• Animal cells and systems
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• v.12 no.1
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• pp.35-39
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• 2008

Menadione induced cell death in cultured C2 myoblasts. By screening synthetic peptide libraries composed of random sequence of hexapeptides, we identified the hexa-peptides pool of(Ala/Ile)-(Ile/Met)-Val-Ile-Asp-(Met/Ser)-$NH_2$ that protected the myoblasts against menadioneinduced cell death. Pre-incubation with the hexapeptide pool reduced the number of cells detached from culture dish substrate and increased the ratio of relative viability against menadione. In addition, the peptides strongly increased the expression of Bcl-2, an anti-apoptotic protein. These results suggest that the hexapeptides might enhance the resistance to cell death against menadione by increasing the expression of Bcl-2.

• BMB Reports
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• v.40 no.4
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• pp.547-553
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• 2007

Many motifs along the 1.2 kb myostatin promoter (MSTNpro) in sheep have been found by the MatInspecter program in our recent study. To further verify the role of the motifs and better understand the transcriptional regulation mechanism of the myostatin gene in sheep, the reporter gene EGFP (enhanced green fluorescent protein) was selected and the wild-type (W) vector MSTNPro$^W$-EGFP or motif-mutational (M) vector MSTNPro$^M$-EGFP were constructed. The transcriptional regulation activities were analyzed by detecting the fluorescence strength of EGFP in C2C12 myoblasts transfected with the vectors. The results showed that E-box (E) 3, E4, E5 and E7, particularly E3, E5 and E7, had important effects on the activity of the 1.2 kb sheep myostatin promoter. In addition, we also detected several other important motifs such as MTBF (muscle-specific Mt binding factor), MEF2 (myocyte enhancer factor 2), GRE (glucocorticoid response elements) and PRE (progesterone response elements) along the sheep myostatin promoter by the mutational analysis.

• Molecules and Cells
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• v.28 no.2
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• pp.119-124
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• 2009

Anti cancer agent 5-FU (Fluoro Uracil) is a prodrug that can be metabolized and then activated to interfere with RNA and DNA homeostasis. However, the majority of administered 5-FU is known to be catabolized in vivo in the liver where Dihydropyrimidine dehydrogenase (DPD) is abundantly expressed to degrade 5-FU. The biological factors that correlate with the response to 5-FU-based chemotherapy have been proposed to include uridine phosphorylase (UPP), thymidine phosphorylase (TPP), p53 and microsatellite instability. Among these, the expression of UPP is known to be controlled by cytokines such as $TNF-{\alpha}$, IL1 and $IFN-{\gamma}$. Our preliminary study using a DNA microarray technique showed that basic fibroblast growth factor (bFGF) markedly induced the expression of UPP1 at the transcription level. In the present study, we investigated whether bFGF could modulate the expression of UPP1 in osteo-lineage cells and examined the sensitivity of these cells to 5-FU mediated apoptosis.