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E inflammatory response and tissue remodeling in tendon healing and also it revealed that; although the severe inflammatory reaction has been developed in response to the collagen implant, but this immune response was due to the remodeling effect of the collagen implant, not its rejection. It has been postulated that inflammation has a major role in tendon healing and if immune response does not p
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Rtner and regulator of KSR1 and the MAPK pathway.One of the main functions of the scaffold protein CNKSR1 is the regulation of other cancer-related signaling pathways integrating output to different intracellular signaling cascades upon cellular stimulation by extracellular cues [11, 12, 17?0]. In breast and cervical cancer cell models, a pro-oncogenic potential has been demonstrated through ERK-i
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Nonevent. All cases with missing information were included in proportional hazard ratio calculations after performing a sensitivity analysis which showed negligible effects of excluding missing data.ImmunohistochemistryImmunohistochemical staining for CNKSR1 (mouse monoclonal antibody CNKSR1 (clone 46), Santa Cruz Biotechnology, TX, USA, #sc-135,870; dilution 1:200) was performed on a Leica BOND-M
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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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Gher nuclear p-ERK expression levels suggests that cellular localization, rather than absolute CNKSR1 expression levels, might be one of the mechanisms of CNKRS1-mediated control of MAPK pathway activity. In this regard, Fisher and colleagues showed in an elegant study with a set of different phosphomimetic mutant constructs that phosphorylation of Tyr 519 recruits CNKSR1 to the nucleus and phosph
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Ed by the current ones, highlight a major role for galectin-1 in GBM invasiveness. The characteristic malignant phenotype of glioblastoma extends beyond aggressive invasion. This tumor develops resistance to chemo- and radio-therapy, it promotes neoangiogenesis, and it seems to benefit from immune privilege. Interestingly, galectin-1 may play a role in promoting each of these phenotypes. While gal
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Ed clones were compared to their GFP control counterparts. (Westerns controlled for loading by -actin IB). (D) Over-expression of galectin-1 promotes invasion. All cell counts were normalized to the parental cell line data. (Westerns controlled for loading by -actin IB).our identification of galectin-1 as a mediator of glioma invasion has been corroborated previously as detailed below. While previ
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Ained parallel sections with a pooled IgG control. This protein-level confirmation of our microarray data gave us the impetus to pursue functional in vitro and in vivo assays with galectin-1 over-expressing GBM cells.Extracellular matrix attachmentResultsIdentification of galectin-1 as a potential mediator of glioma invasionThe quantity of RNA obtained from various xenograft tumors was highly vari

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