基本信息
views: 0
![](https://originalfileserver.aminer.cn/sys/aminer/icon/show-trajectory.png)
Bio
Research Description:
The cystic fibrosis gene product, CFTR, is a multidomain, polytopic plasma membrane protein that belongs to the ATP-Binding Cassette transporter family. The chloride channel activity of CFTR is indispensable for normal transcellular salt and water transport in numerous organs (e.g. gastrointestinal tract, pancreas and sweat duct) and for the homeostasis of airway surface liquid layer. Our long-term goal is to elucidate the molecular and cellular basis of cystic fibrosis, one of the most prevalent genetic diseases in the Caucasian population, caused by mutations interfering with the folding, stability, activity and/or membrane trafficking of the channel. To achieve this goal, we utilize a combination of biochemical, biophysical, cell biological and genetic techniques. Another aspect of our inquiries is to gain insights into the recognition and elimination mechanism of non-native membrane proteins from post-ER/Golgi compartments in mammalian cells. The peripheral quality control of integral membrane proteins likely represents a fundamental protective mechanism against the accumulation of aggregation prone and toxic polypeptides that are generated by cellular stresses or mutations. Using conditionally misfolded model proteins, we aim at identifying the machinery responsible for the disposal of non-native plasma membrane proteins. The structural and biochemical basis of ubiquitin recognition as an endocytic and postendocytic sorting signal is also investigated.
The cystic fibrosis gene product, CFTR, is a multidomain, polytopic plasma membrane protein that belongs to the ATP-Binding Cassette transporter family. The chloride channel activity of CFTR is indispensable for normal transcellular salt and water transport in numerous organs (e.g. gastrointestinal tract, pancreas and sweat duct) and for the homeostasis of airway surface liquid layer. Our long-term goal is to elucidate the molecular and cellular basis of cystic fibrosis, one of the most prevalent genetic diseases in the Caucasian population, caused by mutations interfering with the folding, stability, activity and/or membrane trafficking of the channel. To achieve this goal, we utilize a combination of biochemical, biophysical, cell biological and genetic techniques. Another aspect of our inquiries is to gain insights into the recognition and elimination mechanism of non-native membrane proteins from post-ER/Golgi compartments in mammalian cells. The peripheral quality control of integral membrane proteins likely represents a fundamental protective mechanism against the accumulation of aggregation prone and toxic polypeptides that are generated by cellular stresses or mutations. Using conditionally misfolded model proteins, we aim at identifying the machinery responsible for the disposal of non-native plasma membrane proteins. The structural and biochemical basis of ubiquitin recognition as an endocytic and postendocytic sorting signal is also investigated.
Research Interests
Papers共 264 篇Author StatisticsCo-AuthorSimilar Experts
By YearBy Citation主题筛选期刊级别筛选合作者筛选合作机构筛选
时间
引用量
主题
期刊级别
合作者
合作机构
Yuka Kamada, Yuko Ohnishi, Chikako Nakashima, Aika Fujii, Mana Terakawa, Ikuto Hamano, Uta Nakayamada, Saori Katoh, Noriaki Hirata, Hazuki Tateishi,Ryosuke Fukuda,Hirotaka Takahashi,
The Journal of cell biologyno. 7 (2024)
Scientific datano. 1 (2024): 495-495
FRONTIERS IN PHARMACOLOGY (2024): 1389586-1389586
Yuka Kamada, Yuko Ohnishi, Chikako Nakashima, Aika Fujii, Mana Terakawa, Ikuto Hamano, Uta Nakayamada, Saori Katoh, Noriaki Hirata, Hazuki Tateishi,Ryosuke Fukuda,Hirotaka Takahashi,
bioRxiv (Cold Spring Harbor Laboratory) (2023)
bioRxiv (Cold Spring Harbor Laboratory) (2023)
C. Wang, Z. Yang, A. Aleksandrov,S. Vorobiev, B. Loughlin, Z. Rich, O. Clarke, F. Jiang,C. Brouillette,I. Urbatsch, J. Frank,G. Lukacs,
Journal of Cystic Fibrosis (2023): S167
bioRxiv (Cold Spring Harbor Laboratory) (2023)
Nature Communicationsno. 1 (2023): 1-21
Journal of Cystic Fibrosis (2022)
Load More
Author Statistics
#Papers: 248
#Citation: 14953
H-Index: 64
G-Index: 120
Sociability: 7
Diversity: 0
Activity: 1
Co-Author
Co-Institution
D-Core
- 合作者
- 学生
- 导师
Data Disclaimer
The page data are from open Internet sources, cooperative publishers and automatic analysis results through AI technology. We do not make any commitments and guarantees for the validity, accuracy, correctness, reliability, completeness and timeliness of the page data. If you have any questions, please contact us by email: report@aminer.cn