References
To install AbrahamRT. (2001).Genes Dev.,15, 2177–2196.
Agami R y Bernards R. (2000).The cell,102, 55–66.
Amati B, Dalton S, Brooks MW, Littlewood TD, Evans GI y Land H. (1992).Nature,359, 423–426.
Anderson CW y Carter TH. (1996).current Arrives Microbiol. immune,217, 91–111.
Anderson L, Henderson C y Adachi Y. (2001).minor The cell. Biol.,21, 1719–1508.
Ando T, Kawabe T, Ohara H, Ducommun B e Itoh M. (2001).J. Biol. chemistry,276, 42971–42977.
Asaad NA, Zeng Z-C, Guan J, Thacker J and Iliakis G. (2000).oncogene,19, 5788–5800.
Atchley WR y Fitch WM. (1995).proc. National Academy Saber USA,92, 10217–10221.
Mountaineer CJ and Chestnut MB (2003).Nature,421, 499–506.
Banin S, Moyal L, Shieh S-Y, Tire Y, Anderson CW, Chessa L, Smorodinsky NI, Prives C, Reiss Y, Shiloh Y and Ziv Y. (1998).Science,281, 1674–1677.
Bao S, Tibbetts RS, Brumbaugh KM, Fang Y, Richardson DA, All A, Chen SM, Abraham RT y Wang X-F. (2001).Nature,411, 969–974.
Bartek J, Falck J y Lukas J. (2001).Nat. Rev Mol. cell biol.,2, 877–886.
Bartek J and Lukas C. (2001a).FEBS Lett.,490, 117–122.
Bartek J y Lukas J. (2001b).Current Opinion Cellular Biol.,13, 738–747.
Bell SP y Dutta A. (2002).year Rev. Biochemistry.,71, 333–374.
Bermudez VP, Lindsey-Boltz LA, Cesare AJ, Maniwa Y, Griffith JD, Hurwitz J, and Sancar A. (2003).proc. National Academy Saber USA,100, 1633–1638.
Bernhard EJ, Maity A, Muschel RJ and McKenna WG. (1995).radiate Reign. Biography.,34, 79–83.
Bernhard EJ, McKenna WG and Mussel RJ. (1999).cancer j.,5, 194–204.
Blasina A, Price BD, Turenne GA and McGowan CH. (1999).actual Biol.,9, 1135–1138.
Booher RN, Holman PS y Fattaey A. (1997).J. Biol. chemistry,272, 22300–22306.
Brown EJ y Baltimore D. (2000).Genes Dev.,14, 397–402.
Brush GS and Kelly TJ. (nineteen ninety six).DNA replication mechanisms. Cold Spring Harbor Laboratory Press: Nueva York.
[ PMC free article ] [ PubMed ] Bulavin DV, Amundson SA and Fornace Jr AJ. (2002).Current Genetic Opinion. development,12, 92–97.
Canman CE, Lim D-S, Cimprich KA, Taya Y, Tamai K, Sakaguchi K, Appella E, Chestnut MB and Siliciano JD. (1998).Science,281, 1677–1679.
Chan DW, Son S-C, Block W, Ye R, Khanna KK, Wold MS, Douglas P, Goodarzi AA, Pelley J, Taya Y, Lavin MF y Lees-Miller SP. (2000a).J. Biol. chemistry,275, 7803–7810.
Chan TA, Hermeking H, Lengauer C, Kinzler KW and Vogelstein B. (1999).Nature,401, 616–620.
Chan TA, Hwang PM, Hermeking H, Kinzler KW and Vogelstein B. (2000b).Genes Dev.,14, 1584–1588.
Cleaver JE, Rose R y Mitchell DL. (1990).radiar Res.,124, 294–299.
Cliby WA, Roberts CJ, Cimprich KA, Stringer CM, Lamb JR, Schreiber SL and Friend SH. (1998).EMBÓ J.,17, 159–169.
Cortez D, Guntuku S, Qin J y Elledge SJ. (2001).Science,294, 1713–1716.
Cortez D, Wang Y, Qin J y Elledge SJ. (1999).Science,286, 1162–1166.
Costanzo V, Robertson K, Ying CY, Kim E, Avvedimento E, Gottesman M, Greek D y Gautier J . (2000).minor The cell,6, 649–659.
Crawford DF y Piwnica-Worms H. (2001).J. Biol. chemistry,276, 37166–37177.
D'Amours D, Desnoyers S, D'Silva I and Poirier GG. (1999).biochemistry j,342, 249–268.
De Pamphilis ML. (1999).Bioensayos,21, 5–16.
Desai-Mehta A, Cerosaletti KM and Concannon P. (2001).minor The cell. Biol.,21, 2184–2025.
DeSimone JN, Bengtsson U, Wang Q, Lao XY, Redpath JL y Stanbridge EJ. (2003).radiar Res.,159, 72–85.
DiBiase SJ, Zeng Z-C, Chen R, Hyslop T, Curran Jr WJ and Iliakis G. (2000).Cancer Res.,60, 1245–1253.
Donaldson AD y Blow JJ. (2001).actual Biol.,11, R979–R982.
medico gp. (2000).biochemistry Biography. minutes,1471, M43–M56.
Draetta G y Eckstein J. (1997).biochemistry Biography. minutes,1332, M53–M63.
