abe, Kenji Sakimura, Tomotake Kanki, Mica Ohara-Imaizumi

    Diabetologia   2022年10月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science and Business Media LLC  

    DOI: 10.1007/s00125-022-05800-8

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    その他リンク: https://link.springer.com/article/10.1007/s00125-022-05800-8/fulltext.html

  • Fis1 ablation in the male germline disrupts mitochondrial morphology and mitophagy, and arrests spermatid maturation. 国際誌

    Grigor Varuzhanyan, Mark S Ladinsky, Shun-Ichi Yamashita, Manabu Abe, Kenji Sakimura, Tomotake Kanki, David C Chan

    Development (Cambridge, England)   148 ( 16 )   2021年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Male germline development involves choreographed changes to mitochondrial number, morphology, and organization. Mitochondrial reorganization during spermatogenesis was recently shown to require mitochondrial fusion and fission. Mitophagy, the autophagic degradation of mitochondria, is another mechanism for controlling mitochondrial number and physiology, but its role during spermatogenesis is largely unknown. During post-meiotic spermatid development, restructuring of the mitochondrial network results in packing of mitochondria into a tight array in the sperm midpiece to fuel motility. Here, we show that disruption of mouse Fis1 in the male germline results in early spermatid arrest that is associated with increased mitochondrial content. Mutant spermatids coalesce into multinucleated giant cells (GCs) that accumulate mitochondria of aberrant ultrastructure and numerous mitophagic and autophagic intermediates, suggesting a defect in mitophagy. We conclude that Fis1 regulates mitochondrial morphology and turnover to promote spermatid maturation.

    DOI: 10.1242/dev.199686

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  • The optineurin/TIA1 pathway inhibits aberrant stress granule formation and reduces ubiquitinated TDP-43. 国際誌

    Taichi Kakihana, Masahiko Takahashi, Yoshinori Katsuragi, Shun-Ichi Yamashita, Junya Sango, Tomotake Kanki, Osamu Onodera, Masahiro Fujii

    iScience   24 ( 7 )   102733 - 102733   2021年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron disease characterized by the formation of cytoplasmic ubiquitinated TDP-43 protein aggregates in motor neurons. Stress granules (SGs) are stress-induced cytoplasmic protein aggregates containing various neuropathogenic proteins, including TDP-43. Several studies have suggested that SGs are the initial site of the formation of pathogenic ubiquitinated TDP-43 aggregates in ALS neurons. Mutations in the optineurin (OPTN) and TIA1 genes are causative factors of familial ALS with TDP-43 aggregation pathology. We found that both OPTN depletion and ALS-associated OPTN mutations upregulated the TIA1 level in cells recovered from heat shock, and this upregulated TIA1 increased the amount of ubiquitinated TDP-43. Ubiquitinated TDP-43 induced by OPTN depletion was localized in SGs. Our study suggests that ALS-associated loss-of-function mutants of OPTN increase the amount of ubiquitinated TDP-43 in neurons by increasing the expression of TIA1, thereby promoting the aggregation of ubiquitinated TDP-43.

    DOI: 10.1016/j.isci.2021.102733

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  • Mitophagy reporter mouse analysis reveals increased mitophagy activity in disuse-induced muscle atrophy. 国際誌

    Shun-Ichi Yamashita, Masanao Kyuuma, Keiichi Inoue, Yuki Hata, Ryu Kawada, Masaki Yamabi, Yasuyuki Fujii, Junko Sakagami, Tomoyuki Fukuda, Kentaro Furukawa, Satoshi Tsukamoto, Tomotake Kanki

    Journal of cellular physiology   2021年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Muscle disuse induces atrophy through increased reactive oxygen species (ROS) released from damaged mitochondria. Mitophagy, the autophagic degradation of mitochondria, is associated with increased ROS production. However, the mitophagy activity status during disuse-induced muscle atrophy has been a subject of debate. Here, we developed a new mitophagy reporter mouse line to examine how disuse affected mitophagy activity in skeletal muscles. Mice expressing tandem mCherry-EGFP proteins on mitochondria were then used to monitor the dynamics of mitophagy activity. The reporter mice demonstrated enhanced mitophagy activity and increased ROS production in atrophic soleus muscles following a 14-day hindlimb immobilization. Results also showed an increased expression of multiple mitophagy genes, including Bnip3, Bnip3l, and Park2. Our findings thus conclude that disuse enhances mitophagy activity and ROS production in atrophic skeletal muscles and suggests that mitophagy is a potential therapeutic target for disuse-induced muscle atrophy.

    DOI: 10.1002/jcp.30404

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  • MITOL promotes cell survival by degrading Parkin during mitophagy. 国際誌

    Isshin Shiiba, Keisuke Takeda, Shun Nagashima, Naoki Ito, Takeshi Tokuyama, Shun-Ichi Yamashita, Tomotake Kanki, Toru Komatsu, Yasuteru Urano, Yuuta Fujikawa, Ryoko Inatome, Shigeru Yanagi

    EMBO reports   22 ( 3 )   e49097   2021年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Parkin promotes cell survival by removing damaged mitochondria via mitophagy. However, although some studies have suggested that Parkin induces cell death, the regulatory mechanism underlying the dual role of Parkin remains unknown. Herein, we report that mitochondrial ubiquitin ligase (MITOL/MARCH5) regulates Parkin-mediated cell death through the FKBP38-dependent dynamic translocation from the mitochondria to the ER during mitophagy. Mechanistically, MITOL mediates ubiquitination of Parkin at lysine 220 residue, which promotes its proteasomal degradation, and thereby fine-tunes mitophagy by controlling the quantity of Parkin. Deletion of MITOL leads to accumulation of the phosphorylated active form of Parkin in the ER, resulting in FKBP38 degradation and enhanced cell death. Thus, we have shown that MITOL blocks Parkin-induced cell death, at least partially, by protecting FKBP38 from Parkin. Our findings unveil the regulation of the dual function of Parkin and provide a novel perspective on the pathogenesis of PD.

