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3. Kinase Activity of PAR1b, Which Mediates Nuclear Translocation of the BRCA1 Tumor Suppressor, Is Potentiated by Nucleic Acid-Mediated PAR1b Multimerization

Author

Nishikawa, Hiroko, Christiany, Priscillia, Hayashi, Takeru, Iizasa, Hisashi, Yoshiyama, Hironori, Hatakeyama, Masanori, Nishikawa, Hiroko, Christiany, Priscillia, Hayashi, Takeru, Iizasa, Hisashi, Yoshiyama, Hironori, and Hatakeyama, Masanori

Abstract

PAR1b is a cytoplasmic serine/threonine kinase that controls cell polarity and cell-cell interaction by regulating microtubule stability while mediating cytoplasmic-to-nuclear translocation of BRCA1. PAR1b is also a cellular target of the CagA protein of Helicobacter pylori, which leads to chronic infection causatively associated with the development of gastric cancer. The CagA-PAR1b interaction inactivates the kinase activity of PAR1b and thereby dampens PAR1b-mediated BRCA1 phosphorylation, which reduces the level of nuclear BRCA1 and thereby leads to BRCAness and BRCAness-associated genome instability underlying gastric carcinogenesis. While PAR1b can multimerize within the cells, little is known about the mechanism and functional role of PAR1b multimerization. We found in the present study that PAR1b was multimerized in vitro by binding with nucleic acids (both single- and double-stranded DNA/RNA) via the spacer region in a manner independent of nucleic-acid sequences, which markedly potentiated the kinase activity of PAR1b. Consistent with these in vitro observations, cytoplasmic introduction of double-stranded DNA or expression of single-stranded RNA increased the PAR1b kinase activity in the cells. These findings indicate that the cytoplasmic DNA/RNA contribute to nuclear accumulation of BRCA1 by constitutively activating/potentiating cytoplasmic PAR1b kinase activity, which is subverted in gastric epithelial cells upon delivery of H. pylori CagA oncoprotein.

Published
2022

8. Time-resolved magnetic resonance angiography as a follow-up method for visceral artery aneurysm treated with coil-embolisation

Author

Kawai, Tatsuya, primary, Shimohira, Masashi, additional, Suzuki, Kazushi, additional, Ohta, Kengo, additional, Kurosaka, Kenichiro, additional, Hashizume, Takuya, additional, Nishikawa, Hiroko, additional, Muto, Masahiro, additional, Arai, Nobuyuki, additional, Kan, Hirohito, additional, and Shibamoto, Yuta, additional

Published
2018
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15. Differential Mechanisms for SHP2 Binding and Activation Are Exploited by Geographically Distinct Helicobacter pyloriCagA Oncoproteins

Author

Hayashi, Takeru, Senda, Miki, Suzuki, Nobuhiro, Nishikawa, Hiroko, Ben, Chi, Tang, Chao, Nagase, Lisa, Inoue, Kaori, Senda, Toshiya, and Hatakeyama, Masanori

Abstract

Helicobacter pyloriEast Asian CagA is more closely associated with gastric cancer than Western CagA. Here we show that, upon tyrosine phosphorylation, the East Asian CagA-specific EPIYA-D segment binds to the N-SH2 domain of pro-oncogenic SHP2 phosphatase two orders of magnitude greater than Western CagA-specific EPIYA-C. This high-affinity binding is achieved via cryptic interaction between Phe at the +5 position from phosphotyrosine in EPIYA-D and a hollow on the N-SH2 phosphopeptide-binding floor. Also, duplication of EPIYA-C in Western CagA, which increases gastric cancer risk, enables divalent high-affinity binding with SHP2 via N-SH2 and C-SH2. These strong CagA bindings enforce enzymatic activation of SHP2, which endows cells with neoplastic traits. Mechanistically, N-SH2 in SHP2 is in an equilibrium between stimulatory “relaxed” and inhibitory “squeezed” states, which is fixed upon high-affinity CagA binding to the “relaxed” state that stimulates SHP2. Accordingly, East Asian CagA and Western CagA exploit distinct mechanisms for SHP2 deregulation.

