2450MHz电磁波对细胞转化和热休克蛋白的影响及其机理的研究
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摘要
电子技术的迅速发展，以及微波、射频等电子产品日趋广泛的应用，使职业人员和公众受到各种频段电磁波(electromagnetic fields，EMF)照射剂量日益增加。环境电磁场对健康的影响越来越受到人们的关注，特别是环境电磁场与肿瘤发生之间的关系更是关注的焦点。虽然EMF与癌症相关的研究已有许多，但至今尚未获得一致的结论。绝大多数肿瘤的发生表现为多阶段多步骤的复杂过程。这个过程大致可以分为三个阶段：激发阶段，促进阶段和增殖阶段。若高频电磁场(high frequency electromagnetic field，HFEMF)与癌症的发生相关则HFEMF在癌症发生过程中至少参与一个发展阶段(激发和／或促进阶段)。French等近来提出HFEMF的能量可能扮演着应激诱导物的作用，它引起蛋白构型的改变，这种改变继而引起暴露细胞热休克蛋白(heat shock proteins，HSPs)的改变，从而干扰正常细胞的调节，最终增加癌症发生的危险性。但精确的机制还不清楚。
本研究首先检测2450 MHz HFEMF对20-甲基胆蒽(20-Methylcholanthrene，MC)诱导的C3H10T1／2细胞(8克隆)细胞转化的影响；其次，以HSP70和HSP27作为应激标志研究2450 MHz HFEMFs是否
In recent years, there has been a rapid increase in the use of devices and systems employing electromagnetic energy. People are concerned about the association between environmental electromagnetic fields (EMF) and cancer. The possible mechanisms of the induced effects remain unclear, although a number of theoretical models have been proposed. Tumor formation is considered to be a multi-step process including initiation (mutation), promotion and progression. Whatsoever, if EMF could contribute to the carcinogenic progress, it would affect one or more steps (initiation and/or promotion) in the neoplastic transformation process. A recent publication by French et al. suggests that RF field energy primarily acts as a stress inducer, causing changes in protein conformation, which in turn cause a synthesis of heat shock proteins (HSPs) in exposed cells and tissues. These changes may disturb the normal regulation of the cells and ultimately lead to an increased risk of cancer. However, the exact mechanisms remain unknown.
First, this study was to investigate the possible effects of 2450 MHz continuous wave (CW) high frequency electromagnetic fields (HFEMFs) at different specific absorption rates (SARs) on 20-Methylcholanthrene (MC) induced transformation in C3H10T1/2 cells; second, we investigated whether
本研究首先检测2450 MHz HFEMF对20-甲基胆蒽(20-Methylcholanthrene，MC)诱导的C3H10T1／2细胞(8克隆)细胞转化的影响；其次，以HSP70和HSP27作为应激标志研究2450 MHz HFEMFs是否
In recent years, there has been a rapid increase in the use of devices and systems employing electromagnetic energy. People are concerned about the association between environmental electromagnetic fields (EMF) and cancer. The possible mechanisms of the induced effects remain unclear, although a number of theoretical models have been proposed. Tumor formation is considered to be a multi-step process including initiation (mutation), promotion and progression. Whatsoever, if EMF could contribute to the carcinogenic progress, it would affect one or more steps (initiation and/or promotion) in the neoplastic transformation process. A recent publication by French et al. suggests that RF field energy primarily acts as a stress inducer, causing changes in protein conformation, which in turn cause a synthesis of heat shock proteins (HSPs) in exposed cells and tissues. These changes may disturb the normal regulation of the cells and ultimately lead to an increased risk of cancer. However, the exact mechanisms remain unknown.
First, this study was to investigate the possible effects of 2450 MHz continuous wave (CW) high frequency electromagnetic fields (HFEMFs) at different specific absorption rates (SARs) on 20-Methylcholanthrene (MC) induced transformation in C3H10T1/2 cells; second, we investigated whether
引文
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2. P. R.Liburdy. Calcium signaling in lymphocytes and ELF fields: evidence for an electric field metric and a site of interaction involving calcium ion channels. FEBS Lett 1992, 301: 53-59.
3. P. S. Barnes. Effect of electromagnetic field on the rate of chemical reactions. Biophysics1996, 41: 801-807.
4. S. Prausnitz, C. Susskind. Effects of chronic microwave irradiation on mice. IRE Trans. Biomed. Electron. 1962, 9: 104-108.
