-
1
-
-
0032999346
-
Sister chromatid exchanges are mediated by homologous recombination in vertebrate cells
-
Many DNA-damaging agents induce sister chromatid exchanges (SCEs). Using the chicken DT40 cell line with defined defects in HR or NHEJ, it is shown that Rad51 and Rad54, but not Ku70, affect the spontaneous or mitomycin C-induced SCE frequency.
-
Sonoda E., Sasaki M.S., Morrison C., Yamaguchi-Iwai Y., Takata M., Takeda S. Sister chromatid exchanges are mediated by homologous recombination in vertebrate cells. Mol Cell Biol. 19:1999;5166-5169. Many DNA-damaging agents induce sister chromatid exchanges (SCEs). Using the chicken DT40 cell line with defined defects in HR or NHEJ, it is shown that Rad51 and Rad54, but not Ku70, affect the spontaneous or mitomycin C-induced SCE frequency.
-
(1999)
Mol Cell Biol
, vol.19
, pp. 5166-5169
-
-
Sonoda, E.1
Sasaki, M.S.2
Morrison, C.3
Yamaguchi-Iwai, Y.4
Takata, M.5
Takeda, S.6
-
2
-
-
0033213392
-
Brca1 controls homology-directed repair
-
-/- mouse cells are selectively deficient in homologous recombination measured by targeted integration of transfected DNA as well as by DSB repair by homologous recombination.
-
-/- mouse cells are selectively deficient in homologous recombination measured by targeted integration of transfected DNA as well as by DSB repair by homologous recombination.
-
(1999)
Mol Cell
, vol.4
, pp. 511-518
-
-
Moynahan, M.E.1
Chiu, J.W.2
Koller, B.H.3
Jasin, M.4
-
3
-
-
0033560796
-
The DNA-dependent protein kinase
-
Smith G.S.M., Jackson S.P. The DNA-dependent protein kinase. Genes Dev. 13:1999;916-934.
-
(1999)
Genes Dev
, vol.13
, pp. 916-934
-
-
Smith, G.S.M.1
Jackson, S.P.2
-
4
-
-
0033167979
-
DNA-dependent protein kinase is not required for the p53-dependent response to DNA damage
-
The defective p53 response in the DNA-PK deficient SCGR11 cell line - which was considered to reflect the interdependence of p53 and DNA-PK - is here shown to be a consequence of a p53 mutation. In cells expressing a wild-type p53, p53 activation is demonstrated in the absence of a functional DNA-PK. This is in agreement with several other lines of evidence which indicate that p53-related checkpoint functions are activated independently of DNA-PK.
-
Jimenez G.S., Bryntesson F., Torres-Arzayus M.I., Priestly A., Beeche M., Saito S., Sakaguchi K., Appella E., Jeggo P.A., Taccioli G.E.et al. DNA-dependent protein kinase is not required for the p53-dependent response to DNA damage. Nature. 400:1999;81-83. The defective p53 response in the DNA-PK deficient SCGR11 cell line - which was considered to reflect the interdependence of p53 and DNA-PK - is here shown to be a consequence of a p53 mutation. In cells expressing a wild-type p53, p53 activation is demonstrated in the absence of a functional DNA-PK. This is in agreement with several other lines of evidence which indicate that p53-related checkpoint functions are activated independently of DNA-PK.
-
(1999)
Nature
, vol.400
, pp. 81-83
-
-
Jimenez, G.S.1
Bryntesson, F.2
Torres-Arzayus, M.I.3
Priestly, A.4
Beeche, M.5
Saito, S.6
Sakaguchi, K.7
Appella, E.8
Jeggo, P.A.9
Taccioli, G.E.10
-
5
-
-
0033119394
-
DNA binding of Xrcc4 protein is associated with V(D)J recombination but not with stimulation of DNA ligase IV
-
XRCC4 is shown to exhibit cooperative binding to DNA. This stimulates the adenylation of DNA ligase IV. The phosphorylated form of XRCC4 is shown to lack DNA-binding activity.
-
Modesti M., Hesse J.E., Gellert M. DNA binding of Xrcc4 protein is associated with V(D)J recombination but not with stimulation of DNA ligase IV. EMBO J. 18:1999;2008-2018. XRCC4 is shown to exhibit cooperative binding to DNA. This stimulates the adenylation of DNA ligase IV. The phosphorylated form of XRCC4 is shown to lack DNA-binding activity.