Published
2017
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17. Differential Diagnosis between Pancreatic Ductal Adenocarcinoma from Chronic Pancreatitis with Thin Slice Table Incremental CE-CT

Author

ミウラ, キミコ, ミウラ, ゴウジ, ホンジョウ, カズミツ, ニシカワ, ヒロコ, ササイ, カズヒコ, タナカ, リクオ, ナカダ, タイシ, ナカニシ, タカシ, Miura, Kimiko, Miura, Gouji, Honjou, Kazumitsu, Nishikawa, Hiroko, Sasai, Kazuhiko, Tanaka, Rikuo, Nakada, Taishi, Nakanishi, Takashi, 三浦, 公子, 三浦, 剛史, 本城, 和光, 西川, 浩子, 佐々井, 一彦, 田中, 睦雄, 中田, 太志, 中西, 敬, ミウラ, キミコ, ミウラ, ゴウジ, ホンジョウ, カズミツ, ニシカワ, ヒロコ, ササイ, カズヒコ, タナカ, リクオ, ナカダ, タイシ, ナカニシ, タカシ, Miura, Kimiko, Miura, Gouji, Honjou, Kazumitsu, Nishikawa, Hiroko, Sasai, Kazuhiko, Tanaka, Rikuo, Nakada, Taishi, Nakanishi, Takashi, 三浦, 公子, 三浦, 剛史, 本城, 和光, 西川, 浩子, 佐々井, 一彦, 田中, 睦雄, 中田, 太志, and 中西, 敬

Published
1990

19. Tethering of SCFDia2 to the Replisome Promotes Efficient Ubiquitylation and Disassembly of the CMG Helicase

Author

Maculins, Timurs, Nkosi, Pedro Junior, Nishikawa, Hiroko, and Labib, Karim

Subjects
Agricultural and Biological Sciences(all), Biochemistry, Genetics and Molecular Biology(all)
Abstract

SummaryDisassembly of the Cdc45-MCM-GINS (CMG) DNA helicase, which unwinds the parental DNA duplex at eukaryotic replication forks, is the key regulated step during replication termination but is poorly understood [1, 2]. In budding yeast, the F-box protein Dia2 drives ubiquitylation of the CMG helicase at the end of replication, leading to a disassembly pathway that requires the Cdc48 segregase [3]. The substrate-binding domain of Dia2 comprises leucine-rich repeats, but Dia2 also has a TPR domain at its amino terminus that interacts with the Ctf4 and Mrc1 subunits of the replisome progression complex [4, 5], which assembles around the CMG helicase at replication forks [6]. Previous studies suggested two disparate roles for the TPR domain of Dia2, either mediating replisome-specific degradation of Mrc1 and Ctf4 [4] or else tethering SCFDia2 (SCF [Skp1/cullin/F-box protein]) to the replisome to increase its local concentration at replication forks [5]. Here, we show that SCFDia2 does not mediate replisome-specific degradation of Mrc1 and Ctf4, either during normal S phase or in response to replication stress. Instead, the tethering of SCFDia2 to the replisome progression complex increases the efficiency of ubiquitylation of the Mcm7 subunit of CMG, both in vitro and in vivo. Correspondingly, loss of tethering reduces the efficiency of CMG disassembly in vivo and is synthetic lethal in combination with a disassembly-defective allele of CDC48. Residual ubiquitylation of Mcm7 in dia2-ΔTPR cells is still CMG specific, highlighting the complex regulation of the final stages of chromosome replication, about which much still remains to be learned.

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20. CT Findings of Malignant Lymphoma of the Anterior Mediastinum -Differentistion from Invasive Thymoma

Author

マツモト, ツネオ, シマブクロ, メイコ, オキタ, イサオ, ヒロセ, タカオ, ヤマカワ, キミコ, ナカムラ, ヒロシ, サカモト, エイイチ, カリノ, ユウイチ, モリタニ, カズコ, ヒガシ, ユウイチロウ, ニシガウチ, カズヤ, ミウラ, ゴウシ, スダ, ヒロキ, ニシカワ, ヒロコ, チョウジ, タカシ, ナカニシ, タカシ, Matsumoto, Tsuneo, Shimabukuro, Meiko, Okita, Isao, Hirose, Takao, Yamakawa, Kimiko, Nakamura, Hiroshi, Sakamoto, Eiichi, Karino, Yuuichi, Moritani, Kazuko, Higashi, Yuuichirou, Nishigauchi, Kazuya, Miura, Goushi, Suda, Hiroki, Nishikawa, Hiroko, Chouji, Takashi, Nakanishi, Takashi, 松本, 常男, 島袋, 明子, 沖田, 功, 広瀬, 孝男, 山川, 公子, 中村, 洋, 坂本, 英一, 狩野, 裕一, 森谷, 和子, 東, 祐一郎, 西垣内, 一哉, 三浦, 剛史, 須田, 博喜, 西川, 浩子, 丁子, 卓, 中西, 敬, マツモト, ツネオ, シマブクロ, メイコ, オキタ, イサオ, ヒロセ, タカオ, ヤマカワ, キミコ, ナカムラ, ヒロシ, サカモト, エイイチ, カリノ, ユウイチ, モリタニ, カズコ, ヒガシ, ユウイチロウ, ニシガウチ, カズヤ, ミウラ, ゴウシ, スダ, ヒロキ, ニシカワ, ヒロコ, チョウジ, タカシ, ナカニシ, タカシ, Matsumoto, Tsuneo, Shimabukuro, Meiko, Okita, Isao, Hirose, Takao, Yamakawa, Kimiko, Nakamura, Hiroshi, Sakamoto, Eiichi, Karino, Yuuichi, Moritani, Kazuko, Higashi, Yuuichirou, Nishigauchi, Kazuya, Miura, Goushi, Suda, Hiroki, Nishikawa, Hiroko, Chouji, Takashi, Nakanishi, Takashi, 松本, 常男, 島袋, 明子, 沖田, 功, 広瀬, 孝男, 山川, 公子, 中村, 洋, 坂本, 英一, 狩野, 裕一, 森谷, 和子, 東, 祐一郎, 西垣内, 一哉, 三浦, 剛史, 須田, 博喜, 西川, 浩子, 丁子, 卓, and 中西, 敬