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6. A.Szudzinski, A. Pietraszek, M. Janiak, M. Kalczak, S. Szmigielski. Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave radiation. Arch. Dermatol.Res.1982, 274: 303-312.
7. R.Santini, M.Honsi, P. Deschaux, H. Pacheco. B16 melanoma development in black mice exposed to low-level microwave radiation. Bioelectromagnetics1988, 9: 105-107.
8. H. C. Pitot, Y. P. Dragan, Facts and theories concerning the mechanisms of carcinogenesis. FASEB J 1991, 5: 2280-2286.
9. R. Y. Wu, H. Chiang, B. J. Shao, N.G. Li, Y. D. Fu. Effects of 2.45 GHz microwave radiation and phorbol ester 12-0-tetradecanoylphorbol-13-acetate or dimethylhydrazine-induced colon cancer in mice. Bioelectromagnetics 1994, 15:531-538.
10. C. A. Reznikoff, J. S.Bertram, D.W. Brankow, C. Heidelberger, Quantitative and qualitative studies of chemical transformation of cloned C3H10T1/2 mouse embryo cellssensitive to postconfluence inhibition of cell division. Cancer Res. 1973, 33: 3239-3249.
11. M.Terzaghi, J. B. Little, X-radiation-induced transformation in a C3H mouse embryo-derived cell line. 1976, Cancer Res. 36: 1367-1374.
12. A. Han, M. Elkind, Transformation of mouse C3H/10T1/2 cells by single and fractionated doses of X-rays and fission-spectrum neutrons. Cancer Res: 1979, 39, 123-130.
13. J.Miyakoshi, M.Yoshida, H.Yaguchi, G. R. Ding, Exposure to extremely low frequency magnetic fields suppresses X-Ray-induced transformation in mouse C3HIOT1/2 cells. Biochemical and Biophysical Research Communications 2000, 271:323-327.
14. G. Lazzi, O. P.Gandhi. "On the Optimal Design of the PML Absorbing Boundary Condition for the FDTD Code," 1EEE Transactions on Antennas and Propagation, 1997, Vol.5, pp.914-916.
15. C. A. Reznikoff, D.W. Brankow, C. Heidelberger. Establishment and characterization of a cloned line of C3H mouse embryo cells sensitive to postconfluence inhibition of division. Cancer Res. 1973, 33: 3231-3238.
16. E.J. Hall. Oncogenic transformation systems involving mammalian cells in vitro to determine the relative risks of different treatment modalities. Strahlentherapie 1984, 160:725-731.
17. E. P. Clark, G M.Hahn, J.B.Little. Hyperthermic modulation of X-ray-induced oncogenic transformation in C3H 10T1/2 cells. Radiat. Res. 1981, 88:619-622
18. S.Szmigielski, A. Szudzinski, A.Pietraszek, M.Bielec, M.Janiak, J. K. Wrembel. Accelerated development of spontaneous and benzopyrene-induced skin cancer in mice exposed to 2450-MHz microwave radiation. Bioelectromagnetics 1982, 3:179-191.
19. T. K.Hei, R. S.Krauss, S. X. Liu, E. J. Hall, I. B. Weinstein. Effects of increased expression of protein kinase C on radiation-induced cell transformation. Carcinogenesis1994, 15: 365-370.
20. L. L.Kunz, R. B.Johnson, D.Thomson, J.Crowley, C. K.Chou, A. W. Guy. Evaluation of longevity, cause of death, and histopatho-logical findings. Vol. 8 of Effects of Long-Term Low-Level Radiation Exposure on Rats, Report 1985, USAFSAM TR-85-11, USAF School of Aerospace Medicine, Brooks Air Force Base, T. X.
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25. U.Kikkawa, Y. Takai, Y.Tanaka, R. Miyake Y. Nishizuka. Protein kinase c as a possible receptor protein of tumor-promoting phorbol esters. J. Biol. Chem. 1983, 258: 11442-11445.
26. W. R.Adey. Biological effects of radio frequency electromagnetic radiation. In Interaction of Electromagnetic Waves with biological systems (J. C. Lin, Ed), 1988, pp.1-33. Plenum, New York.
27. R. A. Luben, C. D. Cain, Chen, M.C Rosen, W. R. Adey. Effects of electromagnetic stimuli on bone and bone cells in vitro: Inhibition of responses to parathyroid hormone by low-energy, low-frequency fields. Proc. Natl. Acad. Sci. USA 1982, 79: 4180-4183.