Durocher D y Jackson SP. (2001).Current Opinion Cellular Biol.,13, 225–231.
Dutta A y Bell SP. (1997).Ana. Rev. Cell Biol.,13, 293–332.
(Video) DNA DamageEdwards RJ, Bentley NJ y Carr AM. (1999).Nat. Cell Biol.,1, 393–398.
Eisenman RN y Cooper YES. (1995).Nature,378, 438–439.
Elia AEH, Cantley LC y Yaffe MB. (2003).Science,299, 1228–1231.
Elledge SJ. (1996).Science,274, 1664–1672.
Falck J, Mailand N, Syljuasen RG, Bartek J and Lukas J. (2001).Nature,410, 842–847.
Falck J, Petrini JHJ, Williams BR, Lukas J and Bartek J. (2002).Nat. Ginetta.,30, 290–294.
Friedberg EC, Walker GC and Siede W. (1995).DNA repair mutagenesis. Prensa ASM: Washington, DC.
Furnari B , Blasina A , Boddy MN , McGowan CH and Russell P .minor Biol. The cell,10, 833–845.
Galaktionov K, Chen X y Beach D. (1996).Nature,382, 511–517.
Gatei M, Scott SP, Filippovitch I, Soronika N, Lavin MF, Weber B y Khanna KK. (2000a).Cancer Res.,60, 3299–3304.
Gatei M, Young D, Cerosaletti KM, Desai-Mehta A, Spring K, Kozlov S, Lavin MF, Gatti RA, Concannon P y Khanna KK. (2000b).Nat. Ginetta.,25, 115–119.
Giaccia AJ and Kastan MB. (one thousand nine hundred ninety eight).Genes Dev.,12, 2973–2983.
Glover DM, Hagan IM y Tavares AAM. (1998).Genes Dev.,12, 3777–3787.
Goldberg M, Stucki M, Falck J, D'Amours D, Rahman D, Pappin D, Bartek J and Jackson SP. (2003).Nature,421, 952–956.
Gottifredi V, Shieh SY, Tire Y and Prives C. (2001).proc. National Academy Saber USA,98, 1036–1041.
Graves PR, Yu L, Schwarz JK, Gales J, Sausville EA, O'Connor PM and Cellar-Worms H. (2000).J. Biol. chemistry,275, 5600–5605.
Green CM, Erdjument-Bromage H, Tempst P y Lowndes NF. (2000).actual Biol.,10, 39–42.
Griffiths DJ, Barbet NC, McCready S, Lehmann AR y Carr AM. (1995).EMBÓ J.,14, 5812–5823.
Guan J, DiBiase S and Iliakis G (2000).Nucleic Acids Res.,28, 1183–1192.
Guo CY, D'Anna JA and Larner JM. (1999).radiar Res.,151, 125–132.
Guo Z, Kumagai A, Wang SX y Dunphy WG. (2000).Genes Dev.,14, 2745–2756.
Hagting A, Karlsson C, Clute P, Jackman M y Pines J. (1998).EMBÓ J.,17, 4127–4138.
Harper JW, Adami GR, Wei N, Keyomarsi K and Elledge SJ. (1993).The cell,75, 805–816.
Harris EE, Kao GD, Muschel RJ and McKenna WG. (1998).Cancer treatment. Beef.,93, 169–190.
Hartwell LH and Kastan MB. (1994).Science,266, 1821–1828.
Hartwell LH and Weinert TA. (1989).Science,246, 629–634.
Hermeking H, Lengauer C, Polyak K, He T-C, Zhang L, Thiagalingam S, Kinzler KW y Vogelstein B. (1997).minor The cell,1, 3–11.
Hermeking H, Rago C, Schuhmacher M, Li Q, Barrett JF, Obaya AJ, O'Connell BC, Mateyak MK, Tam W, Kohlhuber F, Dang CV, Sedivy JM, Eick D, Vogelstein B, and Kinzler KW. (2000).proc. National Academy Saber USA,97, 2229–2234.
Hickman ES, Moroni MC y Helin K. (2002).Current Genetic Opinion. development,12, 60–66.
Hirao A, Kong YY, Matsuoka S, Wakeham A, Ruland J, Yoshida H, Liu D, Elledge SJ y Mak TW. (2000).Science,287, 1824–1827.
Hoeijmakers JHJ. (2001).Nature,411, 366–374.
Houldsworth J y Lavin MF. (1980).Nucleic Acids Res.,8, 3709–3720.
Hwang A, Maity A, McKenna WG and Muschel RJ. (1995).J. Biol. chemistry,270, 28419–28424.
Iliakis G. (1988).in t. J. Radiat. Biol.,53, 541–584.
Iliakis G. (1997).Semin. oncol.,24, 602–615.
Jackson SP. (2002).carcinogenesis,23, 687–696.
Jeggo PA. (1997).mutated. Nothing.,384, 1–14.
Jeggo PA. (1998).Adv. Ginetta.,38, 186–218.
Jin P, Gu Y y Morgan DO. (1996).J. cell. Biol.,134, 963–970.
Jin P, Hardy S y Morgan DO. (1998).J. Cell Biol.,141, 875–885.
Kang D, Chen J, Wong J y Fang G. (2002).J. Cell Biol.,156, 249–259.