    DOI: 10.15252/embr.201949097

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  • Association and dissociation between the mitochondrial Far complex and Atg32 regulate mitophagy. 国際誌

    Aleksei Innokentev, Kentaro Furukawa, Tomoyuki Fukuda, Tetsu Saigusa, Keiichi Inoue, Shun-Ichi Yamashita, Tomotake Kanki

    eLife   9   2020年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Mitophagy plays an important role in mitochondrial homeostasis. In yeast, the phosphorylation of the mitophagy receptor Atg32 by casein kinase 2 is essential for mitophagy. This phosphorylation is counteracted by the yeast equivalent of the STRIPAK complex consisting of the PP2A-like protein phosphatase Ppg1 and Far3-7-8-9-10-11 (Far complex), but the underlying mechanism remains elusive. Here we show that two subpopulations of the Far complex reside in the mitochondria and endoplasmic reticulum, respectively, and play distinct roles; the former inhibits mitophagy via Atg32 dephosphorylation, and the latter regulates TORC2 signaling. Ppg1 and Far11 form a subcomplex, and Ppg1 activity is required for the assembling integrity of Ppg1-Far11-Far8. The Far complex preferentially interacts with phosphorylated Atg32, and this interaction is weakened by mitophagy induction. Furthermore, the artificial tethering of Far8 to Atg32 prevents mitophagy. Taken together, the Ppg1-mediated Far complex formation and its dissociation from Atg32 are crucial for mitophagy regulation.

    DOI: 10.7554/eLife.63694

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  • Atg43 tethers isolation membranes to mitochondria to promote starvation-induced mitophagy in fission yeast. 国際誌

    Tomoyuki Fukuda, Yuki Ebi, Tetsu Saigusa, Kentaro Furukawa, Shun-Ichi Yamashita, Keiichi Inoue, Daiki Kobayashi, Yutaka Yoshida, Tomotake Kanki

    eLife   9   2020年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Degradation of mitochondria through mitophagy contributes to the maintenance of mitochondrial function. In this study, we identified that Atg43, a mitochondrial outer membrane protein, serves as a mitophagy receptor in the model organism Schizosaccharomyces pombe to promote the selective degradation of mitochondria. Atg43 contains an Atg8-family-interacting motif essential for mitophagy. Forced recruitment of Atg8 to mitochondria restores mitophagy in Atg43-deficient cells, suggesting that Atg43 tethers expanding isolation membranes to mitochondria. We found that the mitochondrial import factors, including the Mim1-Mim2 complex and Tom70, are crucial for mitophagy. Artificial mitochondrial loading of Atg43 bypasses the requirement of the import factors, suggesting that they contribute to mitophagy through Atg43. Atg43 not only maintains growth ability during starvation but also facilitates vegetative growth through its mitophagy-independent function. Thus, Atg43 is a useful model to study the mechanism and physiological roles, as well as the origin and evolution, of mitophagy in eukaryotes.

    DOI: 10.7554/eLife.61245

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  • FKBP8 LIRL-dependent mitochondrial fragmentation facilitates mitophagy under stress conditions. 査読 国際誌

    Seung-Min Yoo, Shun-Ichi Yamashita, Hyunjoo Kim, DoHyeong Na, Haneul Lee, Seo Jin Kim, Dong-Hyung Cho, Tomotake Kanki, Yong-Keun Jung

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology   34 ( 2 )   2944 - 2957   2020年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Mitochondrial quality control maintains mitochondrial function by regulating mitochondrial dynamics and mitophagy. Despite the identification of mitochondrial quality control factors, little is known about the crucial regulators coordinating both mitochondrial fission and mitophagy. Through a cell-based functional screening assay, FK506 binding protein 8 (FKBP8) was identified to target microtubule-associated protein 1 light chain 3 (LC3) to the mitochondria and to change mitochondrial morphology. Microscopy analysis revealed that the formation of tubular and enlarged mitochondria was observed in FKBP8 knockdown HeLa cells and the cortex of Fkbp8 heterozygote-knockout mouse embryos. Under iron depletion-induced stress, FKBP8 was recruited to the site of mitochondrial division through budding and colocalized with LC3. FKBP8 was also found to be required for mitochondrial fragmentation and mitophagy under hypoxic stress. Conversely, FKBP8 overexpression induced mitochondrial fragmentation in HeLa cells, human fibroblasts and mouse embryo fibroblasts (MEFs), and this fragmentation occurred in Drp1 knockout MEF cells, FIP200 knockout HeLa cells and BNIP3/NIX double knockout HeLa cells, but not in Opa1 knockout MEFs. Interestingly, we found an LIR motif-like sequence (LIRL), as well as an LIR motif, at the N-terminus of FKBP8 and LIRL was essential for both inducing mitochondrial fragmentation and binding of FKBP8 to OPA1. Together, we suggest that FKBP8 plays an essential role in mitochondrial fragmentation through LIRL during mitophagy and this activity of FKBP8 together with LIR is required for mitophagy under stress conditions.

    DOI: 10.1096/fj.201901735R

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  • Gemcitabine induces Parkin-independent mitophagy through mitochondrial-resident E3 ligase MUL1-mediated stabilization of PINK1. 査読 国際誌

    Ryoko Igarashi, Shun-Ichi Yamashita, Tomohiro Yamashita, Keiichi Inoue, Tomoyuki Fukuda, Takeo Fukuchi, Tomotake Kanki

    Scientific reports   10 ( 1 )   1465 - 1465   2020年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Mitophagy plays an important role in the maintenance of mitochondrial homeostasis. PTEN-induced kinase (PINK1), a key regulator of mitophagy, is degraded constitutively under steady-state conditions. During mitophagy, it becomes stabilized in the outer mitochondrial membrane, particularly under mitochondrial stress conditions, such as in treatment with uncouplers, generation of excessive mitochondrial reactive oxygen species, and formation of protein aggregates in mitochondria. Stabilized PINK1 recruits and activates E3 ligases, such as Parkin and mitochondrial ubiquitin ligase (MUL1), to ubiquitinate mitochondrial proteins and induce ubiquitin-mediated mitophagy. Here, we found that the anticancer drug gemcitabine induces the stabilization of PINK1 and subsequent mitophagy, even in the absence of Parkin. We also found that gemcitabine-induced stabilization of PINK1 was not accompanied by mitochondrial depolarization. Interestingly, the stabilization of PINK1 was mediated by MUL1. These results suggest that gemcitabine induces mitophagy through MUL1-mediated stabilization of PINK1 on the mitochondrial membrane independently of mitochondrial depolarization.

    DOI: 10.1038/s41598-020-58315-w

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  • Glaucoma-Associated Mutations in the Optineurin Gene Have Limited Impact on Parkin-Dependent Mitophagy 査読

    Chernyshova K, Inoue K, Yamashita SI, Fukuchi T, Kanki T

    Invest Opthalmol Vis Sci   60 ( 10 )   3625 - 3635   2019年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1167/iovs.19-27184.

