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Miguel A Zaballos Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III (ISCIII), Madrid, Spain

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Pilar Santisteban Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid (UAM), Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Instituto de Salud Carlos III (ISCIII), Madrid, Spain

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variant (TCV-PTC). PTC is mostly related to mutations that activate the MAPK (mitogen-activated protein kinase) signaling pathway, such as RET , NTRK (neurotrophic receptor tyrosine kinase) and ALK (anaplastic lymphoma kinase) gene rearrangements or

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Y L Bao
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K Tsuchida
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B Liu
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A Kurisaki
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T Matsuzaki
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H Sugino
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interfered with TH promoter activation by activin A and bFGF (Fig. 7D ). These data indicate the important role of the Smad signaling pathway for TH regulation by activin A and bFGF. Activation of ERK1/2 MAPK is required for the

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G Almeida-Pereira Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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T Vilhena-Franco Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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R Coletti Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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S Q Cognuck Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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H V P Silva Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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L L K Elias Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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J Antunes-Rodrigues Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil

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phospholipase C, protein kinase C (PKC) and members of the mitogen-activated protein kinase family (MAPK; extracellular signal-regulated kinases 1 and 2 (ERK1/2), p38MAPK and c-Jun N-terminal Kinase (JNK)) ( Mehta & Griendling 2007 ). MAPK proteins are

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A G Kayali Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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A Stotland Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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K V Gunst Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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M Kritzik Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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G Liu Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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S Dabernat Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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Y-Q Zhang Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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W Wu Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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N Sarvetnick Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France

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activated, after which they can activate MAPK ( Bonfini et al. 1996 , Schlessinger 2000 ). Another major signaling pathway activated by growth factors, the PI3 kinase pathway phosphorylates phosphatidylinositols, yielding lipid products that bind the

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Jodie M Fleming Rutgers, The State University of New Jersey, 108 Foran Hall, 59 Dudley Road, New Brunswick, New Jersey 08901-8520, USA

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Jeffrey A Brandimarto Rutgers, The State University of New Jersey, 108 Foran Hall, 59 Dudley Road, New Brunswick, New Jersey 08901-8520, USA

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Wendie S Cohick Rutgers, The State University of New Jersey, 108 Foran Hall, 59 Dudley Road, New Brunswick, New Jersey 08901-8520, USA

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regulation of these two IGFBP by IGF-I via analysis of intracellular signaling pathways. In the present study, we found that both the PI3K and the MAPK pathways were required for IGF-I to increase IGFBP-3 and -5 in MF. However, an unexpected and

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Juliana I Candelaria Department of Animal Science, University of California Davis, Davis, California, USA

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Maria B Rabaglino Department of Applied Mathematics and Computer Science, Technical University of Denmark, Kongens Lyngby, Denmark

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Anna C Denicol Department of Animal Science, University of California Davis, Davis, California, USA

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against p44/42 MAPK (4695, Cell Signaling Technology) or a rabbit isotype IgG overnight in a humidified chamber at 4°C. After washing, 1 µg/mL FITC-conjugated donkey anti-rabbit secondary antibody was added for 1 h at RT, followed by 10 min incubation with

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Pedro A Orihuela Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile
Millennium Institute for Fundamental and Applied Biology, Santiago, Chile

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Alexis Parada-Bustamante Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile
Millennium Institute for Fundamental and Applied Biology, Santiago, Chile

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Lidia M Zuñiga Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile
Millennium Institute for Fundamental and Applied Biology, Santiago, Chile

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Horacio B Croxatto Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile
Millennium Institute for Fundamental and Applied Biology, Santiago, Chile

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and MAPK signalling cascades in this nongenomic pathway. First we examined the role of IP3 and MAPK on accelerated oocyte transport induced by E 2 . The effect of E 2 on the levels of IP3 or phosphorylated MAPK p44/42 in the rat oviduct was then

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Danielle Brown
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Amiya P Sinha Hikim Division of Endocrinology, Division of Endocrinology, Charles Drew University, Los Angeles, California 90059, USA

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Ekaterina L Kovacheva
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Indrani Sinha-Hikim
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Notch signaling in T-mediated muscle fiber hypertrophy. Mitogen-activated protein kinases (MAPKs) comprise a family of serine/threonine kinases that function as critical mediators of variety of extracellular signals ( Johnson & Lapadat 2002 , Wada

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Helena C Barbosa
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Silvana Bordin Departamento de Fisiologia e Biofísica, Departamento de Fisiologia e Biofísica, Beta Cell Development and Function Group, CENEXA, Instituto de Biologia, Universidade Estadual de Campinas, 13083-970 Campinas-SP, São Paulo-SP, Brazil

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Gabriel Anhê Departamento de Fisiologia e Biofísica, Departamento de Fisiologia e Biofísica, Beta Cell Development and Function Group, CENEXA, Instituto de Biologia, Universidade Estadual de Campinas, 13083-970 Campinas-SP, São Paulo-SP, Brazil

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Shanta J Persaud Departamento de Fisiologia e Biofísica, Departamento de Fisiologia e Biofísica, Beta Cell Development and Function Group, CENEXA, Instituto de Biologia, Universidade Estadual de Campinas, 13083-970 Campinas-SP, São Paulo-SP, Brazil

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James Bowe Departamento de Fisiologia e Biofísica, Departamento de Fisiologia e Biofísica, Beta Cell Development and Function Group, CENEXA, Instituto de Biologia, Universidade Estadual de Campinas, 13083-970 Campinas-SP, São Paulo-SP, Brazil

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Maria I Borelli Departamento de Fisiologia e Biofísica, Departamento de Fisiologia e Biofísica, Beta Cell Development and Function Group, CENEXA, Instituto de Biologia, Universidade Estadual de Campinas, 13083-970 Campinas-SP, São Paulo-SP, Brazil

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Juan J Gagliardino Departamento de Fisiologia e Biofísica, Departamento de Fisiologia e Biofísica, Beta Cell Development and Function Group, CENEXA, Instituto de Biologia, Universidade Estadual de Campinas, 13083-970 Campinas-SP, São Paulo-SP, Brazil

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Antonio C Boschero
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-154), and anti-phospho MAPK3/1 -Thr202/Tyr204 (mouse monoclonal sc-7383) antibodies were from Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA; and anti-phospho P70S6K -Thr389 (mouse polyclonal, #9206S) was from Cell Signaling Technology Inc

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Kotaro Horiguchi Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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Ken Fujiwara Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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Cimi Ilmiawati Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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Motoshi Kikuchi Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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Takehiro Tsukada Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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Tom Kouki Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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Takashi Yashiro Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan

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and cyclin D1 production, which suggests that integrin β1 receives laminin as a signal on FS cells and that its signaling activates MAPK signaling cascades, leading to cyclin D1 transcription and contributing to cell cycle progression. However, there

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