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Erved association of CNKSR1 expression and survival outcome suggests scaffolding proteins of the RAS-MAPK pathway may account, in part, for the observed heterogeneity of PDAC biology, and clinically may aid in improved future patient stratification.MethodsStudy participants and tissue microarray (TMA) compositionDe-identified cancer tissues included in this analysis were confirmed to be pancreatic
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Rotein expression levels in pancreatic tumors compared to matched, uninvolved controls (p = 0.004).CNKSR1 expression levels are heterogeneous in pancreatic adenocarcinomaTo examine if CNKSR1 expression is dysregulated in pancreas cancer we first compared CNKSR1 expression measured by intensity of immunostaining in 13 randomly chosen matched tumor and normal pancreaticCombining cases from all three
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Ells stained [24, 25]. CNKSR1 expression was evaluated based on intensity semiquantitatively on a four-tier scale (0 = negative, 1 = weak/background, 2 = moderate/positive, 3 = strongly positive). CNKSRshows minimal expression in lymphoid tissues according to RNA-Seq data and immunohistochemical staining from the Human Protein Atlas (Human Protein Atlas available from www.proteinatlas.org) [26]. S
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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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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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That is relatively over-expressed at the tumor periphery. These graphical representations of gene expression data compare the relative expression of galectin-1 from the core and edge of tumors to pooled data from normal mouse brain samples. (Graphics from GeneSpringW).created. To ensure that galectin-1 over-expression would not enhance proliferation of the U87MG line (and hence alter the interpret
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Radial migration assay was performed as previously described [30,31]. In a blinded fashion, various U87Gal-1 clones were analyzed and compared to U87GFP controls and parental U87MG cells. Of each clone, 2500 cells were allowed to sediment through a cooled manifold onto laminin-coated cell culture wells (Creative Scientific Methods, Inc., Phoenix, AZ). The manifold and slide were incubated together
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Time intervals in a time-dependent experiment. Expression and phosphorylation of ERK (Thr-202/Tyr204) and MEK-1 (Ser-217/221) was determined by western blotting. B) The effect of Triphala on the kinase activity of ERK was determined using a kit from Cell Signaling Technology, measuring the phosphorylation of Elk-1 at Ser-383. C, D) Effect of ERK inhibitor on Triphala induced apoptosis and activati

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