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  • The PP2A-like Protein Phosphatase Ppg1 and the Far Complex Cooperatively Counteract CK2-Mediated Phosphorylation of Atg32 to Inhibit Mitophagy 査読

    Kentaro Furukawa, Tomoyuki Fukuda, Shun-ichi Yamashita, Tetsu Saigusa, Yusuke Kurihara, Yutaka Yoshida, Hiromi Kirisako, Hitoshi Nakatogawa, Tomotake Kanki

    Cell Reports   23 ( 12 )   3579 - 3590   2018年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier B.V.  

    Mitophagy plays an important role in mitochondrial quality control. In yeast, phosphorylation of the mitophagy receptor Atg32 by casein kinase 2 (CK2) upon induction of mitophagy is a prerequisite for interaction of Atg32 with Atg11 (an adaptor protein for selective autophagy) and following delivery of mitochondria to the vacuole for degradation. Because CK2 is constitutively active, Atg32 phosphorylation must be precisely regulated to prevent unrequired mitophagy. We found that the PP2A (protein phosphatase 2A)-like protein phosphatase Ppg1 was essential for dephosphorylation of Atg32 and inhibited mitophagy. We identified the Far complex proteins, Far3, Far7, Far8, Far9, Far10, and Far11, as Ppg1-binding proteins. Deletion of Ppg1 or Far proteins accelerated mitophagy. Deletion of a cytoplasmic region (amino acid residues 151–200) of Atg32 caused the same phenotypes as in ppg1Δ cells, which suggested that dephosphorylation of Atg32 by Ppg1 required this region. Therefore, Ppg1 and the Far complex cooperatively dephosphorylate Atg32 to prevent excessive mitophagy. Mitophagy in yeast is initiated by CK2-mediated phosphorylation of the mitophagy receptor Atg32. However, how this phosphorylation is prevented under non-mitophagy-inducing conditions is unclear. Furukawa et al. show that the PP2A-like protein phosphatase Ppg1 and the Far complex negatively regulate mitophagy by counteracting CK2-mediated phosphorylation of Atg32.

    DOI: 10.1016/j.celrep.2018.05.064

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  • Detection of iron depletion- and hypoxia-induced mitophagy in mammalian cells 査読

    Shun-ichi Yamashita, Tomotake Kanki

    Methods in Molecular Biology   1782   315 - 324   2018年

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    記述言語:英語   掲載種別:論文集(書籍)内論文   出版者・発行元:Humana Press Inc.  

    Mitochondrial autophagy or mitophagy is a process that selectively degrades mitochondria via autophagy. It is believed that mitophagy degrades damaged or unnecessary mitochondria and is important for maintaining mitochondrial homeostasis. To date, it is known that several stimuli can induce mitophagy. However, some of these stimuli (including iron depletion, hypoxia, and nitrogen starvation) induce mild mitophagy, which is difficult to detect by measuring the decrease in mitochondrial mass. Recently, we have successfully detected mitophagy induced under these conditions using mito-Keima as a reporter. In this chapter, we describe the protocols for induction and detection of iron depletion- and hypoxia-induced mitophagy using the mito-Keima-expressing cells.

    DOI: 10.1007/978-1-4939-7831-1_18

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  • Detection of Hypoxia-Induced and Iron Depleition-Induced Mitophagy in Mammalian Cells. 査読

    Yamashita S, Kanki T

    Methods in Molecular Biology   1759   141 - 149   2018年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/7651_2017_19

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  • Parkin非依存的マイトファジーにおけるPINK1の機能解析

    五十嵐 遼子, 山下 俊一, クセニヤ・チェルニショワ, 福地 健郎, 神吉 智丈

    眼科臨床紀要   10 ( 8 )   692 - 692   2017年8月

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    記述言語:日本語   出版者・発行元:眼科臨床紀要会  

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  • 正常眼圧緑内障を発症させるオプチニューリン遺伝子変異とミトコンドリア分解の関係

    クセニヤ・チェルヌショワ, 山下 俊一, 五十嵐 遼子, 福地 健郎, 神吉 智丈

    眼科臨床紀要   10 ( 8 )   691 - 692   2017年8月

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    記述言語:日本語   出版者・発行元:眼科臨床紀要会  

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  • How autophagy eats large mitochondria: Autophagosome formation coupled with mitochondrial fragmentation 査読

    Shun-ichi Yamashita, Tomotake Kanki

    AUTOPHAGY   13 ( 5 )   980 - 981   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:TAYLOR & FRANCIS INC  

    Mitochondrial autophagy (mitophagy) is thought to be a multi-step pathway wherein mitochondria are first divided into small fragments, which are subsequently recognized by the phagophore. DNM1L (dynamin 1 like) plays a pivotal role in mitochondrial division; however, its role in mitophagy remains controversial. In our recent study, we examined the contribution of DNM1L to mitophagy and showed that mitophagy and mitochondrial division occur even in DNM1L-defective cells. Furthermore, time-lapse imaging of mitophagy showed that DNM1L-independent mitochondrial division occurs concomitantly with autophagosome formation. Upstream factors of autophagosome formation, i.e., RB1CC1/FIP200, ATG14, and WIPIs, are required for mitochondrial division, whereas ATG5 and ATG3 are dispensable. These results indicate that a portion of the tubular mitochondria is first recognized and then divided into small fragments by a phagophore-mediated event, independently of DNM1L. This autophagic process suggests that autophagy has the potential to degrade substrates larger than autophagosomes.

    DOI: 10.1080/15548627.2017.1291113

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  • Assessing pexophagy in mammalian cells 査読

    Shun-Ichi Yamashita, Yukio Fujiki

    Methods in Molecular Biology   1595   243 - 248   2017年

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    記述言語:英語   掲載種別:論文集(書籍)内論文   出版者・発行元:Humana Press Inc.  

    In mammalian cells several hundred peroxisomes are maintained by a balance between the biogenesis and turnover by peroxisome homeostasis. Pexophagy, a form of autophagy specific for peroxisomes, is the main pathway for peroxisome degradation, but molecular mechanisms of mammalian pexophagy are largely unknown. This is due to the lack of well-established pexophagy-inducing conditions in mammalian cells. Recently, several conditions that induce pexophagy were described for mammalian cells, involving ubiquitin and adaptor proteins of autophagy. In this chapter, we describe the protocol for Pex3-induced pexophagy, the more readable and highly inducible pexophagy condition in mammalian cells.

    DOI: 10.1007/978-1-4939-6937-1_23

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  • Experimental systems to study yeast pexophagy 査読

    Shun-Ichi Yamashita, Masahide Oku, Yasuyoshi Sakai, Yukio Fujiki

    Methods in Molecular Biology   1595   249 - 255   2017年

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    記述言語:英語   掲載種別:論文集(書籍)内論文   出版者・発行元:Humana Press Inc.  

