在現代生活中，由於家用電器地使用越來越普及，人類已不知不覺暴露於家用電器產生的極低頻電磁場(extremely low-frequency electromagnetic fields；ELF-EMFs) 中。因此，近三十年來，極低頻電磁場是否會危害人類的健康也受到大眾媒體與科學家廣泛關注與討論。對於極低頻電磁場所造成的生物效應研究常有不同的結論，然而這些不一致的結果可能由於不同的實驗條件，例如：實驗對象、照射條件(連續或間歇性)、照射時間及沒有嚴謹的電磁波磁場照射系統(例如：溫度控制及照射環境控制)所導致。在本研究中，我們透過基因表現、蛋白質表現及細胞層級等不同實驗方法，探討極低頻電磁場對於人類角質細胞之生物效應，證實人類皮膚角質細胞Immortalized nontumorigenic human keratinocytes (HaCaT; p53-mutated type)在1.5 mT，60 Hz 極低頻電磁場照射144 小時，會觸發ATM-Chk2-p21 pathway抑制細胞生長，引起細胞G1 phase arrest而降低細胞增生能力。透過西方墨點法，得知極低頻電磁場引發ATM/Chk2 signaling cascades，增加p21蛋白質表現量。相對地，利用siRNA將CHK2 基因 knockdown後，HaCaT 細胞之G1 phase arrest現象即消失。因此，本研究認為極低頻電磁場影響ATM-Chk2-p21 pathway造成HaCaT 細胞發生G1 phase arrest。
進一步，利用相同的照射系統與實驗設計，評估極低頻電磁場是否會在不同的人類皮膚角質細胞primary normal human epidermal keratinocytes (NHEK; primary type)造成相似於HaCaT 細胞之效應。實驗結果證實，極低頻電磁場不會影響NHEK 細胞之細胞生長、細胞增生、細胞週期分布及ATM signaling pathway。本研究發現兩種不同的人類皮膚角質細胞對於極低頻電磁場有不同的反應。進一步以極低頻電磁場同時照射HaCaT細胞與 NHEK細胞168 小時，觀察細胞之生長曲線，其結果呈現相同結論。
因此，本研究經嚴謹測試之磁場照射控制系統，以基因表現、蛋白質表現及細胞層級等方法證實不同的細胞株對於極低頻電磁場有不同的反應(cell type specific response)，這可能是目前極低頻電磁場呈現出不一致生物效應現象的原因之一。

In daily life, humans are exposed to the extremely low-frequency electromagnetic fields (ELF-EMFs) generated by electric appliances, and public concern is increasing regarding the biological effects of such exposure. Numerous studies have yielded inconsistent results regarding the biological effects of ELF-EMF exposure. This study showed that ELF-EMFs activate the ATM-Chk2-p21 pathway in HaCaT cells to decrease cell proliferation. To present well-founded results, we comprehensively evaluated the biological effects of ELF-EMFs at the transcriptional, protein, and cellular levels. Human HaCaT cells from an immortalized epidermal keratinocyte cell line were exposed to a 1.5 mT, 60 Hz ELF-EMF for 144 h. The ELF-EMF caused G1 arrest and decreased colony formation. Protein expression experiments revealed that ELF-EMFs induced the activation of the ATM/Chk2 signaling cascades. In addition, the p21 protein, a regulator of cell cycle progression at G1 and G2/M, exhibited a higher level of expression in exposed HaCaT cells compared with the expression of sham-exposed cells. The ELF-EMF-induced G1 arrest was diminished when the CHK2 gene expression (which encodes checkpoint kinase 2; Chk2) was suppressed by specific small interfering RNA (siRNA). These findings indicated that ELF-EMFs activated the ATM-Chk2-p21 pathway in HaCaT cells resulting in cell cycle arrest at the G1 phase.