Like GD, McKenna WG and Muschel RJ. (1999).J. Biol. chemistry,274, 34779–34784.
Cada MB (2001).Nature,410, 766–767.
Chestnut MB and Lim D-S. (2000).Nat. Rev Mol. cell biol.,1, 179–186.
Kawabe T , Suganuma M , Ando T , Kimura M , Hori H and Okamoto T . (2002).oncogene,21, 1717–1726.
Khanna KK y Jackson SP. (2001).Nat. Ginetta.,27, 247–254.
(Video) DNA damage checkpoint and p53Khanna KK, Keating KE, Kozlov S, Scott S, Gatei M, Hobson K, Taya Y, Gabrielli B, Chan D, Lees-Miller SP and Lavin MF. (1998).Nat. Ginetta.,20, 398–400.
Kim S-T, Lim D-S, Canman CE and Kastan MB. (1999).J. Biol. chemistry,274, 37538–37543.
Kim ST, Xu B y Kastan MB. (2002).Genes Dev.,sixteen, 560–570.
Lamb JR, Petit-Frere C, Broughton BC, Lehmann AR y Green MHL. (1989).in t. J. Radiat. Biol.,56, 125–130.
Larner JM, Lee H y Hamlin JL. (1997).cancer survival,29, 25–45.
Larner JM, Lee H, Little RD, Dijkwell PA, Schildkraut CL and Hamlin JL. (1999).Nucleic Acids Res.,27, 803–809.
Larson JS, Tonkinson JL y Lai MT. (1997).Cancer Res.,57, 3351–3355.
Lavin MF y Schroeder AL. (1988).mutated. Nothing.,193, 193–206.
Lee CH y Chung JH. (2001).J. Biol. chemistry,276, 30537–30541.
Lee H, Larner JM y Hamlin JL. (1997).proc. National Academy Saber USA,94, 526–531.
Lee J, Kumagai A y Dunphy WG. (2001).minor Biol. The cell,12, 551–563.
Lee M and nurse P . (1988).Genetic trends.,4, 287–290.
Lees-Miller SP. (1996).Biochemistry Cellular Biol.,74, 503–512.
Lehmann AR, Arlett CF, Burke JF, Green MHL, James MR y Lowe JE. (1986).in t. J. Radiat. Biol.,49, 639–643.
Leone G, DeGregori J, Sears R, Jakoi L and Nevins JR. (1997).Nature,387, 422–425.
Li J, Meyer AN y Donoghue DJ. (1995).minor Biol. The cell,6, 1111–1124.
Li S, Ting NSY, Zheng L, Chen P-L, Ziv Y, Shiloh Y, Lee EY-HP y Lee W-H. (2000).Nature,406, 210–215.
Lim D-S, Kim S-T, Xu B, Maser RS, Lin J, Petrini JHJ and Chestnut MB. (2000).Nature,404, 613–617.
Lindsey-Boltz LA, Bernudez VP, Hurwitz J, and Sancar A. (2001).proc. National Academy Saber USA,98, 11236–11241.
Liu F-F, Stanton JJ, Wu Z y Cellar-Worms H. (1997).minor The cell. Biol.,17, 571–583.
Liu Q, Guntuku S, Cui XS, Matsuoka S, Cortez D, Tamai K, Luo G, Carattini-Rivera S, DeMayo F, Bradley A, Donehower LA and Elledge SJ. (2000).Genes Dev.,14, 1448–1459.
Lopez-Girona A, Kanoh J and Russell P. (2001).actual Biol.,11, 50–54.
Lou Z, Minter-Dykhouse K, Wu X y Chen J. (2003).Nature,421, 957–961.
Gap-Huhle C. (1982).radiar Res.,89, 298–308.
Lukas C, Bartkova J, Latella L, Falck J, Mailand N, Schroeder T, Sehested M, Lukas J and Bartek J. (2001).Cancer Res.,61, 4990–4993.
Lupardus PJ, Byun T, Yee M-c, Hekmat-Nejad M y Cimprich KA. (2002).Genes Dev.,sixteen, 2327–2332.
Lydall D y Weinert T. (1995).Science,270, 1488–1491.
Mailand N, Falck J, Lukas C, Syljuasen RG, Welcker M, Bartek J y Lukas J. (2000).Science,288, 1425–1429.
Maity A, Hwang A, Janss A, Phillips P, McKenna WG y Muschel RJ. (1996).oncogene,13, 1647–1657.
Maity A, McKenna WG y Muschel RJ. (1994).Radioter. oncol.,31, 1–13.
Marcu KB, Bossone SA and Patel AJ. (1992).year Rev. Biochemistry.,61, 809–860.
Maser RS, Mirzoeva OK, Wells J, Olivares H, Williams BR, Zinkel RA, Farnham PJ y Petrini JHJ. (2001).minor The cell. Biol.,21, 6006–6016.
Matsuoka S, Huang M y Elledge SJ. (1998a).Science,282, 1893–1897.
Matsuoka S, Huang M y Elledge SJ. (1998b).Science,282, 1893–1897.
Matsuoka S, Rotman G, Ogawa A, Shiloh Y, Tamai K y Elledge SJ. (2000).process Nat. Saber Academy EE.UU,97, 10389–10394.
McKenna WG. (1995).37th Annual Meeting, American Society for Therapeutic Radiology and Oncology. Miami Beach, Florida.
