Zobrazeno 1 - 10
of 98
pro vyhledávání: '"Masahiko Igarashi"'
Autor:
Satoshi Okano, Akira Yasui, Shin-ichiro Kanno, Kennichi Satoh, Masahiko Igarashi, Osamu Nakajima
Publikováno v:
Journal of Diabetes Research, Vol 2019 (2019)
Our earlier studies demonstrated that cysteine414- (zinc-binding site of mCRY1-) alanine mutant mCRY1 transgenic mice (Tg mice) exhibit diabetes characterized by the reduction of β-cell proliferation and by β-cell dysfunction, presumably caused by
Externí odkaz:
https://doaj.org/article/ba38f06fd21e400a953dfcc0bb1362f1
Autor:
SATOSHI OKANO, AKIRA YASUI, KENNICHI SATOH, SHIN-ICHIRO KANNO, MASAHIKO IGARASHI, OSAMU NAKAJIMA
Publikováno v:
Diabetes. 71
Cysteine414 (zinc-binding site of mCRY1) -alanine mutant mCRY1 transgenic mice (TG) show diabetes characterized by the reduction of β-cell proliferation due to the characters of senescence-associated secretory phenotype (SASP) in β-cells as we have
Autor:
Satoshi Okano, Akira Yasui, Shin-ichiro Kanno, Kennichi Satoh, Masahiko Igarashi, Osamu Nakajima
Regulator of G protein signaling proteins (RGSs) are involved in regulating β-cell functions. This study was conducted to examine the cellular responses to the occurrence of β-cell dedifferentiation in terms of the changes of expression levels of R
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::909ecb7bda1092a4a22e35e015305369
https://doi.org/10.21203/rs.3.rs-1395694/v1
https://doi.org/10.21203/rs.3.rs-1395694/v1
Autor:
Kennichi Satoh, Osamu Nakajima, Masahiko Igarashi, Shin-Ichro Kanno, Akira Yasui, Satoshi Okano
Publikováno v:
Diabetes. 70
Our preceding studies demonstrated that cysteine414 (zinc-binding site of mCRY1) - alanine mutant mCRY1 transgenic mice (TG mice) exhibit diabetes characterized by the reduction of β-cell proliferation caused by senescence-associated secretory pheno
Autor:
Akira Yasui, Osamu Nakajima, Shin-Ichro Kanno, Kennichi Satoh, Masahiko Igarashi, Satoshi Okano
Publikováno v:
Diabetes. 69
We have demonstrated that cysteine414 (zinc-binding site of mCRY1)-alanine mutant mCRY1 transgenic mice (Tg mice) show diabetes characterized by the reduction of β-cell proliferation and by β-cell dysfunction due to SASP (senescence-associated secr
Autor:
Satoshi Okano, Masahiko Igarashi, Osamu Nakajima, Kennichi Satoh, Shin Ichiro Kanno, Akira Yasui
Publikováno v:
Diabetes. 68
The transgenic mice ubiquitously expressing the zinc-binding site-mutant CRY1 (C414A-CRY1) show early onset diabetes mellitus similar to human MODY characterized by β-cell dysfunction. In the Tg mice with age, atypical ductal structures emerged insi
Autor:
Osamu Nakajima, Kennichi Satoh, Akira Yasui, Masahiko Igarashi, Satoshi Okano, Shin Ichiro Kanno
Publikováno v:
Journal of Diabetes Research
Journal of Diabetes Research, Vol 2019 (2019)
Journal of Diabetes Research, Vol 2019 (2019)
Our earlier studies demonstrated that cysteine414- (zinc-binding site of mCRY1-) alanine mutant mCRY1 transgenic mice (Tg mice) exhibit diabetes characterized by the reduction of β-cell proliferation and by β-cell dysfunction, presumably caused by
Autor:
Masahiko Igarashi, Kennichi Satoh, Osamu Nakajima, Shin Ichiro Kanno, Akira Yasui, Satoshi Okano
Publikováno v:
Diabetes. 67
Cryptochrome (CRY) proteins play indispensable roles in the mammalian circadian clock. We previously generated transgenic mice ubiquitously expressing mCRY1 with a mutation in cysteine414 (the zinc-binding site of CRY1). The Tg mice overexpressing th
Publikováno v:
Rinsho byori. The Japanese journal of clinical pathology. 62(9)
It is well known that dyslipidemia is one of the most crucial risk factors for atherosclerosis, including cardiovascular diseases (ASCVD). In order to prevent the onset of ASCVD, the Japan Atherosclerotic Society (JAS) published the JAS Guidelines in
Autor:
Seijiro Mori, Masafumi Kuzuya, Yasuhito Tanaka, Koutaro Yokote, Tetsuro Miki, Masahiko Igarashi, Shinya Yoshimoto, Minoru Takemoto, Akira Shimamoto
Publikováno v:
Geriatrics & Gerontology International. 13:475-481
Aim: Werner syndrome (WS) is an autosomal recessive disorder of progeroid symptoms and signs. It is caused by mutations in the WRN gene, which encodes a RecQ DNA helicase. The aim of this study was to revise the diagnostic criteria for Japanese Werne