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Background : Apoptoss plays a major role in cellular proliferation and differentiation in tumor cells. Bcl-2, proto-oncogene, is known to inhibit apoptotic cell death of tumor cells. The high expression of bcl-2 in human melanoma cells over transforrned keratinocytes has been reported. The Loton group indicated that the growth of human melanoma cells exposed to ret.inoids was inhibit ed and their cellular melanin content incrensed over that of the untreat,ed ce1Ls. The Veis group reported that bcl-2 defieient mice showed hypopigmented hair. Which suggests that bcl-2 may in volve melanogenesis. The Above mentioned findings may suggest that. bcl-2 and retinoids may play a role in melanoms biology. Objective : We under ook this study to elucidate a possible relationship between retinoids and bcl-2 expvessions in human melanoma cell lines. Methods : We analysed bcl-2 expressions from SK 28 cells(melanoma cell lines) after pretreat ment with retinoids using flow cytometry and imtnunoblotting. Results : 1. In the results of the preliminary studies, we found that cultured human keratinocytes, fibro blasts and melanocytes n the resting state showed expressions of bcl-2. The latter showed a four fold expression of bcl-2. 2. Expression of bcl-2 was detected in SK 28, a human melanoma cell line, in the resting state. 3. After incubation with isotretinoin or etretinate treatment at 37℃, for 48 hours, this treated group showed a more ir creased expression of bcl-2 than the control group. Conclusion : Our data may explain that the mechanism of ret.inoids indur,ing inhibition of mela noma cell growth may be partly due to upregulation of bcl-2 expression. The high base-line ex pression of bcl-2 in melanoma cells may tell us why these pigment cells can survive against oxi dative products generated during melanogenesis. (Korean J Dermatol 1997;35(6): 1088-1094)
Background : Nerve growth factor(NGF), brain derived neurotrophic factor(BDNF), neurotropin 3(NT-3) and neurotropir-4/5 are neurotrophic factors necessary for the development and maintenance of specific neurors. The tyrosine protein kinase(trk) receptors exhibit specificity for differ ent neurotrophins. NGF is the cognate ligand for the trk A receptor, BDNF binds to trk B receptor and NT-3 binds to irk A, trk B and trk C receptors, Since melanoma cells are devived from neural ectoderm, growth factors which affect. neuronal tissue may have a role in melanoma biology. Objective : The purpose of this study is to demonstrate the presence of trk receptors in rnelanoma cells and observe th effect of K-252a on these melanoma cells growth and differentiation. Methods : After K-252a over a range of 0-200nM was added into their cell lines, we exam ined cell viability of SK 28 and SK 30 cells. We performed this to examine the expression of the trk by flow cytometry and immunoblotting. Results : 1. The incubation of SK 28 cells and SK 30 cells with K-252a resulted in a dose dependent inhibition of cell proliferation. 2. In the flowcytometry, SK 28 cells and SK 30 cells showed a high expression of trk A and trk B, not trk C. 3. Using immunoblottiiig, trk in SK 28 cells and SK 30 cells was not expressed. Cpnclusions : These results indicate that. the identification of tyrosine protein kinase reeeptors and their inhibitor which affect differentiation and growth of a melanoma may provide an additional therapeutic option for treatment of melanoma. (Korean J Dermatol 1997;35(6): 1151-1158)