McKenna WG, Iliakis G, Weiss MC, Bernhard EJ and mussel RJ. (1991).radiar Res.,125, 283–287.
Melchionna R, Chen X-B, Blasina A and McGowan CH. (2000).Nat. Cell Biol.,2, 762–765.
Metzger L y Iliakis G. (1991).in t. J. Radiat. Biol.,59, 1325–1339.
Morgan DO. (1995).Nature,374, 131–134.
Shell RJ, Zhang HB, Iliakis G y McKenna WG. (1992).radiar Res.,132, 153–157.
Black ea. (1998).Current Opinion Cellular Biol.,10, 776–783.
Norbury C and the nurse P. (1992).year Rev. Biochemistry.,61, 441–470.
nurse p. (1990).Nature,344, 503–508.
nurse p. (1994).The cell,79, 547–550.
nurse p. (1997).The cell,91, 865–867.
(Video) Biological Effects of RadiationNyberg KA, Michelson RJ, Putnam CW, and Weinert TA. (2002).Rev. year Genet.,36, 617–656.
O'Connell MJ, Walworth NC y Carr AM. (2002).Cell Biol Trends.,10, 296–303.
Paciotti V, Clerici M, Lucchini G and Longhese MP. (2000).Genes Dev.,14, 2046–2059.
Pintor RB. (1981).mutated. Nothing.,84, 183–190.
Pintor RB. (1986).in t. J. Radiat. Biol.,49, 771–781.
Painter RB and Young BR. (1980).process Nat. Saber Academy EE.UU,77, 7315–7317.
Parker AE, Van de Weyer I, Laus MC, Oostveen I, Yon J, Verhasselt P y Luyten WHML. (1998).J. Biol. chemistry,273, 18332–18339.
Parker LL and Cellar-Worms H. (1992).Science,257, 1955–1957.
Paulovich AG, Toczyski DP and Hartwell LH. (1997).The cell,88, 315–321.
Peng C-Y, Graves PR, Thoma RS, Wu Z, Shaw AS y Cellar-Worms H. (1997).Science,277, 1501–1505.
Petrini JH. (2000).Current Opinion Cellular Biol.,12, 293–296.
Pinos J. (1995).Semin. Cancer Biol.,6, 63–72.
Pines J y Hunter T. (1991).J. Cell Biol.,115, 1–17.
Pines J y Hunter T. (1994).EMBÓ J.,13, 3772–3781.
Bodega-Worms H. (1999).Nature,401, 535–537.
Powell SN, DeFrank JS, Connell P, Eogan M, Preffer F, Dombkowski D, Tang W y Friend S. (1995).Cancer Res.,55, 1643–1648.
Rhind N y Russell P. (2000).J. Cell Science.,113, 3889–3896.
Rotman G y Shiloh Y. (1998).human mol Geneta.,1998, 1555–1563.
Rotman G y Shiloh Y. (1999).oncogene,18, 6135–6144.
Rouse J y Jackson SP. (2000).EMBÓ J.,19, 5801–5812.
Sampath D y Plunkett W. (2001).current Opinion oncol.,13, 484–490.
Sánchez Y, Wong C, Thoma RS, Richman R, Wu Z, Cellar-Worms H y Elledge SJ. (1997).Science,277, 1497–1501.
Santoni-Rugiu E, Falck J, Mailand N, Bartek J and Lucas J. (2000).minor The cell. Biol.,20, 3497–3509.
Schultz LB, Chehab NH, Malikzay A and Halazonetis TD. (2000).J. Cell Biol.,151, 1381–1390.
Scolnick DM and Halazonetis TD. (2000).Nature,406, 430–435.
Scully R y Livingston DM. (2000).Nature,408, 429–442.
Senderowicz AM y Sausville EA. (2000).J.Nat. cancer institute,92, 376–387.
Seoane J, Le H-V and Massague J. (2002).Nature,419, 729–734.
Sheen J-H y Dickson RB. (2002).minor The cell. Biol.,22, 1819–1833.
Sherr CJ. (1995).Trends Biol. science,20, 187–191.
Sherr CJ. (1996).Science,274, 1672–1677.
Sherr CJ y Roberts JM. (1995).Genes Dev.,9, 1149–1163.
Sherr CJ y Roberts JM. (1999).Genes Dev.,13, 1501–1512.
Shiloh Y. (2001).Current Genetic Opinion. development,11, 71–77.
Sillje HHW and Nigg EA. (2003).Science,299, 1190–1192.
Smeets MFMA, Mooren EHM, Abdel-Wahab AHA, Bartelink H y Begg AC. (1994).radiar Res.,140, 153–160.
Smith GCM, Cary RB, Lakin ND, Hann BC, Teo S-H, Chen DJ y Jackson SP. (1999).proc. National Academy Saber USA,96, 11134–11139.
Smith GCM y Jackson SP. (1999).Genes Dev.,13, 916–934.
Smith S. (2001).Biochemical trends. science,26, 175–180.
Smits VAJ, Klompmaker R, Arnaud L, Rijksen G, Nigg EA and Medema RH. (2000).Nat. Cell Biol.,2, 672–676.
Smits VAJ and Medema RH. (2001).biochemistry Biography. minutes,1519, 1–12.
