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Osine phosphorylation controls the function of CNK1 as a molecular switch in signal transduction. Biochim Biophys Acta (BBA) - Mol Cell Res. 2015; 1853(11, Part A):2847?5. Winter JM, Yeo CJ, Brody JR. Diagnostic, prognostic, and predictive biomarkers in pancreatic cancer. J Surg Oncol. 2013;107(1):15?2. Brennan MF, Kattan MW, Klimstra D, Conlon K. Prognostic Nomogram for patients undergoing resect
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E atrophy in these animals. It has been shown that the physical activity and weight bearing on the injured limb, has a significant correlation with collagen production and density of the injured area of the tendon [10,12,24]. Lower DTEC and higher TRDEC together with a higher transverse diameter of the injured area of the ITTs, specifically during the initial weeks after injury, could comprehensiv
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Ability was randomly developed and the peri-tendinous fibroblasts proliferated not only in the injured area, but also they randomly invaded into the peri-tendinous tissues such as skin, subcutaneous fascia and muscle and proliferated and manufactured a haphazard granulation tissue throughout these structures. Thus, the potential of the healing response of the ICTs was divided into different region
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Activation of ERK with induction of apoptosis by various chemopreventive and chemotherapeutic agents [39-41]. In fact, oxidants have been shown to activate ERK by taking over the growth factor receptor signaling pathways [42-46]. Moreover, ERK may get activated in response to DNA damage and can phosphorylate p53 in vitro [23,24,47-49]. We found that exposure of Capan-2 or BxPC-3 cells with apoptos
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Tin S, Mathieu V, Kiss R, Lefranc F: Galectins and gliomas. Brain Pathol 2010, 20:17?7. Mariani L, Beaudry C, McDonough WS, Hoelzinger DB, Kaczmarek E, Ponce F, Coons SW, Giese A, Seiler RW, Berens ME: Death-associated protein 3 (Dap3) is overexpressed in invasive glioblastoma cells in vivo and in glioma cell lines with induced motility phenotype in vitro. Clin Cancer Res 2001, 7:2480?489. Mariani
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Action of the tumor [22,36]. Indeed, abrogating galectin-1 expression renders tumor cells more susceptible to temozolamide treatment [22,41]. Finally, galectin-1 induces apoptosis of activated T-cells [42-46], prevents host animals from mounting tumor vaccine-induced immunity [47], and may cooperate with TGF-beta in GBM-induced immunosuppression [48,49]. In sum, galectin-1 expression may inversely
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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura
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Man T lymphocytes. J Immunol 1998, 161:2114?119. 47. Rubinstein N, Alvarez M, Zwirner NW, Toscano MA, Ilarregui JM, Bravo A, Mordoh J, Fainboim L, Podhajcer OL, Rabinovich GA: Targeted inhibition of galectin-1 gene expression in tumor cells results in heightened T cellmediated rejection; A potential mechanism of tumor-immune privilege. Cancer Cell 2004, 5:241?51. 48. Kuppner MC, Hamou MF, Sawamura