    Peroxisome abundance is tightly regulated according to the physiological contexts, through regulations of both proliferation and degradation of the organelles. Here, we describe detailed methods to analyze processes for autophagic degradation of peroxisomes, termed pexophagy, in yeast organisms. The assay systems include a method for biochemical detection of pexophagy completion, and one for microscopic visualization of specialized membrane structures acting in pexophagy. As a model yeast organism utilized in studies of pexophagy, the methylotrophic yeast Komagataella phaffii (Pichia pastoris) is referred to in this chapter and related information on the studies with baker’s yeast (Saccharomyces cerevisiae) is also included. The described techniques facilitate elucidation of molecular machineries for pexophagy and understanding of peroxisome-selective autophagic pathways.

    DOI: 10.1007/978-1-4939-6937-1_24

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  • Mitochondrial division occurs concurrently with autophagosome formation but independently of Drp1 during mitophagy 査読

    Shun-ichi Yamashita, Xiulian Jin, Kentaro Furukawa, Maho Hamasaki, Akiko Nezu, Hidenori Otera, Tetsu Saigusa, Tamotsu Yoshimori, Yasuyoshi Sakai, Katsuyoshi Mihara, Tomotake Kanki

    JOURNAL OF CELL BIOLOGY   215 ( 5 )   649 - 665   2016年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ROCKEFELLER UNIV PRESS  

    Mitophagy is thought to play an important role in mitochondrial quality control. Mitochondrial division is believed to occur first, and autophagosome formation subsequently occurs to enwrap mitochondria as a process of mitophagy. However, there has not been any temporal analysis of mitochondrial division and autophagosome formation in mitophagy. Therefore, the relationships among these processes remain unclear. We show that the mitochondrial division factor Dnm1 in yeast or Drp1 in mammalian cells is dispensable for mitophagy. Autophagosome formation factors, such as FIP200, ATG14, and WIPIs, were essential for the mitochondrial division for mitophagy. Live-cell imaging showed that isolation membranes formed on the mitochondria. A small portion of the mitochondria then divided from parental mitochondria simultaneously with the extension of isolation membranes and autophagosome formation. These findings suggest the presence of a mitophagy process in which mitochondrial division for mitophagy is accomplished together with autophagosome formation.

    DOI: 10.1083/jcb.201605093

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  • Constitutive Activation of PINK1 Protein Leads to Proteasome-mediated and Non-apoptotic Cell Death Independently of Mitochondrial Autophagy 査読

    Shiori Akabane, Kohei Matsuzaki, Shun-ichi Yamashita, Kana Arai, Kei Okatsu, Tomotake Kanki, Noriyuki Matsuda, Toshihiko Oka

    JOURNAL OF BIOLOGICAL CHEMISTRY   291 ( 31 )   16162 - 16174   2016年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Phosphatase and tensin homolog-induced putative kinase 1 (PINK1), a Ser/Thr kinase, and PARKIN, a ubiquitin ligase, are causal genes for autosomal recessive early-onset parkinsonism. Multiple lines of evidence indicate that PINK1 and PARKIN cooperatively control the quality of the mitochondrial population via selective degradation of damaged mitochondria by autophagy. Here, we report that PINK1 and PARKIN induce cell death with a 12-h delay after mitochondrial depolarization, which differs from the time profile of selective autophagy of mitochondria. This type of cell death exhibited definite morphologic features such as plasma membrane rupture, was insensitive to a pan-caspase inhibitor, and did not involve mitochondrial permeability transition. Expression of a constitutively active form of PINK1 caused cell death in the presence of a pan-caspase inhibitor, irrespective of the mitochondrial membrane potential. PINK1-mediated cell death depended on the activities of PARKIN and proteasomes, but it was not affected by disruption of the genes required for autophagy. Furthermore, fluorescence and electron microscopic analyses revealed that mitochondria were still retained in the dead cells, indicating that PINK1-mediated cell death is not caused by mitochondrial loss. Our findings suggest that PINK1 and PARKIN play critical roles in selective cell death in which damaged mitochondria are retained, independent of mitochondrial autophagy.

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  • Peroxisome homeostasis: Mechanisms of division and selective degradation of peroxisomes in mammals 査読

    Masanori Honsho, Shun-ichi Yamashita, Yukio Fujiki

    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH   1863 ( 5 )   984 - 991   2016年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Peroxisome number and quality are maintained by its biogenesis and turnover and are important for the homeostasis of peroxisomes. Peroxisomes are increased in number by division with dynamic morphological changes including elongation, constriction, and fission. In the course of peroxisomal division, peroxisomal morphogenesis is orchestrated by Pexi11 beta, dynamin-like protein 1 (DLP1), and mitochondrial fission factor (Mff). Conversely, peroxisome number is reduced by its degradation. Peroxisomes are mainly degraded by pexophagy, a type of autophagy specific for peroxisomes. Upon pexophagy, an adaptor protein translocates on peroxisomal membrane and connects peroxisomes to autophagic machineries. Molecular mechanisms of pexophagy are well studied in yeast systems where several specific adaptor proteins are identified. Pexophagy in mammals also proceeds in a manner dependent on adaptor proteins. In this review, we address the recent progress in studies on peroxisome morphogenesis and pexophagy. This article is part of a Special Issue entitled: Peroxisomes edited by Ralf Erdmann. (C) 2015 Elsevier B.V. All rights reserved.

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  • Mitophagy in yeast: Molecular mechanisms and physiological role 査読

    Tomotake Kanki, Kentaro Furukawa, Shun-ichi Yamashita

    BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH   1853 ( 10 )   2756 - 2765   2015年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Mitochondria autophagy (mitophagy) is a process that selectively degrades mitochondria via autophagy. Recently, there has been significant progress in the understanding of mitophagy in yeast. Atg32, a mitochondrial outer membrane receptor, is indispensable for mitophagy. Phosphorylation of Atg32 is an initial cue for selective mitochondrial degradation. Atg32 expression and phosphorylation regulate the induction and efficiency of mitophagy. In addition to Atg32-related processes, recent studies have revealed that mitochondrial fission and the mitochondria-endoplasmic reticulum (ER) contact site may play important roles in mitophagy. Mitochondrial fission is required to regulate mitochondrial size. Mitochondria-ER contact is mediated by the ER-mitochondria encounter structure and is important to supply lipids from the ER for autophagosome biogenesis for mitophagy. Mitophagy is physiologically important for regulating the number of mitochondria, diminishing mitochondrial production of reactive oxygen species, and extending chronological lifespan under caloric restriction. These findings suggest that mitophagy contributes to maintain mitochondrial homeostasis. However, whether mitophagy selectively degrades damaged or dysfunctional mitochondria in yeast is unknown. This article is part of a Special Issue entitled: Mitophagy. (C) 2015 Elsevier B.V. All rights reserved.