Somasundaram K, Zhang H, Zeng YX, Houvras Y, Peng Y, Wu GS, Licht JD, Weber BL y El-Deiry WS. (1997).Nature,389, 187–190.
Stewart GS, Wang B, Rignell CR, Taylor AMR y Elledge SJ. (2003).Nature,421, 961–966.
Stillman B. (1994).The cell,78, 725–728.
Stillman B. (1996).Science,274, 1659–1664.
Stokes MP, Van Hatten R, Lindsay HD and Michael WM. (2002).J. Cell Biol.,158, 863–872.
His L and little JB. (1993).radiar Res.,133, 73–79.
(Video) DNA Damage ResponseSuganuma M, Kawabe T, Hori H, Funabiki T y Okamoto T. (1999).Cancer Res.,59, 5887–5891.
Takai H, Tominaga K, Motoyama N, Minamishima YA, Nagahama H, Tsukiyama T, Ikeda K, Nakayama K y Nakanishi M. (2000).Genes Dev.,14, 1439–1447.
Taylor WR, Agarwall ML, Agarwal A, Stacey D y Stark GR. (1999).oncogene,18, 283–295.
Taylor WR y Stark GR. (2001).oncogene,20, 1803–1815.
Terada Y, Tatsuka M, Jinno S y Okayama H. (1995).Nature,376, 358–362.
Thompson LH and Schild D (2001).mutated. Nothing.,477, 131–153.
Thompson LH and Schild D (2002).mutated. Nothing.,509, 49–78.
Tibbetts RS, Brumbaugh KM, Williams JM, Sarkaria JN, Cliby WA, Shieh S-Y, Taya Y, Prives C y Abraham RT. (1999).Genes Dev.,13, 152–157.
Tibbetts RS, Cortez D, Brumbaugh KM, Scully R, Livingston D, Elledge SJ y Abraham RT. (2000).Genes Dev.,14, 2989–3002.
Tobey RA. (1975).Nature,254, 245–247.
Toyoshima F, Moriguchi T, Wada A, Fukuda M y Nishida E. (1998).EMBÓ J.,17, 2728–2735.
Corbata BK. (1999).year Rev. Biochemistry.,68, 649–686.
van Gent DC, Hoeijmakers JHJ y Kanaar R. (2001).Nat. Rev. Genet.,2, 196–206.
van Vugt MATM, Smits VAJ, Klompmaker R y Medema RH. (2001).J. Biol. chemistry,276, 41656–41660.
Venkitaraman AR. (2001).J. Cell Science.,114, 3591–3598.
Vogelstein B, Lane DP y Levine AJ. (2000).Nature,408, 307–310.
Volkmer E and Karnitz LM. (1999).J. Biol. chemistry,274, 567–570.
Wakayama T, Kondo T, Ando S, Matsumoto K y Sugimoto K. (2001).minor The cell. Biol.,21, 755–764.
Walters RA, Gurley LR y Tobey RA. (1974).Biography. j,14, 99–118.
Walworth North Carolina. (2001).Current Genetic Opinion. development,11, 78–82.
Wang H, Wang X, Iliakis G y Wang Y. (2003a).radiar Res.,159, 420–425.
Wang H, Zeng Z-C, Bui T-A, DiBiase SJ, Qin W, Xia F, Powell SN e Iliakis G. (2001a).Cancer Res.,61, 270–277.
Wang H, Zeng Z-C, Bui T-A, Sonoda E, Takata M, Takeda S and Iliakis G. (2001b).oncogene,20, 2212–2224.
Wang JYY. (2000).Nature,405, 404–405.
Wang X, Wang H, Iliakis G y Wang Y. (2003b).radiar Res.. (in press).
Wang Y, Cortez D, Yazdi P, Neff N, Elledge SJ and Qin J. (2000).Genes Dev.,14, 927–939.
Wang Y, Huq MS, Cheng X and Iliakis G. (1995).radiar Res.,142, 169–175.
Wang Y, Zhou XY, Wang H-Y e Iliakis G. (1999).J. Biol. chemistry,274, 22060–22064.
Weichselbaum RR, Nove J and Little JB. (1978).Nature,271, 261–262.
Volkov TD y Enoch T. (2002).minor Biol. The cell,13, 480–492.
Wu X, Ranganathan V, Weisman DS, Heine WF, Ciccone DN, O'Neill TB, Crick KE, Pierce KA, Lane WS, Rathbun G, Livingston DM y Weaver DT. (2000).Nature,405, 477–482.
[ PubMed ] Xia F, Taghian DG, DeFrank JS, Zeng Z-C, Willers H, Iliakis G and Powell SN. (2001).proc. National Academy Saber USA,98, 8644–8649.
Xie S, Wu H, Wang Q, Cogswell P, Husain I, Conn C, Stambrook P, Jhanwar-Uniyal M y Dai W. (2001).J. Biol. chemistry,276, 43305–43312.
Xiong Y, Zhang H y Beach D. (1992).The cell,71, 505–514.
Xu B, Kim S-t y Kastan MB. (2001).minor The cell. Biol.,21, 3445–3450.
Xu B, Kim S-T, Lim D-S y Kastan MB. (2002).minor The cell. Biol.,22, 1049–1059.
Yamane K, Wu X and Chen J. (2002).minor The cell. Biol.,22, 555–566.
