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Geldanamycin induces CHOP expression through a 4-(2-aminoethyl)-benzenesulfonyl fluoride-responsive serine protease

Cell Research 2007年第2期17卷 184-186页

作者： toru hosoi Kanae Hyoda Yasunobu Okuma Yasuyuki Nomura Koichiro Ozawa Department of Pharmacotherapy Graduate School of Biomedical SciencesHiroshima University1-2-3 KasumiMinami-kuHiroshima 734-8551Japan Department of Pharmacology Graduate School of Pharmaceutical SciencesHokkaido UniversitySapporo 060-0812Japan Department of Pharmacology Faculty of Pharmaceutical SciencesChiba Institute of SciencesChoshiChiba 288-0025Japan

Dear Editor:Geldanamycin is a benzoquinone ansamycin,which wasoriginally described as a tyrosine kinase ***-ever,subsequent studies have revealed that geldanamycinbinds to and inhibits heat-shock protein 90(Hsp90)activity[1].Hsp90 is a molecular chaperone involved in the con-formational maturation of proteins such as mutated p53,Raf-1,Akt,Bcr-Ab1,and *** is suggested that agentsinhibiting Hsp90 have anti-cancer properties,although theprecise molecular mechanisms underlying the anti-cancereffects of geldanamycin are not well *** evidence has suggested that diabetes andneurodegenerative disorders such as Parkinson's andAlzheimer's diseases are related to the disruption ofendoplasmic reticulum(ER)*** response to ERstress,unfolded proteins accumulate and aggregate in theER,which will trigger many rescuer responses,includingthe unfolded protein response(UPR)and ***,geldanamycin has been shownto upregulate ER chaperones and the expression of CHOP[2].Moreover,Hsp90 associates with PERK and IRE1α,ER-resident trans-membrane protein kinases involved inER stress response[3].These observations suggest that

关键词： CHOP benzenesulfonyl fluoride-responsive serine protease ER aminoethyl Geldanamycin induces CHOP expression through a 4

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Neuroprotective Effects of 4-phenylbutyric Acid and Its Derivatives： Possible Therapeutics for Neurodegenerative Diseases

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Journal of Health Science 2017年第1期5卷 9-17页

作者： Seisuke Mimori toru hosoi Masayuki Kaneko Koichiro Ozawa Tetsuto Kanzaki Akinori Nishi Yasuyuki Nomura Department of Clinical Medicine Chiba Institute of Science Choshi 288-0025 Japan Department of Pharmacotherapy Graduate School of Biomedical and Health Sciences Hiroshima University Hiroshima734-8553 Japan Department of Biochemistry Institute of Biomedical & Health Sciences Hiroshima University Hiroshima 734-8553 Japan Department of Drug Informatics Graduate School and Faculty of Pharmaceutical Sciences Chiba University Chiba 260-8675Japan Department of Pharmacology Kurume University School of Medicine Kurume 830-0011 Japan

The pathogenesis of neurodegenerative diseases such as Alzheimer＇s and Parkinson＇s diseases involves the aggregation of denatured and misfolded nascent proteins. Consequently, many pharmacological approaches have been developed to prevent protein aggregation. 4-Phenylbutyric acid （4-PBA） is a chemical chaperone that shows potential as a candidate drug for the treatment of neurodegenerative diseases. The main actions of chemical chaperones are the amelioration of unfolded proteins and the suppression of their aggregation, which result in protective effects against endoplasmic reticulum stress-induced neuronal cell death. Furthermore, 4-PBA exhibits inhibitory activity against histone deacetylases （HDACs）. However, owing to the problematically high doses of 4-PBA currently required for therapeutic efficacy, the optimization of 4-PBA is crucial for its effective medicinal application. In the present review, we summarize the recent advances in research on the basic actions of 4-PBA and its derivatives. We also discuss whether these compounds could be viable therapeutic agents against neurodegenerative diseases.

关键词： 4-Phenylbutyric acid (4-PBA) neurodegenerative diseases chemical chaperone histone deacetylase (HDAC).

