• Asian-Australasian Journal of Animal Sciences
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• v.5 no.3
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• pp.455-459
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• 1992

Five type of formulated diet from agricultural by-products (ABP) were fed to four breedtype of cattle in feedlot. The ABP used are palm kernel cake (PKC), palm press fibre (PPF), palm oil mill effluent (POME), cocoa pod (COP), coffee pulp (COF) and pineapple waste (PAP). The formulated diets are PS (52% PKC, 15% PPF and 30% POME), PF (57% PKC, 20% PPF and 20% POME), PA (2% PKC and 55% PAP), CO (42% PKC and 55% COP) and CF (67% PKC and 30% COF) with 1% urea, 1% NaCl and 1% vitamins premix. The cattle breedtypes are Kedah-Kelantan (KK), Brahman-KK (BK), Hereford-KK (HK) and Sahiwal-Friesian (SF). The result showed that breedtype significantly affect all the carcass characteristic except dressing percentage. Each breedtype has it's specific carcass characteristics. HK cattle gave high marbling, BK has high % of carcass bone, KK has high % of carcass meat and low % of carcass fat (lean meat type) and SF has high % of carcass fat. Diet-type significantly affect the deposition of fat in the carcass. High moisture diets (PA and CO) produced significantly higher % carcass bone, the lowest % carcass fat and the highest % carcass meat (65.3%). PF, CF, PA and CO diets produced 63.4%, 59.9%, 55.3% and 54.1% carcass meat respectively.

• YAKHAK HOEJI
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• v.43 no.2
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• pp.263-273
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• 1999

When glutamate was infected intrathecally, the result is similar to those produced by TPA injected. The involvement of protein kinase C (PKC) in the nociceptive responses in rat dorsal horn neurons of lumbar spinal cord was studied. In test with formalin, a PKC inhibitor (chelerythrine) inhibited dose-dependently the formalin-induced behavior response. Neomycin also inhibited it significantly. But, a PKC activator (12-O-tetradecanoylphorbol-13-ester, TPA) showed reverse effect. When gluatamate was injected intrathecally, we observed the result is smilar to those produced by TPA injection. On the other hand, intrathecal injection of glutamate induced thermal and mechanical hyperalgesia. In Tail-flick test, we examined the involvement of PKC on the glutamate-indeced thermal hyperalgesia. Chelerythrine showed an inhibitory effect and TPA enhanced thermal response. Glutamate decreased the mechanical threshold significantly. A pretreatment of chelerythrine and neomycin inhibited glutamate-induced mechanical hyperalgesia, but the effect of neomycin was not significant. TPA had little effect on the mechanical nociceptive response. These results suggest that the PKC activation through metabotropic receptor at postsynaptic region of spinal cord dorsal horn neurons may influence on the persistent nociception produced by chemical stimulation with formalin, thermal and mechanical hyperalgesia induced by glutamate.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.6
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• pp.497-506
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• 2000

In this work, GLUTs phosphorylations by a downstream effector of PI3-kinase, $PKC-{\zeta},$ were studied, and GLUT4 phosphorylation was compared with GLUT2 phosphorylation in relation to the translocation mechanism. Prior to phosphorylation experiment, $PKC-{\zeta}$ kinase activity was determined as $20.76{\pm}4.09$ pmoles Pi/min/25 ng enzymes. GLUT4 was phosphorylated by $PKC-{\zeta}$ and the phosphorylation was increased on the vesicles immunoadsorpted from LDM and on GLUT4 immunoprecipitated from GLUT4- contianing vesicles of adipocytes treated with insulin. However, GLUT2 in hepatocytes was neither phosphorylated by $PKC-{\zeta}$ nor changed in response to insulin treatment. It was confirmed by measuring the subcellular distribution of GLUT2 based on GLUT2 immunoblot density among the four membrane fractions before and after insulin treatment. Total GLUT2 distributions at PM, LYSO, HDM and LDM were $37.7{\pm}12.0%,\;42.4{\pm}12.1%,\;19.2{\pm}5.0%\;and\;0.7{\pm}1.2%$ in the absence of insulin. Total GLUT2 distribution in the presence of insulin was almost same as that in the absence of insulin. Present data with previous findings suggest that GLUT4 translocation may be attributed to GLUT4 phosphorylation by $PKC-{\zeta}$ but GLUT2 does not translocate because GLUT2 is not phosphorylated by the kinase. Therefore, GLUT phosphorylation may be required in GLUT translocation mechanism.