Yang J, Bardes ESG, Moore JD, Brennan J, Powers MA and Kornbluth S. (1998).Genes Dev.,12, 2131–2143.
[ PubMed ] Yarden RI, Brown-Reoyo S, Sgagias M, Cowan KH and Brody LC. (2002).Nat. Ginetta.,30, 285–289.
Yazdi PT, Wang Y, Zhao S, Patel N, Lee EY-HP y Qin J. (2002).Genes Dev.,sixteen, 571–582.
Yu Q, Geng Y and Sicinski P. (2001).Nature,411, 1017–1021.
Zachos G, Rainey MD y Gillespie DAF. (2003).EMBÓ J.,22, 713–723.
Zhao H, Watkins JL and Cellar-Worms H. (2002).proc. National Academy Saber USA,99, 14795–14800.
Zhao S, Weng Y-C, Yuan S-SF, Lin Y-T, Hsu HC, Lin S-CJ, Gerbino E, Song M-h, Zdzienicka MZ, Gatti RA, Shay JW, Ziv Y, Shiloh Y y Lee EY-HP. (2000).Nature,405, 473–477.
Zhou B-BS, Chaturvedi P, Spring K, Scott SP, Johanson RA, Mishra R, Mattern MR, Winkler JD y Khanna KK. (2000).J. Biol. chemistry,275, 10342–10348.
Zhou B-BS y Elledge SJ. (2000).Nature,408, 433–439.
Zhou X-Y, Wang X, Hu B, Guan J, Iliakis G, and Wang Y. (2002).Cancer Res.,62, 1598–1603.
(Video) DNA Repair and Cell Response to DamageZiegler My Oei SL. (2001).Bioensayos,23, 543–548.
Zou L, Cortez D and Elledge SJ. (2002).Genes Dev.,sixteen, 198–208.
FAQs
Control of DNA damage checkpoints in cells exposed to ionizing radiation? ›
Damage induced in the DNA after exposure of cells to ionizing radiation activates checkpoint pathways that inhibit progression of cells through the G1 and G2 phases and induce a transient delay in the progression through S phase.
What checkpoint is affected by ionizing radiation? ›Abstract. Exposure of cells to DNA-damaging agents, such as ionizing radiation (IR), results in perturbation of cell cycle progression. IR activates cell cycle checkpoints that arrest the cell cycle at the G1/S, S, and G2/M phases.
What will happen to the DNA if we are expose to ionizing radiation? ›Ionizing radiation directly affects DNA structure by inducing DNA breaks, particularly, DSBs. Secondary effects are the generation of reactive oxygen species (ROS) that oxidize proteins and lipids, and also induce several damages to DNA, like generation of abasic sites and single strand breaks (SSB).
What checkpoints occur in the cell cycle after ionizing radiation exposure? ›Cell cycle checkpoints exist at the G1/S and G2/M boundary and are thought to prevent cells from replication or undergoing mitosis, respectively, in the presence of DNA damage. Furthermore, DSB induction can cause slowing of replication by locally inhibiting replication fork progression and new origin firing.
What is the checkpoint for DNA damage? ›A DNA damage checkpoint is a pause in the cell cycle that is induced in response to DNA damage to ensure that the damage is repaired before cell division resumes. Proteins that accumulate at the damage site typically activate the checkpoint and halt cell growth at the G1/S or G2/M boundaries.
What does the G1 checkpoint check for? ›At the G1 checkpoint, cells decide whether or not to proceed with division based on factors such as: Cell size. Nutrients. Growth factors.
What is the G1 damage checkpoint? ›The G1/S checkpoint prevents cells from entering the S phase in the presence of the DNA damage by inhibiting the initiation of replication. There are two signal transduction pathways, one to initiate and one to maintain the G1/S arrest [1].
What happens when biological cells exposed to ionizing radiation? ›Biological effects
Ionizing radiation is more harmful than nonionizing radiation because it has enough energy to remove an electron from an atom and thereby directly damage biological material. The energy is enough to damage DNA, which can result in cell death or cancer.
Direct damage is caused by the ionizing radiation causing an ionization in the DNA molecules itself. Indirect damage is caused by free radicals created in the surrounding cytoplasm of a cell but I was in radiation, which then attack and damage the DNA molecules.
What are the direct and indirect action of ionizing radiation on DNA? ›Direct-type damage results from radiation energy being deposited directly into the DNA, whereas indirect damage occurs when the species created by the interaction of the primary radiation and SEs within the molecular environment surrounding the DNA (e.g., salts, proteins, oxygen and water) react with the molecule.
What are checkpoints in the cell cycle controlled by? ›
The central machines that drive cell cycle progression are the cyclin-dependent kinases (CDKs). These are serine/threonine protein kinases that phosphorylate key substrates to promote DNA synthesis and mitotic progression.
What are the 3 checkpoints in the cell cycle? ›Cell-cycle checkpoints prevent the transmission of genetic errors to daughter cells. There exist three major cell-cycle checkpoints; the G1/S checkpoint, the G2/M checkpoint, and the spindle assembly checkpoint (SAC).
Where are the 3 checkpoints in the cell cycle? ›Each step of the cell cycle is monitored by internal controls called checkpoints. There are three major checkpoints in the cell cycle: one near the end of G1, a second at the G2/M transition, and the third during metaphase.