-
(1999)
EMBO J
, vol.18
, pp. 2008-2018
-
-
Modesti, M.1
Hesse, J.E.2
Gellert, M.3
-
6
-
-
0032933430
-
The C terminus of Ku80 activates the DNA-dependent protein kinase catalytic subunit
-
Analysis of mutations in the hamster Ku80 identifies a carboxy-terminal 178 amino acid region as being essential for stimulation of DNA-PK. This region is distinct from the one which interacts with Ku70.
-
Singleton B.K., Torres-Arzayus M.I., Rottinghaus S.T., Taccioli G.E., Jeggo P.A. The C terminus of Ku80 activates the DNA-dependent protein kinase catalytic subunit. Mol Cell Biol. 19:1999;3267-3277. Analysis of mutations in the hamster Ku80 identifies a carboxy-terminal 178 amino acid region as being essential for stimulation of DNA-PK. This region is distinct from the one which interacts with Ku70.
-
(1999)
Mol Cell Biol
, vol.19
, pp. 3267-3277
-
-
Singleton, B.K.1
Torres-Arzayus, M.I.2
Rottinghaus, S.T.3
Taccioli, G.E.4
Jeggo, P.A.5
-
7
-
-
0033104498
-
Structure of DNA dependent protein kinase: Implications for its regulation by DNA
-
Analysis of DNA-PKcs crystallised on a lipid layer reveals an intriguing three-dimensional structure. On the basis of its affinities for different DNA structures, a model for how DNA-PK might operate in DSB rejoining is proposed.
-
Leuther K.K., Hammarstan O., Kornberg R.D., Chu G. Structure of DNA dependent protein kinase: implications for its regulation by DNA. EMBO J. 18:1999;1114-1123. Analysis of DNA-PKcs crystallised on a lipid layer reveals an intriguing three-dimensional structure. On the basis of its affinities for different DNA structures, a model for how DNA-PK might operate in DSB rejoining is proposed.
-
(1999)
EMBO J
, vol.18
, pp. 1114-1123
-
-
Leuther, K.K.1
Hammarstan, O.2
Kornberg, R.D.3
Chu, G.4
-
8
-
-
0032511976
-
Late embryonic lethality and impaired V(D)J recombination in mice lacking DNA ligase IV
-
Frank K.M., Sekiguchi J.M., Seidl K.J., Swat W., Rathburn G.A., Cheng H.L., Davidson L., Kangaloo L., Alt F.W. Late embryonic lethality and impaired V(D)J recombination in mice lacking DNA ligase IV. Nature. 396:1998;173-177.
-
(1998)
Nature
, vol.396
, pp. 173-177
-
-
Frank, K.M.1
Sekiguchi, J.M.2
Seidl, K.J.3
Swat, W.4
Rathburn, G.A.5
Cheng, H.L.6
Davidson, L.7
Kangaloo, L.8
Alt, F.W.9
-
9
-
-
0032585526
-
Targeted disruption of the gene encoding DNA ligase IV leads to lethality in embryonic mice
-
Barnes D.E., Stamp G., Rosewell I., Denzel A., Lindahl T. Targeted disruption of the gene encoding DNA ligase IV leads to lethality in embryonic mice. Curr Biol. 8:1998;1395-1398.
-
(1998)
Curr Biol
, vol.8
, pp. 1395-1398
-
-
Barnes, D.E.1
Stamp, G.2
Rosewell, I.3
Denzel, A.4
Lindahl, T.5
-
10
-
-
0032417640
-
A critical role for DNA end-joining proteins in both lymphomagenesis and neurogenesis
-
•,8] together implicate mouse DNA ligase IV and XRCC4 in an essential developmental function. Animals defective for either gene exhibit embryonic lethality with a characteristic impairment of central nervous system development as well as the anticipated defect in V(D)J recombination. The inviability of these mice contrasts with the viability of Ku or DNA-PKcs mutant mice which strongly suggests an additional role for DNA ligase IV/XRCC4.
-
•,8] together implicate mouse DNA ligase IV and XRCC4 in an essential developmental function. Animals defective for either gene exhibit embryonic lethality with a characteristic impairment of central nervous system development as well as the anticipated defect in V(D)J recombination. The inviability of these mice contrasts with the viability of Ku or DNA-PKcs mutant mice which strongly suggests an additional role for DNA ligase IV/XRCC4.
-
(1998)
Cell
, vol.95
, pp. 891-902
-
-
Gao, Y.1
Sun, Y.2
Frank, K.M.3
Dikkes, P.4
Fujiwara, Y.5
Seidl, K.J.6
Sekiguchi, J.M.7
Rathburn, G.A.8
Swat, W.9
Wang, J.10
-
11
-
-
0033166623
-
Identification of a defect in DNA ligase IV in a radiosensitive leukaemia patient
-
A human cell line from a radiation-sensitive leukaemia patient is shown to have a mutated DNA ligase IV with a severely limited ability to undergo adenylation. Yeast cells expressing the mutated ligase are extremely sensitive to ionizing radiation and deficient in NHEJ in vitro.
-
Riballo E., Crichlow S.E., Teo S-H., Doherty A.J., Priestly A., Broughton B., Kysela B., Beamish H., Plowman N., Arlett C.F.et al. Identification of a defect in DNA ligase IV in a radiosensitive leukaemia patient. Curr Biol. 9:1999;699-702. A human cell line from a radiation-sensitive leukaemia patient is shown to have a mutated DNA ligase IV with a severely limited ability to undergo adenylation. Yeast cells expressing the mutated ligase are extremely sensitive to ionizing radiation and deficient in NHEJ in vitro.
-
(1999)
Curr Biol
, vol.9
, pp. 699-702
-
-
Riballo, E.1
Crichlow, S.E.2
Teo, S.-H.3
Doherty, A.J.4
Priestly, A.5
Broughton, B.6
Kysela, B.7
Beamish, H.8
Plowman, N.9
Arlett, C.F.10
-
12
-
-
0032127849
-
Role of the human RAD51 protein in homologous recombination and double-stranded break repair
-
Baumann P., West S.C. Role of the human RAD51 protein in homologous recombination and double-stranded break repair. Trends Biochem Sci. 23:1998;247-251.
-
(1998)
Trends Biochem Sci
, vol.23
, pp. 247-251
-
-
Baumann, P.1
West, S.C.2
-
13
-
-
0000391880
-
Evidence for DNA PK-dependent and -independent DNA double-strand break repair pathways in mammalian cells as a function of the cell cycle
-
2 phase does not affect radiation sensitivity or rejoining.
-
2 phase does not affect radiation sensitivity or rejoining.
-
(1997)
Mol Cell Biol
, vol.17
, pp. 1425-1433
-
-
Lee, S.E.1
Mitchell, R.A.2
Cheng, A.3
Hendrickson, E.A.4
-
14
-
-
0032556870
-
Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A
-
New J.H., Sugiyama T., Zaitseva E., Kowalczylkowski S.C. Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A. Nature. 391:1998;407-409.
-
(1998)
Nature
, vol.391
, pp. 407-409
-
-
New, J.H.1
Sugiyama, T.2
Zaitseva, E.3
Kowalczylkowski, S.C.4
-
15
-
-
0032556865
-
Synergistic actions of Rad51 and Rad52 in recombination and DNA repair
-
Benson F.E., Baumann P., West S.C. Synergistic actions of Rad51 and Rad52 in recombination and DNA repair. Nature. 391:1998;401-404.
-
(1998)
Nature
, vol.391
, pp. 401-404
-
-
Benson, F.E.1
Baumann, P.2
West, S.C.3
-
16
-
-
0033594407
-
Binding of double strand breaks in DNA by human Rad52 protein
-
Human Rad52 protein is shown to be an alternative DNA end binding activity to Ku. By analogy to Ku/DNA-PK in NHEJ, it is proposed that end binding by hRad52 initiates the HR repair pathways.
-
Van Dyck E., Stasiak A.Z., Stasiak A., West S.C. Binding of double strand breaks in DNA by human Rad52 protein. Nature. 398:1999;728-731. Human Rad52 protein is shown to be an alternative DNA end binding activity to Ku. By analogy to Ku/DNA-PK in NHEJ, it is proposed that end binding by hRad52 initiates the HR repair pathways.
-
(1999)
Nature
, vol.398
, pp. 728-731
-
-
Van Dyck, E.1
Stasiak, A.Z.2
Stasiak, A.3
West, S.C.4
-
17
-
-
0029909565
-
A mutation in mouse rad51 results in an early embryonic lethal that is suppressed by a mutation in p53
-
-/- mice and radiation sensitivity in embryonic cells. This also appears to be the first indication that the cytotoxic effects of impaired DSB rejoining may be mediated by p53.
-
-/- mice and radiation sensitivity in embryonic cells. This also appears to be the first indication that the cytotoxic effects of impaired DSB rejoining may be mediated by p53.
-
(1996)
Mol Cell Biol
, vol.16
, pp. 7133-7143
-
-
Lim, D.S.1
Hasty, P.2
-
18
-
-
0031741863
-
Targeted inactivation of mouse RAD52 reduces homologous recombination but not resistance to ionizing radiation
-
-/- cells and mice.
-
-/- cells and mice.
-
(1998)
Mol Cell Biol
, vol.18
, pp. 6423-6429
-
-
Rijkers, T.1
Van Den Ouweland, J.2
Morolli, B.3
Rolink, A.G.4
Baarends, W.M.5
Van Sloun, P.P.6
Lohman, P.H.7
Pastink, A.8
-
19
-
-
0030948789
-
Disruption of mouse RAD54 reduces ionizing radiation resistance and homologous recombination
-
-/- animals are viable.
-
-/- animals are viable.
-
(1997)
Cell
, vol.89
, pp. 194-204
-
-
Essers, J.1
Hendricks, R.W.2
Swagemakers, S.M.3
Troelstra, C.4
De Wit, J.5
Bootsma, D.6
Hoeijmakers, J.H.7
Kanaar, R.8
-
20
-
-
0033602450
-
Mouse Rad54 affects DNA conformation and DNA-damage-induced Rad51 foci formation
-
mRad54 is here shown to interact with mRad51 and to be required for formation of DNA damage-induced mRad51 foci.
-
Tan T.L.R., Essers J., Citterio C., Swagemakers S.M.A., de Wit J., Benson F.E., Hoeijmakers J.H.J., Kanar R. Mouse Rad54 affects DNA conformation and DNA-damage-induced Rad51 foci formation. Curr Biol. 9:1999;325-328. mRad54 is here shown to interact with mRad51 and to be required for formation of DNA damage-induced mRad51 foci.
-
(1999)
Curr Biol
, vol.9
, pp. 325-328
-
-
Tan, T.L.R.1
Essers, J.2
Citterio, C.3
Swagemakers, S.M.A.4
De Wit, J.5
Benson, F.E.6
Hoeijmakers, J.H.J.7
Kanar, R.8
-
21
-
-
0032061317
-
XRCC2 and XRCC3, new human Rad51-family members, promote chromosome stability and protect against DNA cross-links and other damages
-
The cloning of these two important RAD51 family members by complementing the extreme mitomycin C sensitivity of deficient hamster cells is described. The interaction between XRCC3/mRad51 is directly demonstrated.
-
Liu N., Lamerdin J.E., Tebbs R.S., Schild D., Tucker J.D., Shen M.R., Brookman K.W., Siciliano M.J., Walter C.A., Fan W.et al. XRCC2 and XRCC3, new human Rad51-family members, promote chromosome stability and protect against DNA cross-links and other damages. Mol Cell. 1:1998;783-793. The cloning of these two important RAD51 family members by complementing the extreme mitomycin C sensitivity of deficient hamster cells is described. The interaction between XRCC3/mRad51 is directly demonstrated.
-
(1998)
Mol Cell
, vol.1
, pp. 783-793
-
-
Liu, N.1
Lamerdin, J.E.2
Tebbs, R.S.3
Schild, D.4
Tucker, J.D.5
Shen, M.R.6
Brookman, K.W.7
Siciliano, M.J.8
Walter, C.A.9
Fan, W.10
-
22
-
-
0033569684
-
XRCC3 promotes homology-directed repair of DNA damage in mammalian cells
-
The authors provide direct evidence for the participation of XRCC3 in homologous recombinational repair of DSBs.
-
Pierce A.J., Johnson R.D., Thompson L.H., Jasin M. XRCC3 promotes homology-directed repair of DNA damage in mammalian cells. Genes Dev. 13:1999;2633-2638. The authors provide direct evidence for the participation of XRCC3 in homologous recombinational repair of DSBs.
-
(1999)
Genes Dev
, vol.13
, pp. 2633-2638
-
-
Pierce, A.J.1
Johnson, R.D.2
Thompson, L.H.3
Jasin, M.4
-
23
-
-
0031031787
-
From BRCA1 to RAP1: A widespread BRCT module closely associated with DNA repair
-
Callebaut I., Mornon J-P. From BRCA1 to RAP1: a widespread BRCT module closely associated with DNA repair. FEBS Lett. 400:1997;25-30.
-
(1997)
FEBS Lett
, vol.400
, pp. 25-30
-
-
Callebaut, I.1
Mornon, J.-P.2
-
24
-
-
0032516654
-
BRCA1 required for transcription-coupled repair of oxidative DNA damage
-
+/+wild-type cells and to be deficient in the selective removal of oxidised thymine bases (thymine glycol) from the transcribed DNA strand.
-
+/+wild-type cells and to be deficient in the selective removal of oxidised thymine bases (thymine glycol) from the transcribed DNA strand.
-
(1998)
Science
, vol.281
, pp. 1009-1012
-
-
Gowen, L.C.1
Avrutskaya, A.A.2
Latour, A.M.3
Koller, B.H.4
Leadon, S.A.5
-
25
-
-
0033618621
-
Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response
-
Human Rad50 is shown to complex with Nibrin and hMre11. hRad50 focus formation is reduced in a human breast carcinoma cell line with homozygous mutation in Brca1. Focus formation is restored by a transfected wild-type Brca1. Correction of the (slight) MMS sensitivity is also achieved by expressing a wild-type Brca1.
-
Zhong Q., Chen C-F., Li S., Chen Y., Wang C-C., Xiao J., Chen P-L., Sharp Z.D., Lee W-H. Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response. Science. 285:1999;747-750. Human Rad50 is shown to complex with Nibrin and hMre11. hRad50 focus formation is reduced in a human breast carcinoma cell line with homozygous mutation in Brca1. Focus formation is restored by a transfected wild-type Brca1. Correction of the (slight) MMS sensitivity is also achieved by expressing a wild-type Brca1.
-
(1999)
Science
, vol.285
, pp. 747-750
-
-
Zhong, Q.1
Chen, C.-F.2
Li, S.3
Chen, Y.4
Wang, C.-C.5
Xiao, J.6
Chen, P.-L.7
Sharp, Z.D.8
Lee, W.-H.9
-
26
-
-
0033527717
-
Requirement of ATM dependent phosphorylation of Brca-1 in the DNA damage response to double-strand breaks
-
-/- cells is, however, much less pronounced than A-T cells, indicating that Brca1 is likely to be only one of the significant targets of ATM.
-
-/- cells is, however, much less pronounced than A-T cells, indicating that Brca1 is likely to be only one of the significant targets of ATM.
-
(1999)
Science
, vol.286
, pp. 1162-1166
-
-
Cortez, D.1
Wang, Y.2
Qin, J.3
Elledge, S.J.4
-
27
-
-
0032159062
-
Stable interaction between the products of the BRCA1 and BRCA2 tumour suppressor genes in mitotic and meiotic cells
-
Chen J., Silver D.P., Walpita D., Cantor S.B., Gazdar A.F., Tomlinson G., Couch F.J., Weber B.L., Ashley T., Livingston D.M., Scully R. Stable interaction between the products of the BRCA1 and BRCA2 tumour suppressor genes in mitotic and meiotic cells. Mol Cell. 2:1998;317-328.
-
(1998)
Mol Cell
, vol.2
, pp. 317-328
-
-
Chen, J.1
Silver, D.P.2
Walpita, D.3
Cantor, S.B.4
Gazdar, A.F.5
Tomlinson, G.6
Couch, F.J.7
Weber, B.L.8
Ashley, T.9
Livingston, D.M.10
Scully, R.11
-
28
-
-
0031990269
-
Involvement of Brca2 in DNA repair
-
-/- embryonic fibroblasts. Interestingly, this DNA-repair defect is associated with apparently normal cell cycle checkpoint controls.