According to the results of HaCaT cells, it is natural to suspect whether ELF-EMFs cause similar effects in a distinct epidermal keratinocyte, primary normal human epidermal keratinocytes (NHEK), by using the same ELF-EMF exposure system and experimental design. In NHEK cells, ELF-EMFs exerted no effects on cell growth, cell proliferation, cell cycle distribution, and the activation of ATM signaling pathway. This study elucidated that the two types of epidermal keratinocytes differently responded to ELF-EMFs. To further validate this finding, the NHEK and HaCaT cells were simultaneously exposed to ELF-EMFs in the same incubator for 168 h and observed the cell growths. The results of simultaneous exposure in the two cell types showed that the NHEK and HaCaT cells exhibited distinct responses to ELF-EMFs.
Thus, the biological effects of ELF-EMFs in epidermal keratinocytes are cell type specific. The findings may partially explain the inconsistent results of previous studies when comparing results across various experimental models. Based on the precise control of the ELF-EMF exposure and rigorous sham-exposure experiments in this study, the experiments at the transcriptional, protein and cellular levels all consistently supported the conclusion.

1. Humans IWGotEoCRt (2002) Non-ionizing radiation, Part 1: static and extremely low-frequency (ELF) electric and magnetic fields. IARC Monogr Eval Carcinog Risks Hum 80: 1-395.
2. International Commission on Non-Ionizing Radiation P (2009) Guidelines on limits of exposure to static magnetic fields. Health Phys 96: 504-514.
3. (2002) Non-ionizing radiation, Part 1: static and extremely low-frequency (ELF) electric and magnetic fields. IARC Monogr Eval Carcinog Risks Hum 80: 1-395.
4. International Commission on Non-Ionizing Radiation P (2010) Guidelines for limiting exposure to time-varying electric and magnetic fields (1 Hz to 100 kHz). Health Phys 99: 818-836.
5. Wertheimer N, Leeper E (1979) Electrical wiring configurations and childhood cancer. Am J Epidemiol 109: 273-284.
6. Savitz DA, Wachtel H, Barnes FA, John EM, Tvrdik JG (1988) Case-control study of childhood cancer and exposure to 60-Hz magnetic fields. Am J Epidemiol 128: 21-38.
7. Feychting M, Forssen U, Floderus B (1997) Occupational and residential magnetic field exposure and leukemia and central nervous system tumors. Epidemiology 8: 384-389.
8. Li CY, Theriault G, Lin RS (1997) Residential exposure to 60-Hertz magnetic fields and adult cancers in Taiwan. Epidemiology 8: 25-30.
9. Feychting M, Ahlbom A, Kheifets L (2005) EMF and health. Annu Rev Public Health 26: 165-189.
10. Roosli M, Lortscher M, Egger M, Pfluger D, Schreier N, et al. (2007) Leukaemia, brain tumours and exposure to extremely low frequency magnetic fields: cohort study of Swiss railway employees. Occup Environ Med 64: 553-559.
11. Chen C, Ma X, Zhong M, Yu Z (2010) Extremely low-frequency electromagnetic fields exposure and female breast cancer risk: a meta-analysis based on 24,338 cases and 60,628 controls. Breast Cancer Res Treat 123: 569-576.
12. Hug K, Grize L, Seidler A, Kaatsch P, Schuz J (2010) Parental occupational exposure to extremely low frequency magnetic fields and childhood cancer: a German case-control study. Am J Epidemiol 171: 27-35.
13. Kheifets L, Ahlbom A, Crespi CM, Feychting M, Johansen C, et al. (2010) A pooled analysis of extremely low-frequency magnetic fields and childhood brain tumors. Am J Epidemiol 172: 752-761.
14. Reid A, Glass DC, Bailey HD, Milne E, de Klerk NH, et al. (2011) Risk of childhood acute lymphoblastic leukaemia following parental occupational exposure to extremely low frequency electromagnetic fields. Br J Cancer 105: 1409-1413.