28. W.D. Winters. Biological functions of immunologically reactive human and canine cellsinfluenced by in vitro exposure to 60-Hz electric and magnetic and magnetic fields. In New York State Power Line Project. Final Report, Contract 218207. 1986, Wadsworth Center for Laboratories and Research, Albany, NY.
29. D. B. Lyle, R.D. Ayotte, A. R. Sheppard, W. R. Adey. Suppression of T-lymphocyte cytotoxicity following exposure to 60Hz sinusoidal electric fields. Bioelectromagnetics 1998, 9: 303-313.
30. C.V. Byus, K. Kartun, S. Pieper, W. R. Adey. Increased ornithine decarboxylase activity in cultured cells exposed to low energy modulated microwave fields and phorbol ester tumor promoters. Cancer Res. 1998, 48: 4222-4226.
31. W. R. Adey. Cell membranes: The electromagnetic environment and cancer promotion. Neurochem Res. 1988, 13: 671-677.
32. W. R. Adey. Electromagnetic fields, cell membrane amplification and cancer promotion. In Wilson B. W, Stevens R. G, Anderson L. E (eds): "Extremely Low Frequency Electromagnetic Fields; The Question of Cancer." Columbus, OH: Battelle Press, 1989, pp 221-249.
33. W. R. Adey. Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in cancer promotion. Environ Health Prospect 1990, 86: 297-305.
34. IEEE Standard for safety levels with Respect to human exposure to radio frequency electromagnetic fields, 3kHz to 300GHz. Standard C95.1, IEEE, 1999, New York.
35. IEEE. recommended practice for determining the peak spatial-average specific absorption rate (SAR) in the human body due to wireless communications devices: computational techniques. Standard P1529-200x, IEEE, draft: SCC-34, SC-2, WG-2-computational dosimetry. 2003, New York.
36. M. A. Stuchly Biological concerns in wireless communications. Crit Rev Biomed Eng 1998, 26:117-151.
37. P. W. French, R. Penny, J.A. Laurence, D.R. McKenzie. Mobile phones, heat shock proteins and cancer. Differentiation 2001.67:93-97.
38. I.J. Benjamin, D.R. McMillan. Stress (heat shock) proteins molecular chaperones in cardiovascular biology and disease. Circ Res 1998. 83: 117-132.
39. R.J.Ellis, S.M.Van der Vies Molecular chaperones. Annu Rev Biochem 1991, 60: 321-347.
40. K. Fritze, C. Wiessner, N. Kuster, C. Sommer, E Gass, D.M. Hermann, M. Kiessling, K.A. Hossmann. Effect of global system for mobile communication microwave exposure on the genomic response of the rat brain. Neuroscience 1997.81:627-639.
41. D. De Pomerai, D. Daniells, H. David, J. Allan, I. Duce, M. Mutwakil, D. Thomas, P. Sewell, J. Tattersall, D. Jones, P.Candido. Non-thermal heat-shock response to microwaves. Nature 2000. 405: 417-418.
42. D. De Pomerai, B. Smith, Dawe A, North K, Smith T, Archer DB, Duce IR, Jones D, Candido EP. Microwave radiation can alter protein conformation without bulk heating. FEBS Lett 2003. 543:93-97.
43. D.Leszczynski, S. (?) J. Reivinen, R. Kuokka Non-thermal activation in human endothelial cells: Molecular mechanism for cancer-and blood-brain barrier-related effects. Differentiation 2002.70:120-129.
44. S.E Cleary, G. Cao, L.M. Liu, EM. Egle, K.R. Shelton. Stress proteins are not induced in mammalian cells exposed to radiofrequency or microwave radiation. Bioelectromagnetics 1997. 18: 499-505.
45. E Tian, T. Nakahara, K. Wake, M. Taki, J. Miyakoshi. Exposure to 2.45 GHz electromagnetic fields induces HSP70 at a high SAR of more than 20 W/kg but not at 5 W/kg in human glioma MO54 cells. Int J Radiat Biol 2002, 78: 433-440.
46. J. Miyakoshi, K. Takemasa, Y. Takashima, G. R. Ding, H. Hirose, S. Koyama. Effects ofexposure to a 1950 MHz Radio-frequency field on expression of HSP70 and HSP27 in human glioma cells. Bioelectromagnetics 2005. 26:251-257.
47. A.P.Arrigo, J. Landry. Expression and function of the low-molecular weight heat shock proteins. In RI Morimoto, TA Tissieres, C Georgopoulous(eds): "biology of Heat Shock Proteins and Molecular Chaperones." Cold Spring Harbor, HY: Cold Spring Harbor Laboratory Press, 1994. pp 335-373.