Published
1989

23. Digital Mammographic Features of Breast Cancer Recurrences and Benign Lesions Mimicking Malignancy Following Breast-Conserving Surgery and Radiation Therapy.

Author

Urano M, Nishikawa H, Goto T, Shiraki N, Matsuo M, Denewar FA, Kondo N, Toyama T, and Shibamoto Y

Subjects
Breast Neoplasms diagnostic imaging, Breast Neoplasms pathology, Diagnosis, Differential, Female, Humans, Magnetic Resonance Imaging, Neoplasm Recurrence, Local pathology, Neoplasm Recurrence, Local therapy, Predictive Value of Tests, Radiotherapy, Adjuvant, Treatment Outcome, Ultrasonography, Mammary, Breast Neoplasms therapy, Mammography, Mastectomy, Segmental adverse effects, Neoplasm Recurrence, Local diagnostic imaging
Abstract

Mammography after breast-conserving surgery and radiation therapy is an important tool for followup. Early diagnosis of local recurrence enables prompt treatment decisions, which may affect patient prognosis. For complicated post-treatment changes, radiologists sometimes have difficulties in interpreting follow-up mammography. Fat necrosis, dystrophic calcifications, suture calcification features, breast edema, seroma and distorted breast are benign changes related to treatment. These findings may mimic or hide tumor recurrence making it difficult to diagnose recurrences or prevent inappropriate biopsies. Recurrent tumors in follow-up mammography show several typical findings such as increasing asymmetric density, enlarging mass, reappearance of breast edema, and micro-calcifications. The purpose of this pictorial review is to demonstrate and discuss mammographic findings of recurrent tumors and important post-treatment changes that may mimic benign or malignant lesions, also using breast ultrasound images or breast magnetic resonance images. Recognizing post-treatment changes may help radiologists to more effectively identify candidates for suspected local recurrences.

Published
2020
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24. Development of risky varices in alcoholic cirrhosis with a well-maintained nutritional status.

Author

Enomoto H, Sakai Y, Iwata Y, Takata R, Aizawa N, Ikeda N, Hasegawa K, Nakano C, Nishimura T, Yoh K, Ishii A, Takashima T, Nishikawa H, Iijima H, and Nishiguchi S

Abstract

Aim: To compare the nutritional status between alcoholic compensated cirrhotic patients and hepatitis C virus (HCV)-related cirrhotic patients with portal hypertension., Methods: A total of 21 patients with compensated cirrhosis (14 with HCV-related cirrhosis and seven with alcoholic cirrhosis) who had risky esophageal varices were investigated. In addition to physical variables, including the body mass index, triceps skinfold thickness, and arm-muscle circumference, the nutritional status was also assessed using the levels of pre-albumin (pre-ALB), retinol-binding protein (RBP) and non-protein respiratory quotient (NPRQ) measured with an indirect calorimeter., Results: A general assessment for the nutritional status with physical examinations did not show a significant difference between HCV-related cirrhosis and alcoholic cirrhosis. However, the levels of pre-ALB and RBP in alcoholic compensated cirrhotic patients were significantly higher than those in HCV-related compensated cirrhotic patients. In addition, the frequency of having a normal nutritional status (NPRQ ≥ 0.85 and ALB value > 3.5 g/dL) in alcoholic compensated cirrhotic patients was significantly higher than that in HCV-related compensated cirrhotic patients., Conclusion: According to our small scale study, alcoholic compensated cirrhotic patients can develop severe portal hypertension even with a relatively well-maintained liver function and nutritional status compared with HCV-related cirrhosis.

Published
2015
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