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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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future human trials. The mitogen-activated protein kinase (MAPK) family of signalling molecules, includes extracellular signal-regulated kinase (ERK)1/2, p38 MAPK, c-Jun N-terminal kinase/ stress-activated protein kinase (JNK/SAPK), ERK3 and ERK5
Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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38 MAPK ( Tajima et al. 2003 , Maizels et al. 1998 , Gonazalez-Robayna et al. 2000). Moore et al. (2001) have identified ERK1/2 as the first intracellular signaling molecules that differentially regulate FSH-induced progesterone and
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-induced MAPK activation, including extracellular receptor kinase 1/2 (ERK1/2) in CHO cells over-expressing OX1R ( Ammoun et al . 2006 a ). Furthermore, roles for intracellular signalling molecules including cAMP (up- and down-regulation) and IP 3 /Ca 2 + were
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mediated by extracellular signaling-regulated kinase 1/2 (ERK1/2), p38MAPK or NF-κB pathway in cardiovascular cells such as smooth muscle cells ( Funakoshi et al . 2001 ) and cardiac fibroblasts ( Omura et al . 2004 ). However, the cellular signaling
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-terminal kinase and p38 MAPK signalling pathways ( Freshney et al . 1994 ). Extracellular signal-regulated kinases 1 and 2 (ERK1/2), albeit mostly activated by mitogenic factors, are also activated by IL1α in selective cases ( Bird et al . 1991 , Waterfield et
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possible involvement of JAK/STAT, MAPK, and PI3K/Akt cascades in GH-induced type II SOCS expression was examined. Using transfection studies in CHO cells, the effects of over-expression of grass carp type II SOCS on (i) JAK 2 /STAT 5 signaling coupled to
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Department of Veterans Affairs Palo Alto Health Care System, Division of Gastroenterology and Hepatology, Department of Immunology, Geriatric Research, Education and Clinical Center (GRECC), 3801 Miranda Avenue, Palo Alto, California 94304, USA
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phosphorylation and activation of MAP kinases ( Lewis et al . 1998 , Martindale & Holbrook 2002 , Matsuzawa & Ichijo 2005 , McCubrey et al . 2006 ). Mitogen-activated protein kinase (MAPK) signal transduction pathways are well-characterized signaling networks
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-total-extracellular signal-regulated kinase (ERK)1/2 MAPK antibodies (Cell Signaling Technology Inc.), anti-phospho- and anti-total-P38 MAPK antibodies (Cell Signaling Technology Inc.), anti-phospho- and anti-total-stress-activated protein kinase/c-Jun NH2-terminal kinase
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Division of Endocrinology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Clinical Research Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA
Division of Endocrinology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, 1107 Elliman Clinical Research Building, 421 East Canfield Avenue, Detroit, Michigan 48201, USA
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intracellular signaling pathways are not well defined relative to specific actions. PTH regulates bone remodeling by activating distinct signaling pathways including MAPK pathways in osteoblasts via PTH receptor-1 (PTH1R; for review, see Datta & Abou