48. P. Chretien, J.Landry. Enhanced constitutive expression of the 27-kDa heat shock proteins in heat-resistant variants from Chinese hamster cells. J Cell Physiol 1988.137: 157-166.
49. J. Landry, P, Chretien, H. Lambert, E. Hickey, L.A.Weber. Heat shock resistance conferred by expression of the human HSP27 gene in rodent cells. J Cell Biol 1989.109:7-15.
50. J.N.Lavoie, H. Lambert, E. Hickey, L.A. Weber, J. Landry. Modulation of cellular thermoresistance and actin filament stability accompanies phosphorylation-induced changes in the oligomeric structure of heat shock protein 27. Mol Cell Biol 1995.15:505-516.
51. J. Huot, F. Houle, D.R. Spitz, J. Landry. HSP27 phosphorylation-mediated resistance against actin fragmentation and cell death induced by oxidative stress. Cancer Res 1996. 56:273-279.
52. K. Ono, J. Han. The p38 signal transudation pathway: activation and function. Cell Signalling 2000. 12:1-13.
53. E. Butt, D. Immler, H.E. Meyer, A. Kotlyarov, K. Laass, M. Gaestel. Heat shock protein 27 is a substrate of cGMP-dependent protein kinase in intact human platelets: phosphorylation-induced actin polymerization caused by HSP27 mutants. J Biol Chem 2001.276:7108-7113.
54. E.T. Maizels, C.A. Peters, M. J.Kline, R, E, Cutler, M. Shanmugam, M. Hunzicker-Dunn.Heat-shock protein-25/27 phosphorylation by the delta isoform of protein kinase C. Biochem J 2003. 332:703-712.
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2. P. R.Liburdy. Calcium signaling in lymphocytes and ELF fields: evidence for an electric field metric and a site of interaction involving calcium ion channels. FEBS Lett 1992, 301: 53-59.
3. P. S. Barnes. Effect of electromagnetic field on the rate of chemical reactions. Biophysics1996, 41: 801-807.
4. S. Prausnitz, C. Susskind. Effects of chronic microwave irradiation on mice. IRE Trans. Biomed. Electron. 1962, 9: 104-108.
5. J. F.Spalding, R.W. Freyman, L. M. Holland. Effects of 800 MHz electromagnetic radiation on body weight activity, hematopoiesis and life span in mice. Health Phys. 1971, 20:421-424.
6. A.Szudzinski, A. Pietraszek, M. Janiak, M. Kalczak, S. Szmigielski. Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave radiation. Arch. Dermatol.Res.1982, 274: 303-312.
7. R.Santini, M.Honsi, P. Deschaux, H. Pacheco. B16 melanoma development in black mice exposed to low-level microwave radiation. Bioelectromagnetics1988, 9: 105-107.
8. H. C. Pitot, Y. P. Dragan, Facts and theories concerning the mechanisms of carcinogenesis. FASEB J 1991, 5: 2280-2286.
9. R. Y. Wu, H. Chiang, B. J. Shao, N.G. Li, Y. D. Fu. Effects of 2.45 GHz microwave radiation and phorbol ester 12-0-tetradecanoylphorbol-13-acetate or dimethylhydrazine-induced colon cancer in mice. Bioelectromagnetics 1994, 15:531-538.
10. C. A. Reznikoff, J. S.Bertram, D.W. Brankow, C. Heidelberger, Quantitative and qualitative studies of chemical transformation of cloned C3H10T1/2 mouse embryo cellssensitive to postconfluence inhibition of cell division. Cancer Res. 1973, 33: 3239-3249.
11. M.Terzaghi, J. B. Little, X-radiation-induced transformation in a C3H mouse embryo-derived cell line. 1976, Cancer Res. 36: 1367-1374.
12. A. Han, M. Elkind, Transformation of mouse C3H/10T1/2 cells by single and fractionated doses of X-rays and fission-spectrum neutrons. Cancer Res: 1979, 39, 123-130.
13. J.Miyakoshi, M.Yoshida, H.Yaguchi, G. R. Ding, Exposure to extremely low frequency magnetic fields suppresses X-Ray-induced transformation in mouse C3HIOT1/2 cells. Biochemical and Biophysical Research Communications 2000, 271:323-327.
14. G. Lazzi, O. P.Gandhi. "On the Optimal Design of the PML Absorbing Boundary Condition for the FDTD Code," 1EEE Transactions on Antennas and Propagation, 1997, Vol.5, pp.914-916.