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  • Mitophagy is primarily due to alternative autophagy and requires the MAPK1 and MAPK14 signaling pathways 査読

    Yuko Hirota, Shun-ichi Yamashita, Yusuke Kurihara, Xiulian Jin, Masamune Aihara, Tetsu Saigusa, Dongchon Kang, Tomotake Kanki

    AUTOPHAGY   11 ( 2 )   332 - 343   2015年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:TAYLOR & FRANCIS INC  

    In cultured cells, not many mitochondria are degraded by mitophagy induced by physiological cellular stress. We observed mitophagy in HeLa cells using a method that relies on the pH-sensitive fluorescent protein Keima. With this approach, we found that mitophagy was barely induced by carbonyl cyanide m-chlorophenyl hydrazone treatment, which is widely used as an inducer of PARK2/Parkin-related mitophagy, whereas a small but modest amount of mitochondria were degraded by mitophagy under conditions of starvation or hypoxia. Mitophagy induced by starvation or hypoxia was marginally suppressed by knockdown of ATG7 and ATG12, or MAP1LC3B, which are essential for conventional macroautophagy. In addition, mitophagy was efficiently induced in Atg5 knockout mouse embryonic fibroblasts. However, knockdown of RAB9A and RAB9B, which are essential for alternative autophagy, but not conventional macroautophagy, severely suppressed mitophagy. Finally, we found that the MAPKs MAPK1/ERK2 and MAPK14/p38 were required for mitophagy. Based on these findings, we conclude that mitophagy in mammalian cells predominantly occurs through an alternative autophagy pathway, requiring the MAPK1 and MAPK14 signaling pathways.

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  • Peroxin Pex14p is the key component for coordinated autophagic degradation of mammalian peroxisomes by direct binding to LC3-II 査読

    Li Jiang, Sayuri Hara-Kuge, Shun-ichi Yamashita, Yukio Fujiki

    GENES TO CELLS   20 ( 1 )   36 - 49   2015年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Pexophagy can be experimentally induced in mammalian cells by removing the culture serum. Pex14p, a peroxisomal membrane protein essential for matrix protein import in docking of soluble receptor Pex5p, is involved in the mammalian autophagic degradation of peroxisomes and interacts with the lipidated form of LC3, termed LC3-II, an essential factor for autophagosome formation, under the starvation condition in CHO-K1 cells. However, molecular mechanisms underlying the Pex14p-LC3-II interaction remain largely unknown. To verify whether Pex14p directly binds LC3-II, we reconstituted an in vitro conjugation system for synthesis of LC3-II. We show here that Pex14p directly interacts with LC3-II via the transmembrane domain of Pex14p. Pex5p competitively inhibited this interaction, implying that Pex14p preferentially binds to Pex5p under the nutrient-rich condition. Moreover, a Pex5p mutant defective in PTS1-protein import lost its affinity for Pex14p under the condition of nutrient deprivation, thereby more likely explaining why Pex14p prefers to interact with LC3-II under the starvation condition in vivo. Together, these results suggest that Pex14p is a unique factor that functions in the dual processes in peroxisomal biogenesis and degradation with the coordination of Pex5p in response to the environmental changes.

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  • The membrane peroxin PEX3 induces peroxisome-ubiquitination-linked pexophagy 査読

    Shun-ichi Yamashita, Kakeru Abe, Yuki Tatemichi, Yukio Fujiki

    AUTOPHAGY   10 ( 9 )   1549 - 1564   2014年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:TAYLOR & FRANCIS INC  

    Peroxisomes are degraded by a selective type of autophagy known as pexophagy. Several different types of pexophagy have been reported in mammalian cells. However, the mechanisms underlying how peroxisomes are recognized by autophagy-related machinery remain elusive. PEX3 is a peroxisomal membrane protein (PMP) that functions in the import of PMPs into the peroxisomal membrane and has been shown to interact with pexophagic receptor proteins during pexophagy in yeast. Thus, PEX3 is important not only for peroxisome biogenesis, but also for peroxisome degradation. However, whether PEX3 is involved in the degradation of peroxisomes in mammalian cells is unclear. Here, we report that high levels of PEX3 expression induce pexophagy. In PEX3-loaded cells, peroxisomes are ubiquitinated, clustered, and degraded in lysosomes. Peroxisome targeting of PEX3 is essential for the initial step of this degradation pathway. The degradation of peroxisomes is inhibited by treatment with autophagy inhibitors or siRNA against NBR1, which encodes an autophagic receptor protein. These results indicate that ubiquitin-and NBR1-mediated pexophagy is induced by increased expression of PEX3 in mammalian cells. In addition, another autophagic receptor protein, SQSTM1/p62, is required only for the clustering of peroxisomes. Expression of a PEX3 mutant with substitution of all lysine and cysteine residues by arginine and alanine, respectively, also induces peroxisome ubiquitination and degradation, hence suggesting that ubiquitination of PEX3 is dispensable for pexophagy and an endogenous, unidentified peroxisomal protein is ubiquitinated on the peroxisomal membrane.

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  • Lag-phase autophagy in the methylotrophic yeast Pichia pastoris 査読

    Shun-ichi Yamashita, Hiroya Yurimoto, Dai Murakami, Mari Yoshikawa, Masahide Oku, Yasuyoshi Sakai

    GENES TO CELLS   14 ( 7 )   861 - 870   2009年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL PUBLISHING, INC  

    When microbes sense environmental changes, they often temporarily attenuate cell growth to adapt to the new situations, showing a lag phase. In this study, we report that the methylotrophic yeast, Pichia pastoris, induced autophagy during the lag phase after the cells were shifted from glucose to methanol medium. Through the autophagic process at least two proteins, aminopeptidase I precursor and cytosolic aldehyde dehydrogenase, were found to be transported into the vacuole, which was dependent on PpAtg11 and PpAtg17, respectively. Notably, PpAtg1 and PpAtg17 were required for early exit from the lag phase during the methanol adaptation. In accordance, phosphorylation states of elongation initiation factor 2 alpha indicated reductions of intracellular amino-acid pools in the atg mutant strains. Together, these data demonstrate the importance of amino acid recycling by autophagy during a cell-remodeling process.