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Familial pancreatic cancer: Concept, management and issues

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World Journal of Gastroenterology 2017年第6期23卷 935-948页

作者： Hiroyuki Matsubayashi Kyoichi Takaori Chigusa Morizane Hiroyuki Maguchi Masamichi Mizuma Hideaki Takahashi Keita Wada Hiroko hosoi Shinichi Yachida Masami Suzuki Risa Usui toru Furukawa Junji Furuse Takamitsu Sato Makoto Ueno Yoshimi Kiyozumi Susumu Hijioka Nobumasa Mizuno Takeshi Terashima Masaki Mizumoto Yuzo Kodama Masako Torishima Takahisa Kawaguchi Reiko Ashida Masayuki Kitano Keiji Hanada Masayuki Furukawa Ken Kawabe Yoshiyuki Majima toru Shimosegawa Division of Endoscopy Shizuoka Cancer Center Clinic of Genetic Medicine Shizuoka Cancer Center Department of Surgery Kyoto University Graduate School of Medicine Division of Hepatobiliary and Pancreatic Oncology National Cancer Center Hospital Center for Gastroenterology Teine-Keijinkai Hospital Department of Surgery Tohoku University Graduate School of Medicine Department of Hepatobiliary and Pancreatic Oncology National Cancer Center Hospital East Department of Surgery Teikyo University School of Medicine Division of Cancer Genomics National Cancer Center Research Institute Institute for Integrated Medical Sciences Tokyo Women’s Medical University Department of Internal Medicine Kyorin University School of Medicine Division of Gastroenterology Yokohama City University Graduate School of Medicine Division of Hepatobiliary and Pancreatic Medical Oncology Kanagawa Cancer Center Department of Gastroenterology Aichi Cancer Center Hospital Department of Gastroenterology Kanazawa University Graduate School of Medicine Department of Surgery Japan Bapist Hospital Department of Gastroenterology and Hepatology Kyoto University Graduate School of Medicine Clinical Genetics Unit Kyoto University Graduate School of Medicine Center for Genomic Medicine Kyoto University Graduate School of Medicine Osaka Medical Center for Cancer and Cardiovascular Diseases Second Department of Internal Medicine Wakayama Medical University Department of Gastroenterology Onomichi General Hospital Department of Gastroenterology NationalKyushu Cancer Center Department of Medicine and Bioregulatory Sciences Kyushu University Graduate School of Medical Science Pancreatic Cancer Action Network Department of Gastroenterology Tohoku University Graduate School of Medicine

Familial pancreatic cancer (FPC) is broadly defined as two first-degree-relatives with pancreatic cancer (PC) and accounts for 4%-10% of PC. Several genetic syndromes, including Peutz-Jeghers syndrome, hereditary pancreatitis, hereditary breast-ovarian cancer syndrome(HBOC), Lynch syndrome, and familial adenomatous polyposis (FAP), also have increased risks of PC, but the narrowest definition of FPC excludes these known syndromes. When compared with other familial tumors, proven genetic alterations are limited to a small proportion (Caucasian) and a younger onset are common also in FPC. In European countries, "anticipation" is reported in FPC families, as with other hereditary syndromes; a trend toward younger age and worse prognosis is recognized in the late years. The resected pancreases of FPC kindred often show multiple pancreatic intraepithelial neoplasia (Pan IN) foci, with various K-ras mutations, similar to colorectal polyposis seen in the FAP patients. As with HBOC patients, a patient who is a BRCA mutation carrier with unresectable pancreatic cancer (accounting for 0%-19% of FPC patients) demonstrated better outcome following platinum and Poly (ADP-ribose) polymerase inhibitor treatment. Western countries have established FPC registries since the 1990 s and several surveillance projects for highrisk individuals are now ongoing to detect early PCs. Improvement in lifestyle habits, including non-smoking, is recommended for individuals at risk. In Japan, the FPC study group was initiated in 2013 and the Japanese FPC registry was established in 2014 by the Japan Pancreas Society.

关键词： familial pancreatic cancer registry high risk genetic surveillance

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