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36 results on '"Tamura, Miyuki"'

8. Supplementary_materials_and_methods-rerevise – Supplemental material for Targeted next-generation sequencing of 50 cancer-related genes in Japanese patients with oral squamous cell carcinoma

Author

Nakagaki, Takafumi, Tamura, Miyuki, Kobashi, Kenta, Omori, Akina, Koyama, Ryota, Idogawa, Masashi, Ogi, Kazuhiro, Hiroyoshi Hiratsuka, Tokino, Takashi, and Sasaki, Yasushi

Subjects
FOS: Clinical medicine, Cell Biology, 111299 Oncology and Carcinogenesis not elsewhere classified
Abstract

Supplemental material, Supplementary_materials_and_methods-rerevise for Targeted next-generation sequencing of 50 cancer-related genes in Japanese patients with oral squamous cell carcinoma by Takafumi Nakagaki, Miyuki Tamura, Kenta Kobashi, Akina Omori, Ryota Koyama, Masashi Idogawa, Kazuhiro Ogi, Hiroyoshi Hiratsuka, Takashi Tokino and Yasushi Sasaki in Tumor Biology

Published
2018
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11. Profiling cancer-related gene mutations in oral squamous cell carcinoma from Japanese patients by targeted amplicon sequencing

Author

Nakagaki, Takafumi, primary, Tamura, Miyuki, additional, Kobashi, Kenta, additional, Koyama, Ryota, additional, Fukushima, Hisayo, additional, Ohashi, Tomoko, additional, Idogawa, Masashi, additional, Ogi, Kazuhiro, additional, Hiratsuka, Hiroyoshi, additional, Tokino, Takashi, additional, and Sasaki, Yasushi, additional

Published
2017
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13. GOUT AND NUCLEIC ACID METABOLISM

Author

Ooyama, Satoko, primary, Hirose, Chihiro, additional, Hori, Kenichiro, additional, Cho, Chie, additional, Sugano, Katsuhiro, additional, Tamura, Miyuki, additional, and Tomita, Kimio, additional

Published
2017
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18. Abstract 3707: Semiconductor-based next-generation sequencing analysis of 409 cancer-related genes for mutations and copy-number variations in oral squamous cell carcinoma

Author

Nakagaki, Takafumi, primary, Sasaki, Yasushi, additional, Idogawa, Masashi, additional, Koyama, Ryota, additional, Kobashi, Kenta, additional, Tamura, Miyuki, additional, Ohashi, Tomoko, additional, Ogi, Kazuhiro, additional, Hiratsuka, Hiroyoshi, additional, and Tokino, Takashi, additional

Published
2016
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25. Identification and characterization of a metastatic suppressor BRMS1L as a target gene of p53.

Author

Koyama, Ryota, Tamura, Miyuki, Nakagaki, Takafumi, Ohashi, Tomoko, Idogawa, Masashi, Suzuki, Hiromu, Tokino, Takashi, and Sasaki, Yasushi

Abstract

The tumor suppressor p53 and its family members, p63 and p73, play a pivotal role in the cell fate determination in response to diverse upstream signals. As transcription factors, p53 family proteins regulate a number of genes that are involved in cell cycle arrest, apoptosis, senescence, and maintenance of genomic stability. Recent studies revealed that p53 family proteins are important for the regulation of cell invasion and migration. Microarray analysis showed that breast cancer metastasis suppressor 1-like ( BRMS1L) is upregulated by p53 family proteins, specifically p53, TAp63γ, and TAp73β. We identified two responsive elements of p53 family proteins in the first intron and upstream of BRMS1L. These response elements are well conserved among mammals. Functional analysis showed that ectopic expression of BRMS1L inhibited cancer cell invasion and migration; knockdown of BRMS1L by si RNA induced the opposite effect. Importantly, clinical databases revealed that reduced BRMS1L expression correlated with poor prognosis in patients with breast and brain cancer. Together, these results strongly indicate that BRMS1L is one of the mediators downstream of the p53 pathway, and that it inhibits cancer cell invasion and migration, which are essential steps in cancer metastasis. Collectively, our results indicate that BRMS1L is involved in cancer cell invasion and migration, and could be a therapeutic target for cancer. [ABSTRACT FROM AUTHOR]

Published
2017
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32. Effects of sleep deprivation on face emotion processing

Author

Tamura, Miyuki, primary, Higuchi, Shigekazu, additional, Hida, Akiko, additional, Aritake, Sayaka, additional, Enomoto, Minori, additional, Kitamura, Shingo, additional, Watanabe, Makiko, additional, Moriguchi, Yoshiya, additional, and Mishima, Kazuo, additional

Published
2010
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36. Pharmacokinetics and Pharmacodynamics of SK-0403, a Novel DPPIV Inhibitor, in Rat: -IC[sub 80] for DPP-IV in Circulation Is Insufficient to Protect Degradation of Intact GLP-1-.

Author

Furuta, Shinji, Goto, Moritaka, Furuta, Yoshiyuki, Yasuda, Yoshika, Nakaya, Keizo, Tamura, Miyuki, Uesugi, Noriko, Kawamura, Satoko, Inoue, Akiharu, Kato, Noriaki, Ishida, Tsutomu, and Matsumoto, Yukiharu

Subjects
PHARMACOKINETICS, PHARMACODYNAMICS, CD26 antigen, GLUCAGON-like peptide 1, METABOLISM, LABORATORY rats
Abstract

Glucagon-like peptide- 1 (GLP-1) is rapidly degraded by DPP-IV which ubiquitously exists in plasma and tissues. It is now known that DPP-IV is the most important enzyme for the inactivation of GLP-1, and only 10-15% of secreted GLP-I reaches the systemic circulation as an active form. In general, the inhibition of plasma DPP-IV activity by 80% or higher is considered sufficient to exhibit maximal effect on glycemic control improvement due to the elevation of intact incretins. However, detail relationship between higher DPP-IV inhibition (over 80%) and the degradation of intact GLP- 1 has not been studied. Therefore, to clarify this relationship, we investigated the effect of SK-0403, a novel DPP-IV inhibitor, on an intact (active) GLP-1 degradation in wistar rats with continuous administration of GLP-1. The active GLP-1 level in plasma significantly increased to 353 pM at IC[sub 80] of SK-0403 for plasma DPP-IV activity compared with control. In addition, the active GLP-1 increased in a concentration-dependent manner at concentrations from 1- to 10-fold IC[sub 80] of SK-0403, and reached a maximum of 445 pM (p<0.05 vs. IC[sub 80]) at 10-fold IC[sub 80]. The same results were obtained from sitagliptin and vildagliptin. The concentration dependency on a GLP-1 degradation was also confirmed based on the experiment in which the endogenous active GLP-1 level after an oral carbohydrate load increased 1.9 times at 10-fold IC[sub 80] compared to the IC[sub 80]. In conclusion, IC[sub 80] of DPP-IV activity in circulation may be insufficient to protect degradation of intact GLP-1. The metabolism of GLP-1 may be involved in tissues DPP-IV as well as plasma DPP-IV. These results suggest that high concentration over IC[sub 80] is necessary to protect the degradation of GLP-1 in the metabolic process. [ABSTRACT FROM AUTHOR]

Published
2007

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