• YAKHAK HOEJI
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• v.39 no.6
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• pp.661-665
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• 1995

Ginsenoside-Rg$_{1}$(G-Rg$_{1}$) has been shown to stimulate DNA synthetic activity in SK-HEP-1 cells. This study was therefore designed to determine in SK-HEP-1 cells whether the stimulatory effect of G-Rg$_{1}$ may be mediated by protein kinase C (PKC) which is known to play a key role in the signal transduction pathway leading to the cell proliferation. Using the tn situ PKC assay method, the PKC enzyme activity was determined in SK-HEP-1 cell cultures in response to G-Rg$_{1}$ at 3*10$^{-5}$ M or phorbol 12-myristate 13-acetate(PMA) at 10$^{-6}$ M which in the enzyme activity by 1.5- and 7-fold, respectively. Furthermore, G-Rg$_{1}$, was also able to synergistically increase the enzyme activity by 11-fold m the cell cultures in the presence of PMA. These stimulatory effects of G-Rg$_{1}$ or PMA on the DNA synthetic activity and the PKC activity were ablished by a specific PKC inhibitor, GF109203X. These results suggest that the stimulatory effect of G-Rg$_{1}$ on the DNA synthetic activity may be partly due to stimulation of PKC-mediated signal transduction pathway leading to the proliferation of SK-HEP-1 cells.

• 대한생식의학회:학술대회논문집
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• 2006.06a
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• pp.6-11
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• 2006

Our previous study demonstrates a rapid activation of atypical PKC${\zeta}$ by the ovulatory dose of LH/hCG. The present study was therefore designed to identify PKC${\zeta}$ regulated-genes in rat ovarian preovulatory granulosa cells. Preovulatory granulosa cells cultured in the presence of myristoylated PKC${\zeta}$ pseudosubstrate peptide were subjected to identify differentially expressed genes by using anneling control primer RT-PCR. As a result, among sixteen genes identified, six genes (testin, glypican-4, retrovirus SC1, connective growth factor, aminolevulinic acid synthase1 and serum- inducible kinase) were rapidly stimulated by hCG. Northern blot analysis demonstrated that all these genes were rapidly stimulated by hCG and declined thereafter. In situ hybridization analysis revealed the expression of these genes in granulosa cells of preovulatory follicles. The present study demonstrates time- and cell-specific expression of PKC${\zeta}$-regulated genes, and may imply that these genes play a specific role(s) during LH-induced ovulation.

• Journal of Microbiology and Biotechnology
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• v.16 no.4
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• pp.550-555
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• 2006

CVB3 is a virulent human pathogen that induces myocarditis and ultimately dilated cardiomyopathy. Although several apoptotic factors are involved in the cell death induced by CVB3, the upstream signal transduction factors of CVB3-induced apoptosis are still unclear. We explored and characterized the role of PKC $\delta$ in CVB3-infected cells. PKC $\delta$ was cleaved after CVB3 infection and was activated at 6 h postinfection. PKC $\delta$ was also translocated into the nucleus via mitochondria after CVB3 infection, and overexpression of wild-type PKC $\delta$ reduced the apoptotic cell death caused by CVB3. These results indicate that PKC $\delta$ has an antiapoptotic role in CVB3 infection.

• Journal of Life Science
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• v.13 no.5
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• pp.551-558
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• 2003

Hepatitis C Virus (HCV) is associated with a severe liver disease and increased frequency in the development of hepatocellular carcinoma. Overexpression of HCV core protein is known to transform fibroblast cells. Phospholipase D (PLD) activity is commonly elevated in response to mitogenic signals, and PLD has been also reported to be overexpressed and hyperactivated in some human cancer. The aim of this study was to understand how PLD can be regulated in HCV core protein-transformed NIH3T3 mouse fibroblast cells. We observed that in unstimulated state, basal PLD activity was higher in NIH3T3 cells overexpressing HCV core protein than in vector-transfected cells. Although expression of PLD and protein kinase C (PKC) in core protein-transformed cells was similar with that of control cells, phorbol 12-myristate 13-acetate (PMA), which is known to activate PKC, stimulated significantly PLD activity in core protein-transformed cells, compared with that of the control cells. PLD activity assay using PKC isozyme-specific inhibitor, and PKC translocation experiment showed that PKC-$\delta$ was mainly involved in the PMA-induced PLD activation in the core-transformed cells. Taken together, these results suggest that PLD might be implicated in core protein-induced transformation.