15. Schuz J, Grell K, Kinsey S, Linet MS, Link MP, et al. (2012) Extremely low-frequency magnetic fields and survival from childhood acute lymphoblastic leukemia: an international follow-up study. Blood Cancer J 2: e98.
16. Lupke M, Frahm J, Lantow M, Maercker C, Remondini D, et al. (2006) Gene expression analysis of ELF-MF exposed human monocytes indicating the involvement of the alternative activation pathway. Biochim Biophys Acta 1763: 402-412.
17. Fedrowitz M, Loscher W (2012) Gene expression in the mammary gland tissue of female Fischer 344 and Lewis rats after magnetic field exposure (50 Hz, 100 muT) for 2 weeks. Int J Radiat Biol 88: 425-429.
18. Loberg LI, Engdahl WR, Gauger JR, McCormick DL (2000) Expression of cancer-related genes in human cells exposed to 60 Hz magnetic fields. Radiat Res 153: 679-684.
19. Nakasono S, Laramee C, Saiki H, McLeod KJ (2003) Effect of power-frequency magnetic fields on genome-scale gene expression in Saccharomyces cerevisiae. Radiat Res 160: 25-37.
20. Luceri C, De Filippo C, Giovannelli L, Blangiardo M, Cavalieri D, et al. (2005) Extremely low-frequency electromagnetic fields do not affect DNA damage and gene expression profiles of yeast and human lymphocytes. Radiat Res 164: 277-285.
21. Henderson B, Kind M, Boeck G, Helmberg A, Wick G (2006) Gene expression profiling of human endothelial cells exposed to 50-Hz magnetic fields fails to produce regulated candidate genes. Cell Stress Chaperones 11: 227-232.
22. Chen G, Lu D, Chiang H, Leszczynski D, Xu Z (2012) Using model organism Saccharomyces cerevisiae to evaluate the effects of ELF-MF and RF-EMF exposure on global gene expression. Bioelectromagnetics 33: 550-560.
23. Huwiler SG, Beyer C, Frohlich J, Hennecke H, Egli T, et al. (2012) Genome-wide transcription analysis of Escherichia coli in response to extremely low-frequency magnetic fields. Bioelectromagnetics 33: 488-496.
24. Simko M, Kriehuber R, Lange S (1998) Micronucleus formation in human amnion cells after exposure to 50 Hz MF applied horizontally and vertically. Mutat Res 418: 101-111.
25. Simko M, Kriehuber R, Weiss DG, Luben RA (1998) Effects of 50 Hz EMF exposure on micronucleus formation and apoptosis in transformed and nontransformed human cell lines. Bioelectromagnetics 19: 85-91.
26. Winker R, Ivancsits S, Pilger A, Adlkofer F, Rudiger HW (2005) Chromosomal damage in human diploid fibroblasts by intermittent exposure to extremely low-frequency electromagnetic fields. Mutat Res 585: 43-49.
27. Heredia-Rojas JA, Rodriguez-De La Fuente AO, del Roble Velazco-Campos M, Leal-Garza CH, Rodriguez-Flores LE, et al. (2001) Cytological effects of 60 Hz magnetic fields on human lymphocytes in vitro: sister-chromatid exchanges, cell kinetics and mitotic rate. Bioelectromagnetics 22: 145-149.
28. Stronati L, Testa A, Villani P, Marino C, Lovisolo GA, et al. (2004) Absence of genotoxicity in human blood cells exposed to 50 Hz magnetic fields as assessed by comet assay, chromosome aberration, micronucleus, and sister chromatid exchange analyses. Bioelectromagnetics 25: 41-48.
29. Testa A, Cordelli E, Stronati L, Marino C, Lovisolo GA, et al. (2004) Evaluation of genotoxic effect of low level 50 Hz magnetic fields on human blood cells using different cytogenetic assays. Bioelectromagnetics 25: 613-619.
30. Hone P, Lloyd D, Szluinska M, Edwards A (2006) Chromatid damage in human lymphocytes is not affected by 50 Hz electromagnetic fields. Radiat Prot Dosimetry 121: 321-324.
