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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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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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Ancer, particularly in BRAF-mutated colorectal cancer. Keywords: Colorectal cancer, BRAF, miRNA, miR-193a-3p, Anti-EGFR therapyBackground RAF family kinases, including BRAF and RAF1, function downstream of RAS as critical regulators of the MEK-ERK MAP kinase signaling pathway [1]. This RAS-RAF-MEKERK cascade is a key pathway, which contributes to human oncogenesis controlling the cell cycle, proli
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Rectal cancer containing a BRAF p.V600E mutation possesses more malignant potential when compared with other genotypes of colorectal cancer, including the KRAS/BRAF-wild-type tumor and the KRAS-mutated tumor. In resectable colon cancer patients treated with adjuvant drug therapy, the BRAF mutation has been associated with poor survival compared to wild-type BRAF [7, 8]. A similar tendency has been
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Y using miRNA microarrayThe genome-wide miRNA expression levels of the 30 colorectal cancers from the screening set were analyzed by the SurePrint G3 Human miRNA Rel. 16.0 microarray (Agilent Technologies, Santa Clara, CA, USA), which covers 1222 human miRNAs, according to the manufacturer's protocol. The microarray data were extracted using the GeneSpring ver. 12.5 (Agilent Technologies). The raw
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Ning (scored by 0, 1+, 2+, and 3+ intensity levels) compared to pancreatic cancers with cytoplasmic CNKSR1 staining only (Mann Whitney U test; 2-tailed). d Cytoplasmic CNKSR1 expression levels (scored semiquantitatively as 0, 1+, 2+, and 3+) and nuclear p-ERK expression levels (scored as positive cells) (Pearson's correlation coefficient test; 2-tailed). e Kaplan-Meier survival analysis of pancr
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Is transcriptionaly regulated by ERK in response to Triphala treatment suggesting ERK as an upstream regulator of p53 in Capan-2 cells. We also observed that Triphala induce apoptosis by ERK activation in BxPC-3 cells, which has mutated p53. This is in part consistent with the observation that activated ERK lead to apoptosis after DNA damage in a p53 independent manner [49]. On the other hand, Tri
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Esults. Embryos at high stage (3 1/3 hpf), 50 epiboly (5 1/4 hpf), 70 epiboly (7 hpf) and tailbud stage (10 hpf) were deyolked, separated by SDS-gel electrophoresis and Coomassie stained (A) or blotted and immunodetected with antibodies against Tubulin (55 kD) and Moesin (78/80 kD apparent molecular weight) (B). Note that total protein amount was lower in deyolked samples, therefore more embryos