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  • Atg26-Mediated Pexophagy Is Required for Host Invasion by the Plant Pathogenic Fungus Colletotrichum orbiculare 査読

    Makoto Asakura, Sachiko Ninomiya, Miki Sugimoto, Masahide Oku, Shun-ichi Yamashita, Tetsuro Okuno, Yasuyoshi Sakai, Yoshitaka Takano

    PLANT CELL   21 ( 4 )   1291 - 1304   2009年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC PLANT BIOLOGISTS  

    The number of peroxisomes in a cell can change rapidly in response to changing environmental and physiological conditions. Pexophagy, a type of selective autophagy, is involved in peroxisome degradation, but its physiological role remains to be clarified. Here, we report that cells of the cucumber anthracnose fungus Colletotrichum orbiculare undergo peroxisome degradation as they infect host plants. We performed a random insertional mutagenesis screen to identify genes involved in cucumber pathogenesis by C. orbiculare. In this screen, we isolated a homolog of Pichia pastoris ATG26, which encodes a sterol glucosyltransferase that enhances pexophagy in this methylotrophic yeast. The C. orbiculare atg26 mutant developed appressoria but exhibited a specific defect in the subsequent host invasion step, implying a relationship between pexophagy and fungal phytopathogenicity. Consistent with this, its peroxisomes are degraded inside vacuoles, accompanied by the formation of autophagosomes during infection-related morphogenesis. The autophagic degradation of peroxisomes was significantly delayed in the appressoria of the atg26 mutant. Functional domain analysis of Atg26 suggested that both the phosphoinositide binding domain and the catalytic domain are required for pexophagy and pathogenicity. In contrast with the atg26 mutant, which is able to form appressoria, the atg8 mutant, which is defective in the entire autophagic pathway, cannot form normal appressoria in the earlier steps of morphogenesis. These results indicate a specific function for Atg26-enhanced pexophagy during host invasion by C. orbiculare.

    DOI: 10.1105/tpc.108.060996

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  • Overexpression and purification of rat peroxisomal membrane protein 22, PMP22, in Pichia pastoris 査読

    Kyoko Egawa, Hiroyuki Shibata, Shun-ichi Yamashita, Hiroya Yurimoto, Yasuyoshi Sakai, Hiroaki Kato

    PROTEIN EXPRESSION AND PURIFICATION   64 ( 1 )   47 - 54   2009年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Peroxisomal membrane protein 22, PMP22, is an integral membrane protein that has four putative transmembrane-spanning regions. First reported as a major component of rat liver peroxisomal membranes and suggested to be involved in the metabolism of reactive oxygen species, its function and structure are still unknown owing to a lack of biochemical and structural experiments. Here we report the overproduction and purification of rat PMP22 (rPMP22) with the use of a methylotrophic yeast, Pichia pastoris, as a host. rPMP22 was localized not to peroxisomal membranes but to membrane compartments such as, the nuclear envelope. Highly pure rPMP22 was obtained in two steps. Several physicochemical assays indicated that the purified preparation should retain its functional structure. Furthermore, fed-batch fermentation yielded 90 mg of rPMP22 protein from 4 L of culture. This is the first report to demonstrate the overproduction of a recombinant rPMP22 in the membrane compartments of P. pastoris. (C) 2008 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.pep.2008.10.004

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  • Functions of PI4P and sterol glucoside are necessary for the synthesis of a nascent membrane structure during pexophagy 査読

    Shun-ichi Yamashita, Masahide Oku, Yasursh Sakai

    AUTOPHAGY   3 ( 1 )   35 - 37   2007年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LANDES BIOSCIENCE  

    We recently showed that, in the yeast Pichia, pastoris, an ergosterol glucoside synthesizing enzyme, Atg26, is recruited to the precursor of the pexophagic structure, micropexophogic membrane apparatus (MIPA), under the regulation of phosphatidylinositol 4'-monophosphate (PI4P)-signaling during pexophagy. Atg26 was found to harbor a novel PI4-binding motif, the GRAM domain. Both lipids, PI4P and sterol glucoside, synthesized by PpPik1 and PpAtg26, respectively, were necessary for pexophagy, in the step where the MIPA was formed. In this addendum, we review these findings, and speculate on the mechanistic and physiological implications of the functions of these lipids during the autophagic process.

    DOI: 10.4161/auto.3311

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  • Role of Vac8 in formation of the vacuolar sequestering membrane during micropexophagy 査読

    Masahide Oku, Taku Nishimura, Takeshi Hattori, Yoshitaka Ano, Shun-ichi Yamashita, Yasuyoshi Sakai

    AUTOPHAGY   2 ( 4 )   272 - 279   2006年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:LANDES BIOSCIENCE  

    Vac8 is a yeast vacuolar membrane protein involved in vacuolar membrane dynamics, e.g., vacuole inheritance and vacuolar membrane fusion. This protein is also necessary for a subset of autophagic pathways that deliver specific cellular components to the vacuole. In this study, we show that the micropexohagy and vacuole inheritance required distinct domain structures of Pichia pastoris Vac:8 (PpVac8). Whereas vacuole inheritance required the Armadillo repeat (ARM) region that resides in the middle part of the protein, micropexophagy did not. Deletion of both the ARM and C-terminal domains inhibited a characteristic of vacuolar dynamics during micropexophagy, i.e., formation of the vacuolar sequestering membrane (VSM). Subsequent analyses indicated that PpVAC8 disruption abolished recruitment of PpAtg11, another protein required for formation of the VSM, to the vacuolar membrane. These results present a novel molecular function of PpVac8 in micropexophagy.

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  • 出芽酵母のオートファジーに必須な遺伝子群 Atg分子による膜動態の制御とペキソファジー (ユビキチン-プロテアソーム系とオートファジー--作動機構と病態生理) -- (オートファジー-リソソーム/液胞系)

    山下 俊一, 阪井 康能

    蛋白質核酸酵素   51 ( 10 )   1474 - 1479   2006年8月

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    記述言語:日本語   出版者・発行元:共立出版  

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  • PI4P-signaling pathway for the synthesis of a nascent membrane structure in selective autophagy 査読

    SI Yamashita, M Oku, Y Wasada, Y Ano, Y Sakai

    JOURNAL OF CELL BIOLOGY   173 ( 5 )   709 - 717   2006年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ROCKEFELLER UNIV PRESS  

    Phosphoinositides regulate a wide range of cellular activities, including membrane trafficking and biogenesis, via interaction with various effector proteins that contain phosphoinositide binding motifs. We show that in the yeast Pichia pastoris, phosphatidylinositol 4'-monophosphate(PI4P) initiates de novo membrane synthesis that is required for peroxisome degradation by selective autophagy and that this PI4P signaling is modulated by an ergosterol-converting PpAtg26 (autophagy-related) protein harboring a novel PI4P binding GRAM (glucosyltransferase, Rab-like GTPase activators, and myotubularins) domain. A phosphatidylinositol-4-OH kinase, PpPik1, is the primary source of PI4P. PI4P concentrated in a protein-lipid nucleation complex recruits PpAtg26 through an interaction with the GRAM domain. Sterol conversion by PpAtg26 at the nucleation complex is necessary for elongation and maturation of the membrane structure. This study reveals the role of the PI4P-signaling pathway in selective autophagy, a process comprising multistep molecular events that lead to the de novo membrane formation.

