Contact |
国際センター 留学生課(京田辺) TEL:0774-65-7453
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Contact |
国際センター 留学生課 TEL:075-251-3257
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Contact |
国際センター 留学生課(京田辺) TEL:0774-65-7453
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Contact |
国際センター 留学生課 TEL:075-251-3257
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Contact |
国際センター 留学生課 TEL:075-251-3257
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For 5 weeks from May 25th to June 27th, APSU-JAPAN: Study at Doshisha University 2025 was held at Imadegawa Campus.
Contact |
国際センター 留学生課 TEL:075-251-3257
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Contact |
国際センター 留学生課(京田辺) TEL:0774-65-7453
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Contact |
国際センター 留学生課 TEL:075-251-3257
|
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Contact |
国際センター 留学生課 TEL:075-251-3257
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We welcomed 5 students from Northeastern University (hereafter referred to as NEU), Boston, U.S.A., and they studied about Japanese language and culture throughout the program. In the culture seminar classes, special visiting lecturers were invited and students tried Flower Arrangement, Tea Ceremony and Calligraphy on campus. They also experienced pottery lesson and Aikido lesson off-campus. Although most of them experienced those activities for the first time, they listened to lecturer’s explanation attentively showing their positive attitudes to learn about Japanese tradition and culture.
In addition to the cultural seminars, students worked on diligently improving their Japanese abilities which they have been studying at least one year at NEU. Through Japanese language classes and conversation sessions with Doshisha students who joined the program as “supporters”, all of them showed remarkable growth. We were surprised to see them making full use of their Japanese language skills in various situations.
Students and supporters not only interacted with each other in the classes, but also shared a lot of time in Kyoto such as strolling Gion area. It seemed they fully enjoyed their stay in Kyoto in many aspects.
Although it was only two weeks that they stayed at Doshisha, we hope they will spend rest of their program in Japan energetically and continue to study Japanese language and culture even after going back to their country.
Contact |
国際センター 留学生課 TEL:075-251-3257
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Contact |
国際センター 留学生課(京田辺) TEL:0774-65-7453
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Contact |
国際センター 留学生課(京田辺) TEL:0774-65-7453
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Contact |
国際センター 留学生課 TEL:075-251-3257
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Contact |
国際センター 留学生課 TEL:075-251-3257
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Dr. Biplab Kumar Dash, Professor Yasuomi Urano, and their research team have uncovered a novel secretion mechanism of an unconventional Parkinson’s disease-related protein mediated by autophagy and secretory autolysosomes.
Proteins are conventionally trafficked and secreted extracellularly via the endoplasmic reticulum-Golgi pathway. Some proteins that bypass this system and use unconventional mechanisms to exit the cell have been implicated in neurodegenerative diseases, inflammation, and cancer. Researchers have elucidated a novel role of autophagy mediated by the formation of “secretory autolysosomes” in the release of PARK7—a protein associated with Parkinson’s disease (PD). Their findings uncover potential pathogenic mechanisms, early biomarkers, and therapeutic targets.
Reference
Biplab Kumar Dash, Yasuomi Urano, Yuichiro Mita, Yuki Ashida, Ryoma Hirose, Noriko Noguchi, Unconventional secretion of PARK7 requires lysosomal delivery via chaperone-mediated autophagy and specialized SNARE complex, Proceedings of the National Academy of Sciences, 2025, Vol. 122 No. 19
DOI :10.1073/pnas.2414790122
https://research.doshisha.ac.jp/news/news-detail-76/
https://www.doshisha.ac.jp/news/detail/001-26Qmmn.html
https://www.eurekalert.org/news-releases/1084893
Image title: Proposed model of 6-OHDA-induced autophagy-based unconventional PARK7 secretion.
Image caption: Oxidative stress induced by 6-OHDA stimulates autophagy flux, which enhances STX17-mediated autolysosome formation, leading to the degradation of autophagosomal contents. However, in response to autophagy promotion by 6-OHDA, a subset of autophagosomes recruits ERGIC R-SNARE SEC22B. The KFERQ-like motifs of monomeric PARK7 selectively bind to HSPA8 chaperones and are recruited to the lysosomal membrane, followed by translocation into the lysosomal lumen via the LAMP2 channel. A pool of PARK7-containing lysosomes fuses with SEC22B-containing autophagosomes to form secretory autolysosomes, which then fuse with the plasma membrane mediated by a unique QabcR–SNARE complex comprising STX3/4, VTI1B, STX8, and SEC22B, releasing PARK7 into the extracellular matrix.
Image credit: Dr. Biplab Kumar Dash from Doshisha University, Japan
Source link: https://www.pnas.org/doi/10.1073/pnas.2414790122
License type: CC BY-NC-ND
Usage restrictions: Credit must be given to the creator. Only non-commercial uses of the work are permitted. No derivatives or adaptations of the work are permitted.
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