15. C. A. Reznikoff, D.W. Brankow, C. Heidelberger. Establishment and characterization of a cloned line of C3H mouse embryo cells sensitive to postconfluence inhibition of division. Cancer Res. 1973, 33: 3231-3238.
16. E.J. Hall. Oncogenic transformation systems involving mammalian cells in vitro to determine the relative risks of different treatment modalities. Strahlentherapie 1984, 160:725-731.
17. E. P. Clark, G M.Hahn, J.B.Little. Hyperthermic modulation of X-ray-induced oncogenic transformation in C3H 10T1/2 cells. Radiat. Res. 1981, 88:619-622
18. S.Szmigielski, A. Szudzinski, A.Pietraszek, M.Bielec, M.Janiak, J. K. Wrembel. Accelerated development of spontaneous and benzopyrene-induced skin cancer in mice exposed to 2450-MHz microwave radiation. Bioelectromagnetics 1982, 3:179-191.
19. T. K.Hei, R. S.Krauss, S. X. Liu, E. J. Hall, I. B. Weinstein. Effects of increased expression of protein kinase C on radiation-induced cell transformation. Carcinogenesis1994, 15: 365-370.
20. L. L.Kunz, R. B.Johnson, D.Thomson, J.Crowley, C. K.Chou, A. W. Guy. Evaluation of longevity, cause of death, and histopatho-logical findings. Vol. 8 of Effects of Long-Term Low-Level Radiation Exposure on Rats, Report 1985, USAFSAM TR-85-11, USAF School of Aerospace Medicine, Brooks Air Force Base, T. X.
21. K. Baicer, G. H. Harrison. Evidence for microwave carcinogenesis in vitro. Carcinogenesis 1985, 6:859-864.
22. K. Balcer, G. H. Harrison, Induction of neoplastic transformation in C3H/10T1/2 cells by 2.45-GHz microwaves and phorbol ester. Radiation Res. 1989, 117:531-537.
23. K. Elizabeth, K.Balcer, H. H.George. Neoplastic transformation of C3H10T1/2 cells following exposure to 120 Hz modulated 2.45 GHz microwaves and phorbol ester tumor promoter. Radiation Res. 1991, 126: 65-72.
24. A. R. Kennedy, G.Murphy, J. B. Little. Effect of time and duration of exposure to 12-O-tetradecanoylphorbol-13-acetate on x-ray transformation of C3H 10T 1/2 cells. Cancer Res.1980, 40, 1915-1920.
25. U.Kikkawa, Y. Takai, Y.Tanaka, R. Miyake Y. Nishizuka. Protein kinase c as a possible receptor protein of tumor-promoting phorbol esters. J. Biol. Chem. 1983, 258: 11442-11445.
26. W. R.Adey. Biological effects of radio frequency electromagnetic radiation. In Interaction of Electromagnetic Waves with biological systems (J. C. Lin, Ed), 1988, pp.1-33. Plenum, New York.
27. R. A. Luben, C. D. Cain, Chen, M.C Rosen, W. R. Adey. Effects of electromagnetic stimuli on bone and bone cells in vitro: Inhibition of responses to parathyroid hormone by low-energy, low-frequency fields. Proc. Natl. Acad. Sci. USA 1982, 79: 4180-4183.
28. W.D. Winters. Biological functions of immunologically reactive human and canine cellsinfluenced by in vitro exposure to 60-Hz electric and magnetic and magnetic fields. In New York State Power Line Project. Final Report, Contract 218207. 1986, Wadsworth Center for Laboratories and Research, Albany, NY.
29. D. B. Lyle, R.D. Ayotte, A. R. Sheppard, W. R. Adey. Suppression of T-lymphocyte cytotoxicity following exposure to 60Hz sinusoidal electric fields. Bioelectromagnetics 1998, 9: 303-313.
30. C.V. Byus, K. Kartun, S. Pieper, W. R. Adey. Increased ornithine decarboxylase activity in cultured cells exposed to low energy modulated microwave fields and phorbol ester tumor promoters. Cancer Res. 1998, 48: 4222-4226.
31. W. R. Adey. Cell membranes: The electromagnetic environment and cancer promotion. Neurochem Res. 1988, 13: 671-677.
32. W. R. Adey. Electromagnetic fields, cell membrane amplification and cancer promotion. In Wilson B. W, Stevens R. G, Anderson L. E (eds): "Extremely Low Frequency Electromagnetic Fields; The Question of Cancer." Columbus, OH: Battelle Press, 1989, pp 221-249.
33. W. R. Adey. Joint actions of environmental nonionizing electromagnetic fields and chemical pollution in cancer promotion. Environ Health Prospect 1990, 86: 297-305.
34. IEEE Standard for safety levels with Respect to human exposure to radio frequency electromagnetic fields, 3kHz to 300GHz. Standard C95.1, IEEE, 1999, New York.
35. IEEE. recommended practice for determining the peak spatial-average specific absorption rate (SAR) in the human body due to wireless communications devices: computational techniques. Standard P1529-200x, IEEE, draft: SCC-34, SC-2, WG-2-computational dosimetry. 2003, New York.
36. M. A. Stuchly Biological concerns in wireless communications. Crit Rev Biomed Eng 1998, 26:117-151.
37. P. W. French, R. Penny, J.A. Laurence, D.R. McKenzie. Mobile phones, heat shock proteins and cancer. Differentiation 2001.67:93-97.
38. I.J. Benjamin, D.R. McMillan. Stress (heat shock) proteins molecular chaperones in cardiovascular biology and disease. Circ Res 1998. 83: 117-132.
39. R.J.Ellis, S.M.Van der Vies Molecular chaperones. Annu Rev Biochem 1991, 60: 321-347.
40. K. Fritze, C. Wiessner, N. Kuster, C. Sommer, E Gass, D.M. Hermann, M. Kiessling, K.A. Hossmann. Effect of global system for mobile communication microwave exposure on the genomic response of the rat brain. Neuroscience 1997.81:627-639.
41. D. De Pomerai, D. Daniells, H. David, J. Allan, I. Duce, M. Mutwakil, D. Thomas, P. Sewell, J. Tattersall, D. Jones, P.Candido. Non-thermal heat-shock response to microwaves. Nature 2000. 405: 417-418.
42. D. De Pomerai, B. Smith, Dawe A, North K, Smith T, Archer DB, Duce IR, Jones D, Candido EP. Microwave radiation can alter protein conformation without bulk heating. FEBS Lett 2003. 543:93-97.
43. D.Leszczynski, S. (?) J. Reivinen, R. Kuokka Non-thermal activation in human endothelial cells: Molecular mechanism for cancer-and blood-brain barrier-related effects. Differentiation 2002.70:120-129.
44. S.E Cleary, G. Cao, L.M. Liu, EM. Egle, K.R. Shelton. Stress proteins are not induced in mammalian cells exposed to radiofrequency or microwave radiation. Bioelectromagnetics 1997. 18: 499-505.
45. E Tian, T. Nakahara, K. Wake, M. Taki, J. Miyakoshi. Exposure to 2.45 GHz electromagnetic fields induces HSP70 at a high SAR of more than 20 W/kg but not at 5 W/kg in human glioma MO54 cells. Int J Radiat Biol 2002, 78: 433-440.
46. J. Miyakoshi, K. Takemasa, Y. Takashima, G. R. Ding, H. Hirose, S. Koyama. Effects ofexposure to a 1950 MHz Radio-frequency field on expression of HSP70 and HSP27 in human glioma cells. Bioelectromagnetics 2005. 26:251-257.
47. A.P.Arrigo, J. Landry. Expression and function of the low-molecular weight heat shock proteins. In RI Morimoto, TA Tissieres, C Georgopoulous(eds): "biology of Heat Shock Proteins and Molecular Chaperones." Cold Spring Harbor, HY: Cold Spring Harbor Laboratory Press, 1994. pp 335-373.
48. P. Chretien, J.Landry. Enhanced constitutive expression of the 27-kDa heat shock proteins in heat-resistant variants from Chinese hamster cells. J Cell Physiol 1988.137: 157-166.
49. J. Landry, P, Chretien, H. Lambert, E. Hickey, L.A.Weber. Heat shock resistance conferred by expression of the human HSP27 gene in rodent cells. J Cell Biol 1989.109:7-15.
50. J.N.Lavoie, H. Lambert, E. Hickey, L.A. Weber, J. Landry. Modulation of cellular thermoresistance and actin filament stability accompanies phosphorylation-induced changes in the oligomeric structure of heat shock protein 27. Mol Cell Biol 1995.15:505-516.
51. J. Huot, F. Houle, D.R. Spitz, J. Landry. HSP27 phosphorylation-mediated resistance against actin fragmentation and cell death induced by oxidative stress. Cancer Res 1996. 56:273-279.
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