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Yirui He The Center of Clinical Research of Endocrinology and Metabolic Diseases in Chongqing and Department of Endocrinology, Chongqing Three Gorges Central Hospital, Chongqing, China
Department of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China

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Cheng Zhang The Center of Clinical Research of Endocrinology and Metabolic Diseases in Chongqing and Department of Endocrinology, Chongqing Three Gorges Central Hospital, Chongqing, China

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Yong Luo The Center of Clinical Research of Endocrinology and Metabolic Diseases in Chongqing and Department of Endocrinology, Chongqing Three Gorges Central Hospital, Chongqing, China

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Jinhua Chen Department of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China

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Mengliu Yang The Center of Clinical Research of Endocrinology and Metabolic Diseases in Chongqing and Department of Endocrinology, Chongqing Three Gorges Central Hospital, Chongqing, China

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Ling Li Key Laboratory of Diagnostic Medicine (Ministry of Education) and Department of Clinical Biochemistry, College of Laboratory Medicine, Chongqing Medical University, Chongqing, China

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Harvest F Gu Department of Clinical Science, Intervention and Technology, Karolinska University Hospital, Karolinska Institutet, Huddinge, Stockholm, Sweden

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Gangyi Yang The Center of Clinical Research of Endocrinology and Metabolic Diseases in Chongqing and Department of Endocrinology, Chongqing Three Gorges Central Hospital, Chongqing, China
Department of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China

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Xianxiang Zhang The Center of Clinical Research of Endocrinology and Metabolic Diseases in Chongqing and Department of Endocrinology, Chongqing Three Gorges Central Hospital, Chongqing, China

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Technology Cat# 3024, RRID:AB_331253), anti-AKT kinase (AKT) (Cell Signaling Technology Cat# 9272, RRID:AB_329827)/anti-phospho-AKT (Cell Signaling Technology Cat# 9271, RRID:AB_329825), anti-mammalian target of rapamycin (mTOR) (Cell Signaling Technology Cat

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Hong-Zhi Sun
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Tong-Wei Yang Key Laboratory of Environment and Genes Related to Diseases, First Affiliated Hospital of Jilin University, Ministry of Education, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, People's Republic of China

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Wei-Jin Zang
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Shu-Fang Wu
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), suggesting that NFKB may regulate the expression of AR. The activation of AKT and NFKB has been involved in the progression of PCa from androgen dependence to independence ( Murillo et al . 2001 , Kikuchi et al . 2003 ). The phosphatidylinositol 3-kinase

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Hong Xu Department of Gastroenterology and Hepatology, Hangzhou Red Cross Hospital, Hangzhou, China

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Yang Zhou Liver Cirrhosis Section, Department of Hepatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Yongxia Liu Department of Clinical Laboratory, Hangzhou Red Cross Hospital, Hangzhou, China

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Jian Ping Liver Cirrhosis Section, Department of Hepatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
Institute of Liver Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai, China

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Qiyang Shou Experimental Animal Research Center, Zhejiang Chinese Medical University, Hangzhou, China

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Fangming Chen Experimental Animal Research Center, Zhejiang Chinese Medical University, Hangzhou, China

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Ru Ruo Department of Pathology, Hangzhou Red Cross Hospital, Hangzhou, China

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( Ahmadieh & Azar 2014 ). In the liver, the insulin receptor substrate 2 (IRS2)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling transduction pathway plays a pivotal role in modulating the glucose metabolic actions of insulin ( Pessin

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S Otabe
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N Wada
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T Hashinaga
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X Yuan
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I Shimokawa Division of Endocrinology and Metabolism, Investigative Pathology, Department of Medicine, Kurume University School of Medicine, 67 Asahimachi, Kurume, Fukuoka 830-0011, Japan

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T Fukutani
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K Tanaka
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T Ohki
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S Kakino
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Y Kurita
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H Nakayama
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Y Tajiri
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K Yamada
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lifespan of this murine model of metabolic syndrome without affecting body weight by attenuating AKT signaling and chronic low-grade inflammation. Materials and Methods Animals KK/Ta mice and C57BL/6N mice as a control were purchased from CLEA Japan (Tokyo

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S Greco Laboratory of Cellular Physiology, Department of Biological and Environmental Sciences and Technologies (DiSTeBA), Ecotekne, Via Provinciale per Monteroni, 73100 Lecce, Italy

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C Storelli Laboratory of Cellular Physiology, Department of Biological and Environmental Sciences and Technologies (DiSTeBA), Ecotekne, Via Provinciale per Monteroni, 73100 Lecce, Italy