What activates the DNA damage checkpoint? ›Damage induced in the DNA after exposure of cells to ionizing radiation activates checkpoint pathways that inhibit progression of cells through the G1 and G2 phases and induce a transient delay in the progression through S phase.
Which checkpoints will the cell cycle stop if DNA damage is detected? ›The G2 Checkpoint
If the checkpoint mechanisms detect problems with the DNA, the cell cycle is halted, and the cell attempts to either complete DNA replication or repair the damaged DNA.
The G1 Checkpoint
The cell will only pass the checkpoint if it is an appropriate size and has adequate energy reserves. At this point, the cell also checks for DNA damage. A cell that does not meet all the requirements will not progress to the S phase.
G2/M checkpoints include the checks for damaged DNA, unreplicated DNA, and checks that ensure that the genome is replicated once and only once per cell cycle. If cells pass these checkpoints, they follow normal transition to the M phase.
What happens at the G2 M checkpoint? ›Abstract. The G2 checkpoint prevents cells from entering mitosis when DNA is damaged, providing an opportunity for repair and stopping the proliferation of damaged cells. Because the G2 checkpoint helps to maintain genomic stability, it is an important focus in understanding the molecular causes of cancer.
What is the G2 checkpoint used for? ›The G2/M checkpoint prevents cells from entering mitosis when DNA is damaged in order to afford these cells an opportunity to repair the damaged DNA before propagating genetic defects to the daughter cells. If the damage is irreparable, checkpoint signaling might activate pathways that lead to apoptosis.
What does G1 checkpoint regulate? ›G1 is usually where critical decisions are made as to whether to enter a resting quiescent stage known as G0 or to continue cycling and commit to replicating the genome and mitosis. The point in G1 where this growth factor–dependent decision is made is known as the restriction point (R).
Why is the DNA damage checkpoint in G1 important? ›
The G1 to S checkpoint prevents replication of damaged DNA. Essentially, this process is able to arrest the cell cycle through the functions of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3 related, which phosphorylate a number of substrate proteins in response to DNA damage.
How is G1 controlled? ›In mammalian cells, G1–S genes are regulated by several E2F transcription factor complexes at different stages of the cell cycle. In yeast, G1–S transcripts can be roughly divided into two groups: SBF- or MBF-dependent genes.
How does ionizing radiation damage biological tissue? ›Direct Damage occurs when radiation damages the DNA directly, causing ionization of the atoms in the DNA molecule. Ionisation of molecule invariably leads to its disruption. Indirect Damage occurs when radiation interacts with non-critical target atoms or molecules, usually water.
What can ionising radiation damage cells cause? ›Radiation of certain wavelengths, called ionizing radiation, has enough energy to damage DNA and cause cancer. Ionizing radiation includes radon, x-rays, gamma rays, and other forms of high-energy radiation.
Can ionizing radiation cause DNA mutations? ›Ionizing radiation damages the genetic material in reproductive cells and results in mutations that are transmitted from generation to generation.
What are the most common effects of ionizing radiation? ›Beyond certain thresholds, radiation can impair the functioning of tissues and/or organs and can produce acute effects such as skin redness, hair loss, radiation burns, or acute radiation syndrome. These effects are more severe at higher doses and higher dose rates.
What is the specific effect of ionizing radiation on cell chromosomes? ›When cells are exposed to radiation or carcinogens, DNA sometimes breaks, and the broken ends may rejoin in different patterns from their original arrangement. The abnormalities that result are termed “chromosome aberrations” and may be visualized at mitosis when cells divide.
What are some types of ionizing radiation that can cause mutations in the DNA of cells? ›High energy ionization radiations such as X-rays and gamma rays cause extensive damage to DNA in the form of destruction to their sugars and nitrogenous bases along with strand breaks. Non-ionizing radiation such as ultraviolet light, on the other hand, induces structural changes in the bases of the DNA.
What are the effects of non-ionizing radiation on DNA? ›While IR directly damages DNA, NIR interferes with the oxidative repair mechanisms resulting in oxidative stress, damage to cellular components including DNA, and damage to cellular processes leading to cancer.
What happens when DNA is damaged? ›At the cellular level, damaged DNA that is not properly repaired can lead to genomic instability, apoptosis, or senescence, which can greatly affect the organism's development and ageing process.
What will happen to the cells if there are no control checkpoints in the various stages of the cell cycle? ›
If a checkpoint fails or if a cell suffers physical damage to chromosomes during cell division, or if it suffers a debilitating somatic mutation in a prior S phase, it may selfdestruct in response to a consequent biochemical anomaly.
What are the two different types of checkpoints? ›There are two types of checkpoints in Hyper-V: standard checkpoints and production checkpoints. Both capture the state, data and configuration details of a running VM. The difference is in data consistency. A standard checkpoint only provides application consistency, not data consistency.
How is the checkpoint system in the cell cycle helpful in making sure that a cell divides normally? ›The DNA Replication Checkpoint Arrests the Cell Cycle
The checkpoints detect various issues found on DNA. Once checkpoint proteins identify these issues, the cell activates signal transduction pathways in order to arrest the progression of the cell cycle and allow adequate time to fix the problems on DNA.
