中电导钙激活钾离子通道(SK4)的研究进展(2)
5.结语
SK4作为一种钾离子通道，在机体的生长发育、增殖分化的过程中的作用，越来越清楚，但仍存在很多疑问，比如：SK4调控细胞增殖及分化的具体机制、肿瘤细胞表达的特异性、应用阻滞剂如何降低其他副作用等。目前将SK4阻滞剂应用于临床为时过早，因为SK4存在于正常细胞的膜表面，单纯应用阻滞剂可能干扰细胞的正常生理过程，但它已经为我们打开了一扇治疗肿瘤、自身免疫病等的一扇门，相信随着分子生物技术的不断进步，人们对各种疾病的发生机制的不断深入了解，对SK4的研究会进一步加深，必将成为研究热点。
参考文献
[1]Fanger, C.M., et al., Calmodulin mediates calcium-dependent activation of the intermediate conductance K-Ca channel, IKCa1. Journal of Biological Chemistry, 1999. 274(9): p. 5746-5754.
, http://www.100md.com
[2]Skaper, S.D., Ion channels on microglia: therapeutic targets for neuroprotection. CNS Neurol Disord Drug Targets, 2011. 10(1): p. 44-56.
[3]Shin, D.H., et al., Inhibition of Ca2+-release-activated Ca2+ channel (CRAC) and K+ channels by curcumin in Jurkat-T cells. J Pharmacol Sci, 2011. 115(2): p. 144-54.
[4]Kohler, R. and P. Ruth, Endothelial dysfunction and blood pressure alterations in K+-channel transgenic mice. Pflugers Arch, 2010. 459(6): p. 969-76.
, 百拇医药
[5]Dyrda, A., et al., Local membrane deformations activate Ca2+-dependent K+ and anionic currents in intact human red blood cells. Plos One, 2010. 5(2): p. e9447.
[6]Brakemeier, S., et al., Shear stress-induced up-regulation of the intermediate-conductance Ca2+-activated K+ channel in human endothelium. Cardiovascular Research, 2003. 60(3): p. 488-496.
[7]Pena, T.L., et al., Ras/MEK/ERK up-regulation of the fibroblast K-Ca channel FIK is a common mechanism for basic fibroblast growth factor and transforming growth factor-beta suppression of myogenesis. Journal of Biological Chemistry, 2000. 275(18): p. 13677-13682.
, http://www.100md.com
[8]Grgic, I., et al., Selective blockade of the intermediate-conductance Ca2+-activated K+ channel supresses proliferation of micro- and macrovascular endothelial cells. Faseb Journal, 2004. 18(4): p. A227-A227.
[9]Haren, N., et al., Intermediate conductance Ca2+ activated K+ channels are expressed and functional in breast adenocarcinomas: correlation with tumour grade and metastasis status. Histology and Histopathology, 2010. 25(10): p. 1247-1255.
, 百拇医药
[10]Ouadid-Ahidouch, H., et al., Functional and molecular identification of intermediate-conductance Ca2+-activated K+ channels in breast cancer cells: association with cell cycle progression. American Journal of Physiology-Cell Physiology, 2004. 287(1): p. C125-C134.
[11]Jager, H., et al., Blockage of intermediate-conductance Ca2+-activated K+ channels inhibit human pancreatic cancer cell growth in vitro. Molecular Pharmacology, 2004. 65(3): p. 630-638.
, 百拇医药
[12]Lallet-Daher, H., et al., Intermediate-conductance Ca2+-activated K+ channels (IKCa1) regulate human prostate cancer cell proliferation through a close control of calcium entry. Oncogene, 2009. 28(15): p. 1792-1806.
[13]Abdullaev, I.F., et al., Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation. Plos One, 2010. 5(8): p. -.