31. Jin YB, Kang GY, Lee JS, Choi JI, Lee JW, et al. (2012) Effects on micronuclei formation of 60-Hz electromagnetic field exposure with ionizing radiation, hydrogen peroxide, or c-Myc overexpression. Int J Radiat Biol 88: 374-380.
32. Lai H, Singh NP (1997) Acute exposure to a 60 Hz magnetic field increases DNA strand breaks in rat brain cells. Bioelectromagnetics 18: 156-165.
33. Ivancsits S, Diem E, Pilger A, Rudiger HW, Jahn O (2002) Induction of DNA strand breaks by intermittent exposure to extremely-low-frequency electromagnetic fields in human diploid fibroblasts. Mutat Res 519: 1-13.
34. Ivancsits S, Diem E, Jahn O, Rudiger HW (2003) Intermittent extremely low frequency electromagnetic fields cause DNA damage in a dose-dependent way. Int Arch Occup Environ Health 76: 431-436.
35. Ivancsits S, Diem E, Jahn O, Rudiger HW (2003) Age-related effects on induction of DNA strand breaks by intermittent exposure to electromagnetic fields. Mech Ageing Dev 124: 847-850.
36. Focke F, Schuermann D, Kuster N, Schar P (2010) DNA fragmentation in human fibroblasts under extremely low frequency electromagnetic field exposure. Mutat Res 683: 74-83.
37. Kim J, Ha CS, Lee HJ, Song K (2010) Repetitive exposure to a 60-Hz time-varying magnetic field induces DNA double-strand breaks and apoptosis in human cells. Biochem Biophys Res Commun 400: 739-744.
38. Kim J, Yoon Y, Yun S, Park GS, Lee HJ, et al. (2012) Time-varying magnetic fields of 60 Hz at 7 mT induce DNA double-strand breaks and activate DNA damage checkpoints without apoptosis. Bioelectromagnetics 33: 383-393.
39. Scarfi MR, Sannino A, Perrotta A, Sarti M, Mesirca P, et al. (2005) Evaluation of genotoxic effects in human fibroblasts after intermittent exposure to 50 Hz electromagnetic fields: a confirmatory study. Radiat Res 164: 270-276.
40. Burdak-Rothkamm S, Rothkamm K, Folkard M, Patel G, Hone P, et al. (2009) DNA and chromosomal damage in response to intermittent extremely low-frequency magnetic fields. Mutat Res 672: 82-89.
41. Vianale G, Reale M, Amerio P, Stefanachi M, Di Luzio S, et al. (2008) Extremely low frequency electromagnetic field enhances human keratinocyte cell growth and decreases proinflammatory chemokine production. Br J Dermatol 158: 1189-1196.
42. Martinez MA, Ubeda A, Cid MA, Trillo MA (2012) The proliferative response of NB69 human neuroblastoma cells to a 50 Hz magnetic field is mediated by ERK1/2 signaling. Cell Physiol Biochem 29: 675-686.
43. Trillo MA, Martinez MA, Cid MA, Leal J, Ubeda A (2012) Influence of a 50 Hz magnetic field and of all-transretinol on the proliferation of human cancer cell lines. Int J Oncol 40: 1405-1413.
44. Gluck B, Guntzschel V, Berg H (2001) Inhibition of proliferation of human lymphoma cells U937 by a 50 Hz electromagnetic field. Cell Mol Biol (Noisy-le-grand) 47 Online Pub: OL115-117.
45. Van Den Heuvel R, Leppens H, Nemethova G, Verschaeve L (2001) Haemopoietic cell proliferation in murine bone marrow cells exposed to extreme low frequency (ELF) electromagnetic fields. Toxicol In Vitro 15: 351-355.
