Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Atsushi, Hayama"'
Publikováno v:
The Journal of the Acoustical Society of America. 117:3636-3644
The present study extends our previous work [Furihata et al., J. Acoust. Soc. Am. 114, 174-184 (2003)] by investigating our electrodynamic planar loudspeaker when driven by a 12 bit digital signal with noise shaping. Changing the structure of the lou
Autor:
Eisei Sohara, Tatemitsu Rai, Shin Suda, Atsushi Hayama, Sei Sasaki, Tomohiro Itoh, Shinichi Uchida, Tatsunori Suzuki
Publikováno v:
Journal of Cellular Physiology. 206:792-798
ClC chloride channels (ClCs) can be classified into two groups in terms of their cellular localizations: ClCs present in the plasma membranes and those residing in intracellular organelles. Members of the latter group, including ClC-3, ClC-4, ClC-5,
Disease-causing mutant WNK4 increases paracellular chloride permeability and phosphorylates claudins
Autor:
Tatemitsu Rai, Kozue Yamauchi, Eisei Sohara, Tomohiro Itoh, Tatsunori Suzuki, Atsushi Hayama, Shinichi Uchida, Katsuki Kobayashi, Shin Suda, Sei Sasaki
Publikováno v:
Proceedings of the National Academy of Sciences. 101:4690-4694
Mutations in the WNK4 gene cause pseudohypoaldosteronism type II (PHAII), an autosomal-dominant disorder of hyperkalemia and hypertension. The target molecules of this putative kinase and the molecular mechanisms by which the mutations cause the phen
Publikováno v:
The Journal of the Acoustical Society of America. 114:174-184
In this paper, an electrodynamic planar loudspeaker driven by a digital signal is experimentally discussed. The digital loudspeaker consists of 22 voice coils, 11 permanent magnets, a diaphragm with streamlined sections molded in plastic, and a suspe
Autor:
Yasuo Uchiyama, Shinichi Uchida, Yujiro Kida, Atsushi Hayama, Sei Sasaki, Junji Ezaki, Masato Koike, Fumiaki Marumo, Masaki Noda, Tatemitsu Rai, Eiki Kominami, Momono Yoshikawa, Katsuki Kobayashi
Publikováno v:
Genes to Cells. 7:597-605
Background: CLC-3 is a member of the CLC chloride channel family and is widely expressed in mammalian tissues. To determine the physiological role of CLC-3, we generated CLC-3-deficient mice (Clcn3–/–) by targeted gene disruption. Results: Togeth
Publikováno v:
Gene. 261:355-364
The human CLC-5 chloride channel is expressed mainly in the kidney and its mutations cause Dent's disease (a familial renal tubular syndrome with hypercalciuria, tubular proteinuria, rickets, nephrocalcinosis, and eventual renal failure). To gain ins
Autor:
Yoshiaki Kondo, Mikio Arisawa, Sei Sasaki, Fumiaki Marumo, Hiroaki Miyazaki, Yoshihiro Matsumura, Shigeru B. H. Ko, Tetuji Morimoto, Wen Liu, Shinichi Uchida, Atsushi Hayama
Publikováno v:
Nature Genetics. 21:95-98
CLC-K1 is a kidney-specific chloride channel that mediates transepithelial chloride transport in the thin ascending limb of Henle's loop (tAL) in the inner medulla 1, 2 . Transport of NaCl in the tAL is thought to be a component of urinary concentrat
Publikováno v:
Biochemical and biophysical research communications. 362(4)
ClC-K chloride channels belong to the CLC chloride channel family and play an important role in transepithelial chloride transport in the kidney. To be functional, ClC-K channels need to be translocated to the plasma membranes after synthesis; the tr
Publikováno v:
Histochemistry and cell biology. 119(6)
Barttin, a gene product of BSND, was identified as a fourth gene responsible for Bartter syndrome. The co-expression of barttin with CLC-K chloride channels has been demonstrated to dramatically induce the expression of CLC-K current. However, it rem
Autor:
Momono, Yoshikawa, Shinichi, Uchida, Junji, Ezaki, Tatemitsu, Rai, Atsushi, Hayama, Katsuki, Kobayashi, Yujiro, Kida, Masaki, Noda, Masato, Koike, Yasuo, Uchiyama, Fumiaki, Marumo, Eiki, Kominami, Sei, Sasaki
Publikováno v:
Genes to cells : devoted to molecularcellular mechanisms. 7(6)
CLC-3 is a member of the CLC chloride channel family and is widely expressed in mammalian tissues. To determine the physiological role of CLC-3, we generated CLC-3-deficient mice (Clcn3-/- ) by targeted gene disruption.Together with developmental ret