Several cell cycle checkpoints function to ensure that incomplete or damaged chromosomes are not replicated and passed on to daughter cells (Figure 14.8). One of the most clearly defined of these checkpoints occurs in G2 and prevents the initiation of mitosis until DNA replication is completed.
What is the restriction point in the cell cycle? ›The point at G1 at which commitment occurs and the cell no longer requires growth factors to complete the cell cycle has been termed the restriction (R) point. The R point has been temporally mapped at 2–3 hours prior to the onset of DNA synthesis.
What are the checkpoints in the cell cycle quizlet? ›What are cell checkpoints? A checkpoint is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cycle can be halted until conditions are favorable. These checkpoints occur near the end of G1, at the G2/M transition, and during metaphase.
What are the 4 stages of the cell cycle? ›The cell cycle is a 4-stage process consisting of Gap 1 (G1), synthesis (S), Gap 2 (G2), and mitosis (M), which a cell undergoes as it grows and divides. After completing the cycle it either starts the process again from G1 or exits through G0.
How do cells detect DNA damage? ›The protein UvrA recognizes damaged DNA and recruits UvrB and UvrC to the site of the lesion. UvrB and UvrC then cleave on the 3′ and 5′ sides of the damaged site, respectively, thus excising an oligonucleotide consisting of 12 or 13 bases.
What is the most restricted checkpoint in the cell cycle? ›The G1 checkpoint, also known as the restriction point in mammalian cells and the start point in yeast, is the point at which the cell becomes committed to entering the cell cycle.
What happens if a cell stops at the G1 checkpoint? ›If the cell stops at the G1 checkpoint, it has been arrested before it can enter the S phase and its chromosomes will be unable to replicate.
What can be affected by ionizing radiation? ›
Ionizing radiation can affect the atoms in living things, so it poses a health risk by damaging tissue and DNA in genes. has sufficient energy to affect the atoms in living cells and thereby damage their genetic material (DNA). Fortunately, the cells in our bodies are extremely efficient at repairing this damage.
What body parts are affected by ionizing radiation? ›Large doses of ionizing radiation can cause acute illness by reducing the production of blood cells and damaging the digestive tract. A very large dose of ionizing radiation can also damage the heart and blood vessels (cardiovascular system), brain, and skin.
What happens at Checkpoint 2? ›G2 checkpoint – DNA quality control
After the second growth phase, the cell checks that the DNA was completely and correctly replicated during the S phase. If it passes it enters the M phase, and if it fails it tries to correct the errors. If the cell is unable to repair the DNA, it undergoes apoptosis.
When cells are exposed to ionizing radiation, they initiate a complex response that includes the arrest of cell cycle progression in G1 and G2, apoptosis and DNA repair.
What does ionizing radiation do to cells? ›Ionizing activity can alter molecules within the cells of our body. That action may cause eventual harm (such as cancer). Intense exposures to ionizing radiation may produce skin or tissue damage.
What is the major effect of ionizing radiation on the cell? ›When ionizing radiation interacts with cells, it can cause damage to the cells and genetic material (i.e., deoxyribonucleic acid, or DNA). If not properly repaired, this damage can result in the death of the cell or potentially harmful changes in the DNA (i.e., mutations).
What cells are most sensitive to ionizing radiation? ›Immature (undifferentiated) hematopoietic cells that have divided (proliferated) from stem cells are highly sensitive to radiation and die due to a small amount of radiation more easily than differentiated cells.
Which part of the cell is the most sensitive to ionizing radiation? ›Lymphocytes (white blood cells) and cells which produce blood are constantly regenerating, and are, therefore, the most sensitive. Reproductive and gastrointestinal cells are not regenerating as quickly and are less sensitive.
What are the 3 major checkpoints and what does each checkpoint do? ›The cell cycle is controlled at three checkpoints. The integrity of the DNA is assessed at the G1 checkpoint. Proper chromosome duplication is assessed at the G2 checkpoint. Attachment of each kinetochore to a spindle fiber is assessed at the M checkpoint.
What happens at the G1 checkpoint and the G2 checkpoint? ›Damage to DNA and other external factors are evaluated at the G1 checkpoint; if conditions are inadequate, the cell will not be allowed to continue to the S phase of interphase. The G2 checkpoint ensures all of the chromosomes have been replicated and that the replicated DNA is not damaged before cell enters mitosis.
What happens at the G2 checkpoint and how is it controlled? ›
The G2/M checkpoint prevents cells from entering mitosis when DNA is damaged in order to afford these cells an opportunity to repair the damaged DNA before propagating genetic defects to the daughter cells. If the damage is irreparable, checkpoint signaling might activate pathways that lead to apoptosis.
How does ionizing radiation halt cell division? ›Exposure to ionizing radiation is known to affect cell-cycle progression: radiation causes DNA damage, and an arrest in cell-cycle progression follows as the cell activates DNA repair mechanisms.
What are the effects of ionizing radiation at cellular and molecular level? ›Ionizing radiation can interact directly with a DNA molecule's atoms. This prevents cells from reproducing. Direct action can also damage critical cellular systems. Sometimes, it can even lead to cancer.
What part of the cell cycle does radiation target? ›It is well known that radiation causes cells to transiently arrest the progression through the cell cycle (Iliakis et al. 2003). This arrest takes place at the so-called cell cycle checkpoints in G1, S, and G2 phases (Fig. 4).