    DOI: 10.1083/jcb.200512142

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  • Emendation of the genus Acidomonas Urakami, Tamaoka, Suzuki and Komagata 1989 査読

    S Yamashita, T Uchimura, K Komagata

    INTERNATIONAL JOURNAL OF SYSTEMATIC AND EVOLUTIONARY MICROBIOLOGY   54 ( 3 )   865 - 870   2004年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SOC GENERAL MICROBIOLOGY  

    The genus Acidomonas and the species Acidomonas methanolica were recharacterized by using the type strain (NIRIC 0498(T)), three reference strains and 10 methanol-utilizing bacteria that were isolated from activated sludge from three different sewage-treatment plants in Tokyo. Based on 16S rDNA sequences, all strains formed a single cluster within the Acetobacteraceae that was clearly different from the genera Acetobacter, Gluconobacter, Gluconacetobacter, Asaia and Kozakia. The 14 strains were identified as a single species, Acidomonas methanolica, by DNA-DNA similarities, showed DNA G + C contents that ranged from 62 to 63 mol% and had Q-10 as the major quinone, accounting for >87% of total ubiquinones. Cells of Acidomonas methanolica had a single polar flagellum (or occasionally polar tuft flagella); this differs from a previous study that described peritrichous flagella. Oxidation of acetate was positive for all strains, but oxidation of lactate was weakly positive and varied with strains. Dihydroxyacetone was not produced from glycerol. Pantothenic acid was an essential requirement for growth. The strains tested grew at mostly the same extent at pH 3.0-8.0. Therefore, Acidomonas methanolica should be regarded as acidotolerant, not aciclophilic. The descriptions of the genus Acidomonas and the species Acidomonas methanolica Urakami, Tamaoka, Suzuki and Komagata 1989 are emended with newly obtained data.

    DOI: 10.1099/ijs.0.02946-0

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▶ 全件表示

書籍等出版物

  • 実験医学増刊Vol.37 No.12:ミトコンドリアと疾患・老化

    井上敬一, 山下 俊一, 神吉智丈( 担当: 共著 ,  範囲: 哺乳類におけるミトコンドリアオートファジーの分子機構)

    羊土社  2019年7月  ( ISBN:9784758103800

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  • BIO Clinica: オートファジーと疾患

    山下俊一, 神吉智丈( 担当: 共著 ,  範囲: ミトコンドリア恒常性の維持とマイトファジー)

    北隆館、ニューサイエンス社  2018年 

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  • 実験医学:ユビキチン化を介したオルガネロファジー

    藤木幸夫, 山下俊一, 奥本寛治, 本庄雅則( 担当: 共著 ,  範囲: ペキソファジー:ペルオキシソームの形成・機能制御と分解機構)

    羊土社  2017年7月  ( ISBN:9784758101653

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  • 蛋白質核酸酵素:ユビキチン-プロテアソーム系とオートファジー

    山下俊一, 阪井康能( 担当: 共著 ,  範囲: 出芽酵母のオートファジーに必須な遺伝子群 Atg分子による膜動態の制御とペキソファジー)

    共立出版  2006年 

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MISC

▶ 全件表示

講演・口頭発表等

  • レセプター介在性マイトファジーの分子機構 招待

    山下俊一, 神吉智丈

    第94回日本生化学会大会  2021年11月 

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    開催年月日: 2021年11月

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  • The role of mitophagy-receptor proteins in mitophagy 招待

    山下 俊一, David Chan, 神吉 智丈

    第42回日本分子生物学会年会  2019年12月 

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    記述言語:日本語   会議種別:口頭発表(招待・特別)  

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  • The contribution of mitophagy to thermogenesis in adipose tissues

    山下 俊一

    第4回温度生物学若手の会  2018年6月 

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    記述言語:日本語   会議種別:ポスター発表  

    開催地:沖縄県  

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  • Mitochondrial division is associated with autophagosome formation during mitophagy 国際会議

    山下 俊一, 神吉 智丈

    Keystone Symposia Mitochondrial Biology, Selective Autophagy  2018年4月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:京都  

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  • Regulation of mitochondrial number in response to changing environmental temperature in adipose tissues

    山下 俊一

    第3回温度生物学若手の会  2018年1月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:愛知県  

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  • Mitochondrial division concurrently with autophagosome formation during mitophagy

    山下 俊一, 神吉 智丈

    2017年度生命科学系学会合同年次大会  2017年12月 

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    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(公募)  

    開催地:兵庫県  

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  • Mitochondria division into small fragment concurrently with autophagosome formation

    山下 俊一, 金 秀蓮, 神吉 智丈

    ミトコンドリアサイエンスワークショップ 2017  2017年7月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:山形県  

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  • Temporal analysis of mitochondrial morphology during mitophagy 国際会議

    山下 俊一, 神吉 智丈

    The 8th International Symposium on Autophagy  2017年5月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:奈良県  

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  • A new model for mitochondrial division during mitophagy 招待 国際会議

    山下 俊一, 金 秀蓮, 神吉 智丈

    KSBMB International Conference 2017  2017年5月 

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    記述言語:英語   会議種別:口頭発表(招待・特別)  

    開催地:釜山、韓国  

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  • Drp1-independent mitochondrial division occurs concurrently with autophagosome formation in mitophagy 招待 国際会議

    山下 俊一

    Joint-Japan-Korea-China Young Investigator Conference (A3)  2017年2月 

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    記述言語:英語   会議種別:口頭発表(招待・特別)  

    開催地:ソウル、韓国  

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  • 温度変化に伴う脂肪組織におけるミトコンドリア分解の解析

    山下 俊一

    第2回温度生物学若手の会  2017年1月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:愛知県  

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  • マイトファジー時に見られるミトコンドリア分裂機構の解析

    山下 俊一

    第10回オートファジー研究会  2016年11月 

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    記述言語:日本語   会議種別:ポスター発表  

    開催地:新潟県  

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  • マイトファジー時に見られるミトコンドリア分裂機構の解析

    山下 俊一

    第89回日本生化学会大会  2016年9月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:宮城県  

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  • マイトファジー時に見られる特殊なミトコンドリア分裂機構

