k8day.io ~ラッキールーレット,1BTCの賞金を勝ち取る!スポーツ ...

<ウェブサイト名>

<現在の時刻>

出典: 標準

International Affairs Students Current Students Alumni Faculty/Staff Careers--> TOHOKU UNIVERSITYCREATING GLOBAL EXCELLENCE Search 日本語 Contact Tohoku University --> About Facts & Figures Facilities Organization Chart History President's Message Top Global University Project Designated National University Global Network Promotional Videos Academics Undergraduate Graduate Courses in English Exchange Programs Summer Programs Double Degree Programs Academic Calendar Syllabus Admissions Undergraduate Admissions Graduate Admissions Fees and Expenses Financial Aid Research Feature Highlights Research Releases University Research News Research Institutes Visitor Research Center Research Profiles Academic Research Staff Campus Life International Support Office IT Services Facilities Dining & Shops Campus Bus Clubs & Circles News University News Research--> Arts & Culture Health & Sports Campus & Community Press Release--> International Visit Alumni Careers Events Exhibits Music Special Event Lecture Alumni--> Map & Directions Campus Maps & Bus--> Facilities Map--> TOHOKUUNIVERSITY About Academics Admissions Research Campus Life News Events International Affairs Students Current Students Alumni Faculty/Staff Promotional Videos Subscribe to our Newsletter Map & Directions Contact Jobs & Vacancies Emergency Information Site Map 日本語 Close Home Research News ASK the enzyme: new potential targets for cancer Research News ASK the enzyme: new potential targets for cancer 2018-01-04 New understandings of how molecules affect the activity of an enzyme could lead to potential targets for the treatment of cancers and neurodegenerative diseases. Atsushi Matsuzawa at Tohoku University and colleagues in Japan used gene silencing techniques and cell culture studies to investigate how molecules regulate an enzyme known as apoptosis signal-regulating kinase 1 (ASK1). Irregular ASK1 activation is linked to some cancers, and inflammatory and neurodegenerative diseases. ASK1 is normally activated in the body by oxidative stress, a process that involves high rates of oxygen metabolism and happens in response to stress, toxins and infections. A variety of molecules are known to regulate ASK1, but how they do this has not been clear. An enzyme called protein arginine methyltransferase 1 (PRMT1) is known to encourage ASK1 to interact with a small protein called thioredoxin (Trx). This interaction effectively turns ASK1 off, interfering with this enzyme's role in initiating a cell-signalling process that ultimately leads to cell death and inflammation. Matsuzawa and his team found that a protein called tripartite motif 48 (TRIM48) starts a process that labels PRMT1 for destruction inside cells. PRMT1 deficiency means that ASK1 and Trx can't interact, which turns ASK1 on. When the researchers turned off the gene that codes for TRIM48, ASK1 failed to be activated by oxidative stress. Tumor suppressive roles of TRIM48-mediated ASK1 activation and cell death When the researchers made the same gene work excessively in cancer cells planted under the skin in mice, they observed cancer cell death and suppression of tumour growth, possibly due to ASK1 hyperactivation. "PRMT1 upregulation may be caused by decreased TRIM48 expression or activity, leading to cancer development and progression," write the researchers in their study published in the journal Cell Reports. "Future studies should determine whether TRIM48 suppresses cancer development and progression through PRMT1 downregulation," they say. Further studies could reveal that the pathways involved in regulating ASK1 activation could act as therapeutic targets in the treatment of ASK1-related diseases, the researchers conclude. Press release in Japanese Publication Details: Title: TRIM48 Promotes ASK1 Activation and Cell Death through Ubiquitination-Dependent Degradation of the ASK1-Negative Regulator PRMT1Authors: Yusuke Hirata, Kazumi Katagiri, Keita Nagaoka, Tohru Morishita, Yuki Kudoh, Tomohisa Hatta, Isao Naguro, Kuniyuki Kano, Tsuyoshi Udagawa, Tohru Natsume, Junken Aoki, Toshifumi Inada, Takuya Noguchi, Hidenori Ichijo and Atsushi MatsuzawaJournal: Cell ReportsDOI: https://doi.org/10.1016/j.celrep.2017.11.007 Contact: Yusuke Hirata Graduate School of Pharmaceutical Sciences Tohoku University Email: [email protected] Atsushi Matsuzawa  Graduate School of Pharmaceutical Sciences Tohoku University Email: [email protected] Archives 2014&#24180; 2015&#24180; 2016&#24180; 2017&#24180; 2018&#24180; 2019&#24180; 2020&#24180; 2021&#24180; 2022&#24180; 2023&#24180; Page Top About Tohoku University Academics Admissions Research Campus Life News Events International Affairs Students Alumni Promotional Videos Subscribe to our Newsletter Map & Directions Contact Tohoku University Jobs & Vacancies Emergency Information Site Map Media Enquiries Parent & Family Support Public Facilities Contact Tohoku University

ホットニュース

ベースボールライブ支払い方法 ウグルカン・チャクル kkポーカー入金ボーナス トミーポール
Copyright ©k8day.io ~ラッキールーレット,1BTCの賞金を勝ち取る!スポーツ ... The Paper All rights reserved.