Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by T Yamazaki
Total Records ( 1 ) for T Yamazaki
  D Yamazaki , S Komazaki , H Nakanishi , A Mishima , M Nishi , M Yazawa , T Yamazaki , R Taguchi and H. Takeshima
  Daiju Yamazaki, Shinji Komazaki, Hiroki Nakanishi, Aya Mishima, Miyuki Nishi, Masayuki Yazawa, Tetsuo Yamazaki, Ryo Taguchi, and Hiroshi Takeshima

TRIC channels function as monovalent cation-specific channels that mediate counter ion movements coupled with ryanodine receptor-mediated Ca2+ release from intracellular stores in muscle cells. Mammalian tissues differentially contain two TRIC channel subtypes: TRIC-A is abundantly expressed in excitable cells, whereas TRIC-B is ubiquitously expressed throughout tissues. Here, we report the physiological role of TRIC-B channels in mouse perinatal development. TRIC-B-knockout neonates were cyanotic owing to respiratory failure and died shortly after birth. In the mutant neonates, the deflated lungs exhibited severe histological defects, and alveolar type II epithelial cells displayed ultrastructural abnormalities. The metabolic conversion of glycogen into phospholipids was severely interrupted in the mutant type II cells, and surfactant phospholipids secreted into the alveolar space were insufficient in the mutant neonates. Moreover, the mutant type II cells were compromised for Ca2+ release mediated by inositol-trisphosphate receptors, despite Ca2+ overloading in intracellular stores. Our results indicate that TRIC-B channels take an active part in Ca2+ signalling to establish specialised functions in type II cells and are thus...

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility