Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage

Checkpoint response to DNA damage involves the activation of DNA repair and G2 lengthening subpathways. The roles of nibrin (NBS1) and the ATM/ATR kinases in the G2 DNA damage checkpoint, evoked by endogenous and radio-induced DNA damage, were analyzed in control, A-T and NBS lymphoblast cell lines....

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Autores principales:	Marcelain,Katherine, de la Torre,Consuelo, González,Patricio, Pincheira,Juana
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2005
Materias:	ataxia-telangiectasia ATM ATR kinases caffeine G2 checkpoint nibrin (Nbs1) Nijmegen breakage syndrome (NBS)
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602005000200007
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spelling	oai:scielo:S0716-976020050002000072007-01-04Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damageMarcelain,Katherinede la Torre,ConsueloGonzález,PatricioPincheira,Juana ataxia-telangiectasia ATM ATR kinases caffeine G2 checkpoint nibrin (Nbs1) Nijmegen breakage syndrome (NBS) Checkpoint response to DNA damage involves the activation of DNA repair and G2 lengthening subpathways. The roles of nibrin (NBS1) and the ATM/ATR kinases in the G2 DNA damage checkpoint, evoked by endogenous and radio-induced DNA damage, were analyzed in control, A-T and NBS lymphoblast cell lines. Short-term responses to G2 treatments were evaluated by recording changes in the yield of chromosomal aberrations in the ensuing mitosis, due to G2 checkpoint adaptation, and also in the duration of G2 itself. The role of ATM/ATR in the G2 checkpoint pathway repairing chromosomal aberrations was unveiled by caffeine inhibition of both kinases in G2. In the control cell lines, nibrin and ATM cooperated to provide optimum G2 repair for endogenous DNA damage. In the A-T cells, ATR kinase substituted successfully for ATM, even though no G2 lengthening occurred. X-ray irradiation (0.4 Gy) in G2 increased chromosomal aberrations and lengthened G2, in both mutant and control cells. However, the repair of radio-induced DNA damage took place only in the controls. It was associated with nibrin-ATM interaction, and ATR did not substitute for ATM. The absence of nibrin prevented the repair of both endogenous and radio-induced DNA damage in the NBS cells and partially affected the induction of G2 lengthening.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.38 n.2-3 20052005-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602005000200007en10.4067/S0716-97602005000200007
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	ataxia-telangiectasia ATM ATR kinases caffeine G2 checkpoint nibrin (Nbs1) Nijmegen breakage syndrome (NBS)
spellingShingle	ataxia-telangiectasia ATM ATR kinases caffeine G2 checkpoint nibrin (Nbs1) Nijmegen breakage syndrome (NBS) Marcelain,Katherine de la Torre,Consuelo González,Patricio Pincheira,Juana Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage
description	Checkpoint response to DNA damage involves the activation of DNA repair and G2 lengthening subpathways. The roles of nibrin (NBS1) and the ATM/ATR kinases in the G2 DNA damage checkpoint, evoked by endogenous and radio-induced DNA damage, were analyzed in control, A-T and NBS lymphoblast cell lines. Short-term responses to G2 treatments were evaluated by recording changes in the yield of chromosomal aberrations in the ensuing mitosis, due to G2 checkpoint adaptation, and also in the duration of G2 itself. The role of ATM/ATR in the G2 checkpoint pathway repairing chromosomal aberrations was unveiled by caffeine inhibition of both kinases in G2. In the control cell lines, nibrin and ATM cooperated to provide optimum G2 repair for endogenous DNA damage. In the A-T cells, ATR kinase substituted successfully for ATM, even though no G2 lengthening occurred. X-ray irradiation (0.4 Gy) in G2 increased chromosomal aberrations and lengthened G2, in both mutant and control cells. However, the repair of radio-induced DNA damage took place only in the controls. It was associated with nibrin-ATM interaction, and ATR did not substitute for ATM. The absence of nibrin prevented the repair of both endogenous and radio-induced DNA damage in the NBS cells and partially affected the induction of G2 lengthening.
author	Marcelain,Katherine de la Torre,Consuelo González,Patricio Pincheira,Juana
author_facet	Marcelain,Katherine de la Torre,Consuelo González,Patricio Pincheira,Juana
author_sort	Marcelain,Katherine
title	Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage
title_short	Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage
title_full	Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage
title_fullStr	Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage
title_full_unstemmed	Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage
title_sort	roles of nibrin and atm/atr kinases on the g2 checkpoint under endogenous or radio-induced dna damage
publisher	Sociedad de Biología de Chile
publishDate	2005
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602005000200007
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Roles of nibrin and ATM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage

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