46. Zhou J, Ming LG, Ge BF, Wang JQ, Zhu RQ, et al. (2011) Effects of 50 Hz sinusoidal electromagnetic fields of different intensities on proliferation, differentiation and mineralization potentials of rat osteoblasts. Bone 49: 753-761.
47. Yoshizawa H, Tsuchiya T, Mizoe H, Ozeki H, Kanao S, et al. (2002) No effect of extremely low-frequency magnetic field observed on cell growth or initial response of cell proliferation in human cancer cell lines. Bioelectromagnetics 23: 355-368.
48. Marcantonio P, Del Re B, Franceschini A, Capri M, Lukas S, et al. (2010) Synergic effect of retinoic acid and extremely low frequency magnetic field exposure on human neuroblastoma cell line BE(2)C. Bioelectromagnetics 31: 425-433.
49. Ivancsits S, Pilger A, Diem E, Jahn O, Rudiger HW (2005) Cell type-specific genotoxic effects of intermittent extremely low-frequency electromagnetic fields. Mutat Res 583: 184-188.
50. Simko M (2007) Cell type specific redox status is responsible for diverse electromagnetic field effects. Curr Med Chem 14: 1141-1152.
51. Boukamp P, Petrussevska RT, Breitkreutz D, Hornung J, Markham A, et al. (1988) Normal keratinization in a spontaneously immortalized aneuploid human keratinocyte cell line. J Cell Biol 106: 761-771.
52. Lehman TA, Modali R, Boukamp P, Stanek J, Bennett WP, et al. (1993) p53 mutations in human immortalized epithelial cell lines. Carcinogenesis 14: 833-839.
53. Huang CL, Shu WY, Tsai ML, Chiang CS, Chang CW, et al. (2011) Repeated small perturbation approach reveals transcriptomic steady states. PLoS One 6: e29241.
54. Chang CW, Chen CR, Huang CY, Shu WY, Chiang CS, et al. (2013) Comparative transcriptome profiling of an SV40-transformed human fibroblast (MRC5CVI) and its untransformed counterpart (MRC-5) in response to UVB irradiation. PLoS One 8: e73311.
55. Schena M, Shalon D, Davis RW, Brown PO (1995) Quantitative monitoring of gene expression patterns with a complementary DNA microarray. Science 270: 467-470.
56. Tsai ML, Chang KY, Chiang CS, Shu WY, Weng TC, et al. (2009) UVB radiation induces persistent activation of ribosome and oxidative phosphorylation pathways. Radiat Res 171: 716-724.
57. Cheng WC, Shu WY, Li CY, Tsai ML, Chang CW, et al. (2012) Intra- and inter-individual variance of gene expression in clinical studies. PLoS One 7: e38650.
58. Ye J, Coulouris G, Zaretskaya I, Cutcutache I, Rozen S, et al. (2012) Primer-BLAST: a tool to design target-specific primers for polymerase chain reaction. BMC Bioinformatics 13: 134.
59. Zhang L, Hou Y, Wang M, Wu B, Li N (2009) A study on the functions of ubiquitin metabolic system related gene FBG2 in gastric cancer cell line. J Exp Clin Cancer Res 28: 78.
60. Hong JH, Gatti RA, Huo YK, Chiang CS, McBride WH (1994) G2/M-phase arrest and release in ataxia telangiectasia and normal cells after exposure to ionizing radiation. Radiat Res 140: 17-23.
61. Chiang CS, Syljuasen RG, Hong JH, Wallis A, Dougherty GJ, et al. (1997) Effects of IL-3 gene expression on tumor response to irradiation in vitro and in vivo. Cancer Res 57: 3899-3903.
62. Wang SC, Wu CC, Wei YY, Hong JH, Chiang CS (2011) Inactivation of ataxia telangiectasia mutated gene can increase intracellular reactive oxygen species levels and alter radiation-induced cell death pathways in human glioma cells. Int J Radiat Biol 87: 432-442.