[14]Schmidt, J., et al., Migration-associated secretion of melanoma inhibitory activity at the cell rear is supported by KCa3.1 potassium channels. Cell Research, 2010. 20(11): p. 1224-1238., http://www.100md.com(张汝超)
SK4作为一种钾离子通道，在机体的生长发育、增殖分化的过程中的作用，越来越清楚，但仍存在很多疑问，比如：SK4调控细胞增殖及分化的具体机制、肿瘤细胞表达的特异性、应用阻滞剂如何降低其他副作用等。目前将SK4阻滞剂应用于临床为时过早，因为SK4存在于正常细胞的膜表面，单纯应用阻滞剂可能干扰细胞的正常生理过程，但它已经为我们打开了一扇治疗肿瘤、自身免疫病等的一扇门，相信随着分子生物技术的不断进步，人们对各种疾病的发生机制的不断深入了解，对SK4的研究会进一步加深，必将成为研究热点。
参考文献
[1]Fanger, C.M., et al., Calmodulin mediates calcium-dependent activation of the intermediate conductance K-Ca channel, IKCa1. Journal of Biological Chemistry, 1999. 274(9): p. 5746-5754.
, http://www.100md.com
[2]Skaper, S.D., Ion channels on microglia: therapeutic targets for neuroprotection. CNS Neurol Disord Drug Targets, 2011. 10(1): p. 44-56.
[3]Shin, D.H., et al., Inhibition of Ca2+-release-activated Ca2+ channel (CRAC) and K+ channels by curcumin in Jurkat-T cells. J Pharmacol Sci, 2011. 115(2): p. 144-54.
[4]Kohler, R. and P. Ruth, Endothelial dysfunction and blood pressure alterations in K+-channel transgenic mice. Pflugers Arch, 2010. 459(6): p. 969-76.
, 百拇医药
[5]Dyrda, A., et al., Local membrane deformations activate Ca2+-dependent K+ and anionic currents in intact human red blood cells. Plos One, 2010. 5(2): p. e9447.
[6]Brakemeier, S., et al., Shear stress-induced up-regulation of the intermediate-conductance Ca2+-activated K+ channel in human endothelium. Cardiovascular Research, 2003. 60(3): p. 488-496.
[7]Pena, T.L., et al., Ras/MEK/ERK up-regulation of the fibroblast K-Ca channel FIK is a common mechanism for basic fibroblast growth factor and transforming growth factor-beta suppression of myogenesis. Journal of Biological Chemistry, 2000. 275(18): p. 13677-13682.
, http://www.100md.com
[8]Grgic, I., et al., Selective blockade of the intermediate-conductance Ca2+-activated K+ channel supresses proliferation of micro- and macrovascular endothelial cells. Faseb Journal, 2004. 18(4): p. A227-A227.
[9]Haren, N., et al., Intermediate conductance Ca2+ activated K+ channels are expressed and functional in breast adenocarcinomas: correlation with tumour grade and metastasis status. Histology and Histopathology, 2010. 25(10): p. 1247-1255.
, 百拇医药
[10]Ouadid-Ahidouch, H., et al., Functional and molecular identification of intermediate-conductance Ca2+-activated K+ channels in breast cancer cells: association with cell cycle progression. American Journal of Physiology-Cell Physiology, 2004. 287(1): p. C125-C134.
[11]Jager, H., et al., Blockage of intermediate-conductance Ca2+-activated K+ channels inhibit human pancreatic cancer cell growth in vitro. Molecular Pharmacology, 2004. 65(3): p. 630-638.
, 百拇医药
[12]Lallet-Daher, H., et al., Intermediate-conductance Ca2+-activated K+ channels (IKCa1) regulate human prostate cancer cell proliferation through a close control of calcium entry. Oncogene, 2009. 28(15): p. 1792-1806.
[13]Abdullaev, I.F., et al., Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation. Plos One, 2010. 5(8): p. -.
[14]Schmidt, J., et al., Migration-associated secretion of melanoma inhibitory activity at the cell rear is supported by KCa3.1 potassium channels. Cell Research, 2010. 20(11): p. 1224-1238., http://www.100md.com(张汝超)