    山下 俊一

    第57回新潟生化学懇話会  2016年6月 

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    記述言語:日本語   会議種別:ポスター発表  

    開催地:新潟県  

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  • Drp1-independent mitochondrial division in mitophagy 国際会議

    山下 俊一

    Young Investigator Conference on Autophagy (A3)  2016年2月 

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    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:新潟県  

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  • マイトファジー時に見られるミトコンドリア形態制御機構

    山下 俊一

    第9回オートファジー研究会  2015年11月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:兵庫県  

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  • Regulation of mitochondrial morphology by Drp1-independent division in mitophagy 招待 国際会議

    山下 俊一

    Joint-Korea-Japan Symposium on Autophagy (A3)  2015年10月 

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    記述言語:英語   会議種別:口頭発表(招待・特別)  

    開催地:ソウル、韓国  

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  • マイトファジーにおけるミトコンドリア形態制御因子の重要性

    山下 俊一

    ミトコンドリアサイエンスワークショップ 2015  2015年7月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

    開催地:千葉県  

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  • マイトファジーにおけるミトコンドリア形態制御因子の重要性 招待

    山下 俊一

    第67回日本細胞生物学会大会  2015年7月 

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    記述言語:日本語   会議種別:シンポジウム・ワークショップ パネル(指名)  

    開催地:東京  

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  • Insight into peroxisome degradation induced by overloading of peroxisome membrane protein in mammalian cells 国際会議

    山下 俊一

    Post-GCOE Retreat with NUS and TLL  2013年3月 

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    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:シンガポール  

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  • Induction of peroxisome degradation by overloading of peroxisome membrane protein in mammalian cells 招待 国際会議

    山下 俊一

    Interact 2012  2012年3月 

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    記述言語:英語   会議種別:口頭発表(招待・特別)  

    開催地:ミュンヘン、ドイツ  

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  • Induction of peroxisome degradation by overloading of peroxisome membrane protein in mammalian cells 国際会議

    山下 俊一, 藤木 幸夫

    9thGCOE international symposium, 8th young investigators forum  2012年1月 

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    記述言語:英語   会議種別:口頭発表(一般)  

    開催地:Fukuoka  

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  • Peroxisome degradation of mammalian cells 国際会議

    山下 俊一, 藤木 幸夫

    7th Global-COE International Symposium and 6th Young Investigators Forum  2011年2月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:ビンタン、インドネシア  

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  • Peroxisome degradation of mammalian cells 国際会議

    山下 俊一, 藤木 幸夫

    The 3rd International Symposium on Protein Community  2010年9月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:奈良県  

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  • Peroxisome homeostasis in autophagy-defective cells 国際会議

    山下 俊一, 藤木 幸夫

    5th International Symposium on Autophagy  2009年9月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:滋賀県  

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  • Role of PpAtg26 in autophagy-related pathways in methylotrophic yeast Pichia pastoris 国際会議

    山下 俊一, 由里本 博也, 阪井 康能

    Gordon Research Conference, Autophagy in Stress, Development and Disease  2008年1月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:カリフォルニア、アメリカ  

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  • Detection of autophagy-related pathways in Pichia pastoris through two distinct autophagy-monitoring systems 国際会議

    山下 俊一, 阪井 康能

    4th International symposium on autophagy  2006年10月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:静岡  

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  • The role of the small GTPase PpYpt7 in pexophagy 国際会議

    山下 俊一, 阪井 康能

    20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB Congress  2006年6月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:京都  

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  • A novel phosphoinositide-signaling required for peroxisome degradation 国際会議

    山下 俊一, 奥 公秀, 阪井 康能

    International symposium on life of protein  2005年11月 

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    記述言語:英語   会議種別:ポスター発表  

    開催地:兵庫県  

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受賞

  • 学長賞(若手教員研究奨励)

    2017年9月   新潟大学   Mitochondrial division occurs concurrently with autophagosome formation but independently of Drp1 during mitophagy

    山下 俊一

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  • 鈴木紘一メモリアル賞

    2013年   日本生化学会   Induction of peroxisome degradation by overloading of peroxisome membrane protein in mammalian cells

    Shun-ichi Yamashita, Kakeru Abe, Yukio Fujiki

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  • 柿内三郎記念奨励研究賞

    2011年   日本生化学会   ペルオキシソーム膜タンパク質の品質管理機構の解析

    山下 俊一

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共同研究・競争的資金等の研究

  • 抗がん剤耐性に関与する新奇マイトファジーの分子機構解明と化学療法への応用

    研究課題/領域番号:22K07207  2022年4月 - 2025年3月

    日本学術振興会  基盤研究(C)  基盤研究(C)

    山下俊一

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    担当区分:研究代表者 

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  • ミトコンドリア関連疾患におけるミトコンドリアDNA分解の重要性とその分子機構の解析

    2018年4月 - 2019年3月

    東京生化学研究会  研究奨励金(I) 

    山下 俊一

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    担当区分:研究代表者  資金種別:競争的資金

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  • オートファジーによって分解されるミトコンドリアの形態制御機構の解明

    2017年4月 - 2020年3月

    日本学術振興会  国際共同研究加速基金(国際共同研究強化) 

    山下 俊一

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    担当区分:研究代表者  資金種別:競争的資金

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  • オートファジーによるミトコンドリアDNA分解の分子機構と生理的意義の解析

    2017年4月 - 2019年3月

    日本学術振興会  若手研究B 

    山下 俊一

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    担当区分:研究代表者  資金種別:競争的資金

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  • 低酸素誘導性ミトコンドリア分解の分子機構と生理的意義

    2015年8月 - 2018年5月

    公益財団法人 武田科学振興財団  医学系研究助成(基礎) 

    山下 俊一

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    担当区分:研究代表者  資金種別:競争的資金

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  • オートファジーによって分解されるミトコンドリアの形態制御機構の解明

    2015年4月 - 2017年3月

    日本学術振興会  若手研究B 

    山下 俊一

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    担当区分:研究代表者  資金種別:競争的資金

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  • 哺乳類ペルオキシソーム分解の分子機構とその生理的意義に関する研究

    2010年4月 - 2013年3月

    日本学術振興会  日本学術振興会特別研究員PD 

    山下 俊一

      詳細を見る

    担当区分:研究代表者  資金種別:競争的資金

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  • 哺乳類ペルオキシソームにおける新規分解経路の解明

    2010年4月 - 2012年3月

    日本学術振興会  若手研究B 

    山下 俊一

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    担当区分:研究代表者  資金種別:競争的資金

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  • Elucidation of intracellular membrane synthesis during pexophagy

    2003年 - 2007年

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    資金種別:競争的資金

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▶ 全件表示