63. Wang SC, Yu CF, Hong JH, Tsai CS, Chiang CS (2013) Radiation therapy-induced tumor invasiveness is associated with SDF-1-regulated macrophage mobilization and vasculogenesis. PLoS One 8: e69182.
64. Kerr MK, Churchill GA (2001) Experimental design for gene expression microarrays. Biostatistics 2: 183-201.
65. Valery C, Grob JJ, Verrando P (2001) Identification by cDNA microarray technology of genes modulated by artificial ultraviolet radiation in normal human melanocytes: relation to melanocarcinogenesis. J Invest Dermatol 117: 1471-1482.
66. Li D, Turi TG, Schuck A, Freedberg IM, Khitrov G, et al. (2001) Rays and arrays: the transcriptional program in the response of human epidermal keratinocytes to UVB illumination. FASEB J 15: 2533-2535.
67. Takao J, Ariizumi K, Dougherty, II, Cruz PD, Jr. (2002) Genomic scale analysis of the human keratinocyte response to broad-band ultraviolet-B irradiation. Photodermatol Photoimmunol Photomed 18: 5-13.
68. Sesto A, Navarro M, Burslem F, Jorcano JL (2002) Analysis of the ultraviolet B response in primary human keratinocytes using oligonucleotide microarrays. Proc Natl Acad Sci U S A 99: 2965-2970.
69. Kanehisa M, Goto S (2000) KEGG: kyoto encyclopedia of genes and genomes. Nucleic Acids Res 28: 27-30.
70. Datto MB, Li Y, Panus JF, Howe DJ, Xiong Y, et al. (1995) Transforming growth factor beta induces the cyclin-dependent kinase inhibitor p21 through a p53-independent mechanism. Proc Natl Acad Sci U S A 92: 5545-5549.
71. Yoon K, Smart RC (2004) C/EBPalpha is a DNA damage-inducible p53-regulated mediator of the G1 checkpoint in keratinocytes. Mol Cell Biol 24: 10650-10660.
72. Aliouat-Denis CM, Dendouga N, Van den Wyngaert I, Goehlmann H, Steller U, et al. (2005) p53-independent regulation of p21Waf1/Cip1 expression and senescence by Chk2. Mol Cancer Res 3: 627-634.
73. Matsuoka S, Huang M, Elledge SJ (1998) Linkage of ATM to cell cycle regulation by the Chk2 protein kinase. Science 282: 1893-1897.
74. Matsuoka S, Rotman G, Ogawa A, Shiloh Y, Tamai K, et al. (2000) Ataxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro. Proc Natl Acad Sci U S A 97: 10389-10394.
75. Bakkenist CJ, Kastan MB (2003) DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation. Nature 421: 499-506.
76. Lee JH, Paull TT (2004) Direct activation of the ATM protein kinase by the Mre11/Rad50/Nbs1 complex. Science 304: 93-96.
77. Abraham RT, Tibbetts RS (2005) Cell biology. Guiding ATM to broken DNA. Science 308: 510-511.
78. Vijayalaxmi, Obe G (2005) Controversial cytogenetic observations in mammalian somatic cells exposed to extremely low frequency electromagnetic radiation: a review and future research recommendations. Bioelectromagnetics 26: 412-430.
79. Manni V, Lisi A, Pozzi D, Rieti S, Serafino A, et al. (2002) Effects of extremely low frequency (50 Hz) magnetic field on morphological and biochemical properties of human keratinocytes. Bioelectromagnetics 23: 298-305.
80. Dehay C, Kennedy H (2007) Cell-cycle control and cortical development. Nat Rev Neurosci 8: 438-450.
81. Malumbres M, Barbacid M (2005) Mammalian cyclin-dependent kinases. Trends Biochem Sci 30: 630-641.
82. Bertoli C, Skotheim JM, de Bruin RA (2013) Control of cell cycle transcription during G1 and S phases. Nat Rev Mol Cell Biol 14: 518-528.