-
-/- embryonic fibroblasts. Interestingly, this DNA-repair defect is associated with apparently normal cell cycle checkpoint controls.
-
(1998)
Mol Cell
, vol.1
, pp. 347-357
-
-
Patel, K.J.1
Yu, V.P.C.C.2
Lee, H.3
Corcoran, A.4
Thistlethwaite, F.C.5
Evans, M.J.6
Colledge, W.H.7
Friedman, L.S.8
Ponder, B.A.J.9
Venkitaraman, A.R.10
-
29
-
-
0032823314
-
Growth retardation, DNA repair defects, and lack of spermatogenesis in BRCA1-deficient mice
-
-/- cells is reversed by selection for an abrogated p53 response. This is another example of p53 controlling the survival of cells with unresolved DSBs.
-
-/- cells is reversed by selection for an abrogated p53 response. This is another example of p53 controlling the survival of cells with unresolved DSBs.
-
(1999)
Mol Cell Biol
, vol.19
, pp. 7061-7075
-
-
Cressman, V.L.1
Backlund, D.C.2
Avrutskaya, A.V.3
Leadon, S.A.4
Godfrey, V.5
Koller, B.H.6
-
30
-
-
0033180301
-
Nijmegen Breakage Syndrome: Consequences of defective DNA double strand break repair
-
Digweed M., Reis A., Sperling K. Nijmegen Breakage Syndrome: consequences of defective DNA double strand break repair. Bioessays. 21:1999;649-656.
-
(1999)
Bioessays
, vol.21
, pp. 649-656
-
-
Digweed, M.1
Reis, A.2
Sperling, K.3
-
31
-
-
0033544724
-
The DNA double-strand break repair gene hMRE11 is mutated in individuals with an Ataxia-Telangiectasia-like disorder
-
Two families diagnosed as A-T are shown to have truncating or missense mutations in hMRE11. Skin fibroblasts from affected individuals exhibit ionising radiation sensitivity and levels of radiation-resistant DNA synthesis comparable to A-T cells. As with A-T and NBS cells, no overt defect in DSB rejoining is observed. hMRE11/Rad50/NBS focus formation is absent in hMRE11 mutant cells which are also defective in JNK activation. The p53 response to ionising radiation serves to distinguish hMRE11 mutant cells from A-T cells. Because of the similarity of clinical phenotypes, the authors suggest that up to 6% of diagnosed A-T patients may actually harbour hMRE11 mutations.
-
Stewart G.S., Maser R.S., Stankovic T., Bressan D.A., Kaplan M.I., Jaspers N.G.J., Raams A., Byrd P.J., Petrini J.H.J., Taylor A.M.R. The DNA double-strand break repair gene hMRE11 is mutated in individuals with an Ataxia-Telangiectasia-like disorder. Cell. 99:1999;577-587. Two families diagnosed as A-T are shown to have truncating or missense mutations in hMRE11. Skin fibroblasts from affected individuals exhibit ionising radiation sensitivity and levels of radiation-resistant DNA synthesis comparable to A-T cells. As with A-T and NBS cells, no overt defect in DSB rejoining is observed. hMRE11/Rad50/NBS focus formation is absent in hMRE11 mutant cells which are also defective in JNK activation. The p53 response to ionising radiation serves to distinguish hMRE11 mutant cells from A-T cells. Because of the similarity of clinical phenotypes, the authors suggest that up to 6% of diagnosed A-T patients may actually harbour hMRE11 mutations.
-
(1999)
Cell
, vol.99
, pp. 577-587
-
-
Stewart, G.S.1
Maser, R.S.2
Stankovic, T.3
Bressan, D.A.4
Kaplan, M.I.5
Jaspers, N.G.J.6
Raams, A.7
Byrd, P.J.8
Petrini, J.H.J.9
Taylor, A.M.R.10
-
32
-
-
0033594904
-
Disruption of mRad50 causes embryonic stem cell lethality, abnormal embryonic development, and sensitivity to ionising radiation
-
-/- cells.
-
-/- cells.
-
(1999)
Proc Natl Acad Sci USA
, vol.96
, pp. 7376-7381
-
-
Luo, G.1
Yao, M.S.2
Bender, C.F.3
Mills, M.4
Bladl, A.R.5
Bradley, A.6
Petrini, J.H.J.7
-
33
-
-
0033485758
-
Mre11 is essential for the maintenance of chromosomal DNA in vertebrate cells
-
-/- mouse cells is seen in chicken cells in which MRE11 is conditionally inactivated. The absence of Mre11 causes proliferative arrest and an increase in spontaneous and radiation-induced chromosome aberrations. The effects are more apparent when combined with a Ku defect, indicating that the NHEJ and SSA HR pathways process DSBs independently.
-
-/- mouse cells is seen in chicken cells in which MRE11 is conditionally inactivated. The absence of Mre11 causes proliferative arrest and an increase in spontaneous and radiation-induced chromosome aberrations. The effects are more apparent when combined with a Ku defect, indicating that the NHEJ and SSA HR pathways process DSBs independently.
-
(1999)
EMBO J
, vol.18
, pp. 6619-6629
-
-
Yamaguchi-Iwai, Y.1
Sonoda, E.2
Sasaki, M.S.3
Morrison, C.4
Haraguchi, T.5
Hiraoka, Y.6
Yamashita, Y.M.7
Yagi, T.8
Takata, M.9
Price, C.10
-
34
-
-
0033538496
-
The Nijmegen Breakage Syndrome protein is essential for Mre11 phosphorylation upon DNA damage
-
Mre11 phosphorylation in response to different DNA-damaging agents is absent in NBS cells. Phosphorylation precedes DNA-damage-dependent Mre11 focus formation, suggesting that a phosphorylated form of Mre11 may be required for participation in DSB repair.
-
Dong Z., Zhong Q., Chen P-L. The Nijmegen Breakage Syndrome protein is essential for Mre11 phosphorylation upon DNA damage. J Biol Chem. 274:1999;19513-19516. Mre11 phosphorylation in response to different DNA-damaging agents is absent in NBS cells. Phosphorylation precedes DNA-damage-dependent Mre11 focus formation, suggesting that a phosphorylated form of Mre11 may be required for participation in DSB repair.
-
(1999)
J Biol Chem
, vol.274
, pp. 19513-19516
-
-
Dong, Z.1
Zhong, Q.2
Chen, P.-L.3
-
35
-
-
0032076248
-
The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: Linkage of double-strand break repair to the cellular DNA damage response
-
The key identification of Nbs1 as p95 and confirmation that Nbs forms a complex with hRad50 and Mre11 which localises to radiation-induced foci in normal, but not NBS, cells. The report suggests a DNA-damage-sensing role for the complex.
-
Carney J.P., Maser R.S., Olivares H., Davis E.M., le Beau M., Yates J.R., Hays L., Morgan W.F., Petrini J.H. The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: linkage of double-strand break repair to the cellular DNA damage response. Cell. 93:1998;477-486. The key identification of Nbs1 as p95 and confirmation that Nbs forms a complex with hRad50 and Mre11 which localises to radiation-induced foci in normal, but not NBS, cells. The report suggests a DNA-damage-sensing role for the complex.
-
(1998)
Cell
, vol.93
, pp. 477-486
-
-
Carney, J.P.1
Maser, R.S.2
Olivares, H.3
Davis, E.M.4
Le Beau, M.5
Yates, J.R.6
Hays, L.7
Morgan, W.F.8
Petrini, J.H.9
-
36
-
-
0033563229
-
Nbs1 potentiates ATP-driven DNA unwinding and endonuclease cleavage by the Mre11/Rad50 complex
-
Analysis of the biochemical properties of a purified recombinant human Rad50/Mre11/Nbs complex indicates that Nbs confers several additional functions on the hRad50/Mre11 heterodimer. The authors also suggest that the tripartite complex may serve a DNA-damage recognition function which may control how DSBs are processed. This decision would be determined partly by the ability of the complex to sense differences in the type of DNA ends present.
-
Paull T.T., Gellert M. Nbs1 potentiates ATP-driven DNA unwinding and endonuclease cleavage by the Mre11/Rad50 complex. Genes Dev. 13:1999;1276-1288. Analysis of the biochemical properties of a purified recombinant human Rad50/Mre11/Nbs complex indicates that Nbs confers several additional functions on the hRad50/Mre11 heterodimer. The authors also suggest that the tripartite complex may serve a DNA-damage recognition function which may control how DSBs are processed. This decision would be determined partly by the ability of the complex to sense differences in the type of DNA ends present.
-
(1999)
Genes Dev
, vol.13
, pp. 1276-1288
-
-
Paull, T.T.1
Gellert, M.2
-
37
-
-
1842366037
-
Two pathways for removal of non-homologous DNA ends during double-strand break repair in Saccharomyces cerevisiae
-
Paques F., Haber J.E. Two pathways for removal of non-homologous DNA ends during double-strand break repair in Saccharomyces cerevisiae. Mol Cell Biol. 17:1997;6765-6771.
-
(1997)
Mol Cell Biol
, vol.17
, pp. 6765-6771
-
-
Paques, F.1
Haber, J.E.2
-
38
-
-
0030834260
-
Role of Saccharomyces cerevisiae Msh2 and Msh3 repair proteins in double-strand break-induced recombination
-
Evidence is presented that the MSH2 and MSH3 mismatch repair proteins may participate in the removal of single-stranded DNA tails during DSB repair by SSA.
-
Sugawara N., Paques F., Colaiacovo M., Haber J.E. Role of Saccharomyces cerevisiae Msh2 and Msh3 repair proteins in double-strand break-induced recombination. Proc Natl Acad Sci USA. 94:1997;9214-9219. Evidence is presented that the MSH2 and MSH3 mismatch repair proteins may participate in the removal of single-stranded DNA tails during DSB repair by SSA.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 9214-9219
-
-
Sugawara, N.1
Paques, F.2
Colaiacovo, M.3
Haber, J.E.4
-
40
-
-
0032718278
-
Separation-of-function mutations in Saccharomyces cervisiae MSH2 that confer mismatch repair defects but do not affect nonhomologous-tail removal during recombination
-
Studamire B., Price G., Sugawara N., Haber J.E., Alani E. Separation-of-function mutations in Saccharomyces cervisiae MSH2 that confer mismatch repair defects but do not affect nonhomologous-tail removal during recombination. Mol Cell Biol. 19:1999;7558-7567.
-
(1999)
Mol Cell Biol
, vol.19
, pp. 7558-7567
-
-
Studamire, B.1
Price, G.2
Sugawara, N.3
Haber, J.E.4
Alani, E.5
-
41
-
-
0030992749
-
Interaction between ATM protein and c-Abl in response to DNA damage
-
Shafman T., Khannah K.K., Kedar P., Spring K., Kozlov S., Yen T., Hobson K., Gatei M., Zhang N., Watters D.et al. Interaction between ATM protein and c-Abl in response to DNA damage. Nature. 387:1997;520-523.
-
(1997)
Nature
, vol.387
, pp. 520-523
-
-
Shafman, T.1
Khannah, K.K.2
Kedar, P.3
Spring, K.4
Kozlov, S.5
Yen, T.6
Hobson, K.7
Gatei, M.8
Zhang, N.9
Watters, D.10
-
42
-
-
0033617368
-
Radiation-induced assembly of Rad51 and Rad52 recombination complex requires ATM and c-Abl
-
The authors demonstrate a radiation-induced ATM and c-Abl dependent phosphorylation of Rad51 which enhances its interaction with Rad52.
-
Chen G., Yuan S-S.F., Liu W., Xu Y., Trujillo K., Song B., Cong F., Goff S.P., Wu Y., Arlinghaus R.et al. Radiation-induced assembly of Rad51 and Rad52 recombination complex requires ATM and c-Abl. J Biol Chem. 274:1999;12748-12752. The authors demonstrate a radiation-induced ATM and c-Abl dependent phosphorylation of Rad51 which enhances its interaction with Rad52.
-
(1999)
J Biol Chem
, vol.274
, pp. 12748-12752
-
-
Chen, G.1
Yuan, S.-S.F.2
Liu, W.3
Xu, Y.4
Trujillo, K.5
Song, B.6
Cong, F.7
Goff, S.P.8
Wu, Y.9
Arlinghaus, R.10
-
43
-
-
0033168376
-
DNA recombination the replication connection
-
Haber J.E. DNA recombination the replication connection. Trends Biochem Sci. 224:1999;271-275.
-
(1999)
Trends Biochem Sci
, vol.224
, pp. 271-275
-
-
Haber, J.E.1
|