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S Marsigliante Laboratory of Cellular Physiology, Department of Biological and Environmental Sciences and Technologies (DiSTeBA), Ecotekne, Via Provinciale per Monteroni, 73100 Lecce, Italy

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activated by BK in MCF-7 cells, paying attention to those pathways previously highlighted in primary normal and cancerous breast cells (i.e. PKCs, PI3K/Akt and ERK1/2 signalling) ( Greco et al. 2004 , 2005 ); furthermore, the possibility that BK is

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Andrea Vasconsuelo Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahía Blanca, Argentina

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Lorena Milanesi Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahía Blanca, Argentina

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Ricardo Boland Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahía Blanca, Argentina

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suggest the ability of the hormone to activate extranuclear receptors ( Bjornstrom & Sjoberg 2005 ). Among the rapid non-transcriptional actions of E 2 , the activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway has been shown in various

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Botao Du
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Masahide Ohmichi
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Kazuhiro Takahashi
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Jun Kawagoe
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Chika Ohshima
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Hideki Igarashi
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Akiko Mori-Abe
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Maki Saitoh
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Tsuyoshi Ohta
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Akira Ohishi
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Masakazu Doshida
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Naohiro Tezuka
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Toshifumi Takahashi
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Hirohisa Kurachi
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consensus sequence for phosphorylation by Akt, and Akt kinase enhances the human telomerase activity through phosphorylation of hTERT ( Kang et al. 1999 ). In addition, it was recently reported that estrogen protects against Aβ- ( Zhang et al. 2001 ) or

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José Edgar Nicoletti-Carvalho
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Tatiane C Araújo Nogueira
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Renata Gorjão Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Institute of Physical Activity Sciences and Sports, Cruzeiro do Sul University, Physiology and Biophysics, Internal Medicine, Pharmacology, Faculty of Medical Sciences, State University of Campinas, Prof. Lineu Prestes Ave #1524. ICB 1- Room 125, 05508-900 Sao Paulo, SP, Brazil

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Carla Rodrigues Bromati
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Tatiana S Yamanaka
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Antonio Carlos Boschero Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Institute of Physical Activity Sciences and Sports, Cruzeiro do Sul University, Physiology and Biophysics, Internal Medicine, Pharmacology, Faculty of Medical Sciences, State University of Campinas, Prof. Lineu Prestes Ave #1524. ICB 1- Room 125, 05508-900 Sao Paulo, SP, Brazil

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Licio Augusto Velloso Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Institute of Physical Activity Sciences and Sports, Cruzeiro do Sul University, Physiology and Biophysics, Internal Medicine, Pharmacology, Faculty of Medical Sciences, State University of Campinas, Prof. Lineu Prestes Ave #1524. ICB 1- Room 125, 05508-900 Sao Paulo, SP, Brazil

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Rui Curi
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Gabriel Forato Anhê Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Institute of Physical Activity Sciences and Sports, Cruzeiro do Sul University, Physiology and Biophysics, Internal Medicine, Pharmacology, Faculty of Medical Sciences, State University of Campinas, Prof. Lineu Prestes Ave #1524. ICB 1- Room 125, 05508-900 Sao Paulo, SP, Brazil

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Silvana Bordin
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). Anti-BCL2 (sc492), anti-signal transducer and activator of transcription 3 (STAT3) (sc483), anti-phospho-STAT3 Tyr (sc8059), anti-CHOP (sc575 and sc793), anti-phospho-AKT1/2/3 Ser (sc33437), anti-tribble3 (TRIB3) (sc34212), and anti

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Daisuke Fujita Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Akiko Tanabe Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Tatsuharu Sekijima Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Hekiko Soen Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Keijirou Narahara Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Yoshiki Yamashita Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Yoshito Terai Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Hideki Kamegai Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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Masahide Ohmichi Department of Obstetrics and Gynecology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-City, Osaka 569-8686, Japan

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roles of the AKT–MTOR and ERK cascades in the regulation of VEGF and endoglin production under hypoxic conditions in the trophoblast-derived cell line, BeWo. Materials and Methods Materials The phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002

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Darryl L Hadsell Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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Walter Olea Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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Nicole Lawrence Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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Jessy George Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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Daniel Torres Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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Takahashi Kadowaki Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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Adrian V Lee Department of Pediatrics,
Department of Molecular and Cellular Biology,
Department of Medicine, The Breast Center, Baylor College of Medicine, USDA/ARS Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030, USA
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

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the serine threonine kinase Akt ( Datta et al. 1997 ). The activation of Akt in response to insulin or IGF-I stimulation mediates the ability of these two hormones to inhibit apoptosis ( Datta et al. 1997 ). However, activation of Akt has also

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