83. Fang G, Yu H, Kirschner MW (1998) Direct binding of CDC20 protein family members activates the anaphase-promoting complex in mitosis and G1. Mol Cell 2: 163-171.
84. Visintin R, Prinz S, Amon A (1997) CDC20 and CDH1: a family of substrate-specific activators of APC-dependent proteolysis. Science 278: 460-463.
85. Harper JW, Adami GR, Wei N, Keyomarsi K, Elledge SJ (1993) The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell 75: 805-816.
86. Cayrol C, Knibiehler M, Ducommun B (1998) p21 binding to PCNA causes G1 and G2 cell cycle arrest in p53-deficient cells. Oncogene 16: 311-320.
87. Ramos-Jerz Mdel R, Villanueva S, Jerz G, Winterhalter P, Deters AM (2013) Persea americana Mill. Seed: Fractionation, Characterization, and Effects on Human Keratinocytes and Fibroblasts. Evid Based Complement Alternat Med 2013: 391247.
88. Pastore S, Lulli D, Potapovich AI, Fidanza P, Kostyuk VA, et al. (2011) Differential modulation of stress-inflammation responses by plant polyphenols in cultured normal human keratinocytes and immortalized HaCaT cells. J Dermatol Sci 63: 104-114.
89. Chaturvedi V, Qin JZ, Denning MF, Choubey D, Diaz MO, et al. (1999) Apoptosis in proliferating, senescent, and immortalized keratinocytes. J Biol Chem 274: 23358-23367.
90. Lewis DA, Hurwitz SA, Spandau DF (2003) UVB-induced apoptosis in normal human keratinocytes: role of the erbB receptor family. Exp Cell Res 284: 316-327.
91. Lewis DA, Zweig B, Hurwitz SA, Spandau DF (2003) Inhibition of erbB receptor family members protects HaCaT keratinocytes from ultraviolet-B-induced apoptosis. J Invest Dermatol 120: 483-488.
92. Lewis DA, Hengeltraub SF, Gao FC, Leivant MA, Spandau DF (2006) Aberrant NF-kappaB activity in HaCaT cells alters their response to UVB signaling. J Invest Dermatol 126: 1885-1892.
93. Petit-Frere C, Capulas E, Lyon DA, Norbury CJ, Lowe JE, et al. (2000) Apoptosis and cytokine release induced by ionizing or ultraviolet B radiation in primary and immortalized human keratinocytes. Carcinogenesis 21: 1087-1095.
94. Isoir M, Buard V, Gasser P, Voisin P, Lati E, et al. (2006) Human keratinocyte radiosensitivity is linked to redox modulation. J Dermatol Sci 41: 55-65.
95. http://www.atcc.org/products/all/PCS-200-010.aspx
96. Okada S, Irie T, Tanaka J, Yasuhara R, Yamamoto G, et al. (2014) Potential role of hematopoietic pre-B-cell leukemia transcription factor-interacting protein in oral carcinogenesis. J Oral Pathol Med.
97. Shiloh Y (2006) The ATM-mediated DNA-damage response: taking shape. Trends Biochem Sci 31: 402-410.
98. Shiloh Y, Ziv Y (2013) The ATM protein kinase: regulating the cellular response to genotoxic stress, and more. Nat Rev Mol Cell Biol 14: 197-210.
99. Kastan MB, Lim DS (2000) The many substrates and functions of ATM. Nat Rev Mol Cell Biol 1: 179-186.
100. Kitagawa R, Kastan MB (2005) The ATM-dependent DNA damage signaling pathway. Cold Spring Harb Symp Quant Biol 70: 99-109.
101. Lee JH, Paull TT (2005) ATM activation by DNA double-strand breaks through the Mre11-Rad50-Nbs1 complex. Science 308: 551-554.
102. Lee JH, Paull TT (2007) Activation and regulation of ATM kinase activity in response to DNA double-strand breaks. Oncogene 26: 7741-7748.
103. Livak KJ, Schmittgen TD (2001) Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods 25: 402-408.