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S of pancreatic cancer. Nature. 2016;531(7592):47?2. 10. Kolch W. Coordinating ERK/MAPK signalling through scaffolds and inhibitors. Nat Rev Mol Cell Biol. 2005;6(11):827?7. 11. McKay MM, Morrison DK. Integrating signals from RTKs to ERK/MAPK. Oncogene. 2007;26(22):3113?1. 12. Kim M, Yan Y, Kortum RL, Stoeger SM, Sgagias MK, Lee K, Lewis RE, Cowan KH. Expression of kinase suppressor of Ras1 enhanc
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Cellbased study expressing mutants of known phosphorylation sites of CNKSR1 in cancer cells identified sites linked to nuclear translocation with concomitant activation of MAPK pathway-driven serum response element (SRE) gene expression providing, for the first time, a direct correlation of cellular CNKSR1 distribution and MAPK pathway signaling output. [21] These findings are in line with the ide
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Eased DTEC and reduction in TRDEC. To prove these statements, we have tested some biophysical characteristics as indices of collagen content of the regenerated tissues at 120 DPI. Compared to the ICTs, the ITTs had a higher dry matter content. They also showed almost similar patterns of water delivery and water uptake characteristics with their normal contralateral tendons. This bio-implant was no
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S unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwis
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Aging revealed a similar hazard ratio (HR) of 1.91 (95 CI: 1.20 to 3.05; data not shown). Other statistically significant variables in the model were, as expected and known from previous clinicopathological multivariate outcome models of pancreas cancer, no resection compared to any resection (HR = 3.78, 95 CI: 2.to 6.85), TNM staging indicating regional lymph nodes (HR = 1.89, 95 Cl: 1.21 to 2
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Nt strategies [10,11]. An ideal scaffold which is designed for tendon tissue engineering should have similar architecture and composition as normalhealthy tendon [11]. In addition, they should have optimum cell cytocompatibility in vitro, and have optimum biodegradability, biocompatibility and healing efficacy in vivo [10,11]. On the other hand, the scaffold should incorporate with the newly regen
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Ing glioblastoma cells to apoptosis. J Clin Oncol 2005, 23: 2411?422. Paulus W, Baur I, Beutler AS, Reeves SA: Diffuse brain invasion of glioma cells requires beta 1 integrins. Lab Invest 1996, 75:819?26. Uhm JH, Gladson CL, Rao JS: The role of integrins in the malignant phenotype of gliomas. Front Biosci 1999, 4:D188 199. Lipinski CA, Tran NL, Bay C, Kloss J, McDonough WS, Beaudry C, Berens ME, L
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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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