• YAKHAK HOEJI
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• v.41 no.5
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• pp.629-637
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• 1997

Tumor necrosis factor-${alpha}$ (TNF) induced a cytotoxic response in ME-180 cervical carcinoma cells in vitro. This cytotoxic response was accompanied by a temporal series of mitogenic stimuli : increased c-fos, c-jun and jun-B expression. Depletion of protein kinase C (PKC) by exposure of ME-180 cells to 100ng/ml phorbol myristate acetate (PMA) for 24hours almost completely abolished TNF-mediated increase in these signals, indicating that a PKC-dependent pathway is involved in TNF-mediated increases in the expression of c-fos, c-jun and jun-B. Characteristics of TNF receptors after exposure to 100ng/ml PMA or 24hours were not altered, suggesting that diminished induction of these oncogenes by TNF after PMA treatment is not due to any changes at the receptor level. To examine whether a PKC-dependent pathway is involved in TNF-mediated cytotoxicity in ME-180 cells, cytotoxicity was measured after depletion of PKC. No apparent changes in cytototoxicity after PKC depletion suggest that a PKC-dependent pathway is not involved in TNF-mediated cytotoxicity. Furthermore, results from cytotoxicity tests after exposure to staurosporine (PKC inhibitor) did not show any changes in the TNF-mediated cytotoxicity, confirming that a PKC-dependent pathway is not involved in this process. These data indicate that 1) TNF induces expression of c-fos, c-jun and jun-B oncogenes via a PKC-dependent pathway and 2) PKC-dependent expression of these three oncogenes by TNF may not be involved in TNF-mediated cytotoxicity in ME-180 cells.

• BMB Reports
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• v.45 no.11
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• pp.659-664
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• 2012

Extracellular superoxide dismutase (EC-SOD) overexpression modulates cellular responses such as tumor cell suppression and is induced by $IFN{\gamma}$. Therefore, we examined the role of EC-SOD in $IFN{\gamma}$-mediated tumor cell suppression. We observed that the dominant-negative protein kinase C delta ($PKC{\delta}$) suppresses $IFN{\gamma}$-induced EC-SOD expression in both keratinocytes and melanoma cells. Our results also showed that $PKC{\delta}$-induced EC-SOD expression was reduced by pretreatment with a PKC-specific inhibitor or a siRNA against $PKC{\delta}$. $PKC{\delta}$-induced EC-SOD expression suppressed cell proliferations by the up-regulation of p21 and Rb, and the downregulation of cyclin A and D. Finally, we demonstrated that increased expression of EC-SOD drastically suppressed lung melanoma proliferation in an EC-SOD transgenic mouse via p21 expression. In summary, our findings suggest that $IFN{\gamma}$-induced EC-SOD expression occurs via activation of $PKC{\delta}$. Therefore, the upregulation of EC-SOD may be effective for prevention of various cancers, including melanoma, via cell cycle arrest.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6017-6022
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• 2012

Background: Resveratrol has been reported to have potential chemopreventive and apoptosis-inducing properties in a variety of tumor cell lines. Objective: In this study, to investigate the effects of resveratrol on protein kinase C (PKC) activity and apoptosis in human colon carcinoma cells, we used HT-29 cells and examined the $PKC{\alpha}$ and ERK1/2 signaling pathways. Methods: To test the effects of resveratrol on the growth of HT-29 cells, the cells were exposed to varying concentrations and assessed with the the MTT cell-viability assay. Fluorescence-activated cell sorter (FACS) analysis was applieded to determine the effects of resveratrol on cell apoptosis. Western blotting was performed to determine the protein levels of $PKC{\alpha}$ and ERK1/2. In inhibition experiments, HT-29 cells were treated with G$\ddot{o}$6976 or PD98059 for 30 min, followed by exposure to $200{\mu}M$ resveratrol for 72 h. Results: Resveratrol had a significant inhibitory effect on HT-29 cell growth. FACS revealed that resveratrol induced apoptosis. Western blotting showed that e phosphorylation of $PKC{\alpha}$ and ERK1/2 was significantly increased in response to resveratrol treatment. Pre-treatment with $PKC{\alpha}$ and ERK1/2 inhibitors (G$\ddot{o}$6976 and PD98059) promoted apoptosis. Conclusion: Resveratrol has significant anti-proliferative effects on the colon cancer cell line HT-29. The PKC-ERK1/2 signaling pathway can partially mediate resveratrol-induced apoptosis of HT-29 cells.