Zobrazeno 1 - 10
of 16
pro vyhledávání: '"Kei-ichi NAKAYAMA"'
Autor:
Yoichi, Shinkai, Shigeo, Koyasu, Kei-Ichi, Nakayama, Kenneth M, Murphy, Dennis Y, Loh, Ellis L, Reinherz, Frederick W, Alt
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 202(5)
Autor:
Monsef Benkirane, Keiko Nakayama, Kei-ichi Nakayama, Rosemary Kiernan, Jean-Claude Labbé, Anna Castro, Thierry Lorca, Stéphane Emiliani
Publikováno v:
Molecular and Cellular Biology. 21:7956-7970
Transcriptional elongation is regulated by both positive and negative transcription elongation factors and is recognized as an important target for transcriptional regulation (37). The human positive transcription elongation factor b (P-TEFb) is comp
Autor:
Kimihiko HATTORI, Kei-ichi NAKAYAMA
Publikováno v:
Kagaku To Seibutsu. 38:653-660
CHIP promotes proteasomal degradation of familial ALS-linked mutant SOD1 by ubiquitinating Hsp/Hsc70
Autor:
Makoto, Urushitani, Junko, Kurisu, Minako, Tateno, Shigetsugu, Hatakeyama, Kei-Ichi, Nakayama, Shinsuke, Kato, Ryosuke, Takahashi
Publikováno v:
Journal of neurochemistry. 90(1)
Over 100 mutants in superoxide dismutase 1 (SOD1) are reported in familial amyotrophic lateral sclerosis (ALS). However, the precise mechanism by which they are degraded through a ubiquitin-proteasomal pathway (UPP) remains unclear. Here, we report t
Autor:
Kei-Ichi, Nakayama
Publikováno v:
Rinsho shinkeigaku = Clinical neurology. 43(11)
Machado-Joseph disease (MJD)/Spinocerebellar ataxia type 3 (SCA3) is neurodegenerative disease which is caused by polyglutamine expansion in a responsible gene product, MJD1/Ataxin3. MJD1 has now been shown to undergo ubiquitylation and degradation b
Autor:
Kouji, Kato, Kenjirou, Kamezaki, Kazuya, Shimoda, Akihiko, Numata, Takashi, Haro, Kenichi, Aoki, Fumihiko, Ishikawa, Ken, Takase, Hiroshi, Ariyama, Tadashi, Matsuda, Toshihiro, Miyamoto, Koji, Nagafuji, Hisashi, Gondo, Kei-Ichi, Nakayama, Mine, Harada
Publikováno v:
British journal of haematology. 123(3)
Interferon (IFN)-alpha and IFN-gamma suppress the growth of haematopoietic progenitor cells. IFN-alpha activates Janus kinase-1 (Jak1) and Tyrosine kinase-2 (Tyk2), followed by the phosphorylation of the signal transducers and activators of transcrip
Publikováno v:
Cancer research. 63(7)
Accumulated evidence suggests that connexin43 (Cx43) serves as a tumor-suppressing gene. We have previously shownA. B. that Cx43 suppressed the G(1)-S phase cell cycle transition via increasing the level of p27 (Zhang, Y. W., et al., Oncogene, 20: 41
Autor:
Koichi, Kitamura, Keiko, Mizuno, Akiko, Etoh, Yoshiko, Akita, Akitomo, Miyamoto, Kei-Ichi, Nakayama, Shigeo, Ohno
Publikováno v:
Genes to cells : devoted to molecularcellular mechanisms. 8(4)
Cell lines that stably over-express protein kinase C (PKC) delta frequently show a decrease in growth rate and saturation density, leading to the hypothesis that PKC delta has a negative effect on cell proliferation. However, the mode of PKC delta ac
Autor:
Taka-aki, Masuda, Hiroshi, Inoue, Hideto, Sonoda, Shinji, Mine, Yasuji, Yoshikawa, Keiko, Nakayama, Kei-Ichi, Nakayama, Masaki, Mori
Publikováno v:
Cancer research. 62(13)
Reduced expression level of p27, a cyclin-dependent kinase inhibitor, is associated with high aggressiveness and poor prognosis of various malignant tumors, including gastric carcinoma. S-phase kinase-associated protein 2 (Skp2), a member of the F-bo
Publikováno v:
Cancer research. 62(4)
The abundance of p27(Kip1), an inhibitor of cell proliferation, is determined by Skp2-dependent proteolysis, the deregulation of which is associated with cancer progression. Lack of Skp2 results in p27(Kip1) accumulation as well as enlargement and po