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PMC0
bibo:doi
10.1371%2Fjournal.ppat.1001342
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_:vb11107476
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dc:title
introduction
n6:contains
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Subject Item
_:vb11107477
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DNA damage resulting from these challenge produces a complex protein kinase signaling cascade that promotes repair of the damaged DNA and activates cell cycle checkpoints or apoptosis [>>1<<]. A central mediator of certain DNA damage response (DDR) pathways is the ataxia telangiectasia mutated (ATM) protein kinase [2]. ATM activation leads to the phosphorylation of numerous proteins that ultimately signal cell cycle arrest and
n3:mentions
n2:17303408
Subject Item
_:vb11107478
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rdf:value
A central mediator of certain DNA damage response (DDR) pathways is the ataxia telangiectasia mutated (ATM) protein kinase [>>2<<]. ATM activation leads to the phosphorylation of numerous proteins that ultimately signal cell cycle arrest and DNA repair and/or apoptosis. Recent data have shown that several viruses, including herpes simplex virus type 1 (HSV-1),
n3:mentions
n2:12556884
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_:vb11107479
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viruses, including herpes simplex virus type 1 (HSV-1), polyomavirus, human papillomavirus (HPV), and human immunodeficiency virus type 1 (HIV-1) require the activation of ATM and/or downstream proteins for a fully permissive infection [>>3<<], [4], [5], [6], [7]. Presumably, these viruses also encode proteins that interfere with downstream DDR signaling that antagonize virus replication through the activation of cell cycle checkpoints or the induction of apoptosis.
n3:mentions
n2:15824307
Subject Item
_:vb11107480
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n3:Context
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including herpes simplex virus type 1 (HSV-1), polyomavirus, human papillomavirus (HPV), and human immunodeficiency virus type 1 (HIV-1) require the activation of ATM and/or downstream proteins for a fully permissive infection [3], [>>4<<], [5], [6], [7]. Presumably, these viruses also encode proteins that interfere with downstream DDR signaling that antagonize virus replication through the activation of cell cycle checkpoints or the induction of apoptosis.
n3:mentions
n2:12679521
Subject Item
_:vb11107481
rdf:type
n3:Context
rdf:value
herpes simplex virus type 1 (HSV-1), polyomavirus, human papillomavirus (HPV), and human immunodeficiency virus type 1 (HIV-1) require the activation of ATM and/or downstream proteins for a fully permissive infection [3], [4], [>>5<<], [6], [7]. Presumably, these viruses also encode proteins that interfere with downstream DDR signaling that antagonize virus replication through the activation of cell cycle checkpoints or the induction of apoptosis.
n3:mentions
n2:15834407
Subject Item
_:vb11107482
rdf:type
n3:Context
rdf:value
herpes simplex virus type 1 (HSV-1), polyomavirus, human papillomavirus (HPV), and human immunodeficiency virus type 1 (HIV-1) require the activation of ATM and/or downstream proteins for a fully permissive infection [3], [4], [5], [>>6<<], [7]. Presumably, these viruses also encode proteins that interfere with downstream DDR signaling that antagonize virus replication through the activation of cell cycle checkpoints or the induction of apoptosis.
n3:mentions
n2:15964848
Subject Item
_:vb11107483
rdf:type
n3:Context
rdf:value
simplex virus type 1 (HSV-1), polyomavirus, human papillomavirus (HPV), and human immunodeficiency virus type 1 (HIV-1) require the activation of ATM and/or downstream proteins for a fully permissive infection [3], [4], [5], [6], [>>7<<]. Presumably, these viruses also encode proteins that interfere with downstream DDR signaling that antagonize virus replication through the activation of cell cycle checkpoints or the induction of apoptosis.
n3:mentions
n2:19798429
Subject Item
_:vb11107484
rdf:type
n3:Context
rdf:value
Human cytomegalovirus (HCMV) infection activates multiple DDR proteins, including ATM and the downstream effector protein, p53 [>>8<<], [9], [10]. The p53 transcription factor plays an important role in responding to certain cellular stresses as well as in regulating cell cycle progression.
n3:mentions
n2:16103197
Subject Item
_:vb11107485
rdf:type
n3:Context
rdf:value
Human cytomegalovirus (HCMV) infection activates multiple DDR proteins, including ATM and the downstream effector protein, p53 [8], [>>9<<], [10]. The p53 transcription factor plays an important role in responding to certain cellular stresses as well as in regulating cell cycle progression.
n3:mentions
n2:17151099
Subject Item
_:vb11107486
rdf:type
n3:Context
rdf:value
Human cytomegalovirus (HCMV) infection activates multiple DDR proteins, including ATM and the downstream effector protein, p53 [8], [9], [>>10<<]. The p53 transcription factor plays an important role in responding to certain cellular stresses as well as in regulating cell cycle progression.
n3:mentions
n2:15105295
Subject Item
_:vb11107487
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It has been proposed that the activation of p53 helps to elicit the cell cycle arrest in HCMV infected fibroblasts by modulating p21 levels [>>11<<] or by facilitating viral gene expression [12].
n3:mentions
n2:12062798
Subject Item
_:vb11107488
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It has been proposed that the activation of p53 helps to elicit the cell cycle arrest in HCMV infected fibroblasts by modulating p21 levels [11] or by facilitating viral gene expression [>>12<<]. However, the functional relevance of ATM in HCMV replication has been unclear. Although others have concluded that ATM does not contribute to HCMV replication [9], it seems reasonable to reconsider the role of ATM in this process given
n3:mentions
n2:16912290
Subject Item
_:vb11107489
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Although others have concluded that ATM does not contribute to HCMV replication [>>9<<], it seems reasonable to reconsider the role of ATM in this process given that downstream factors of ATM activation are required for efficient replication of HCMV and that ATM contributes to the replication of other DNA viruses.
n3:mentions
n2:17151099
Subject Item
_:vb11107490
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has been noted that the cellular environment of HCMV infected cells is “G1/S-arrest”, yet these cells exhibit some biochemical properties of S and G2 phase, such as cyclin E and cyclin B kinase activation and pRb hyperphosphorylation [>>13<<], [14], [15], [16]. One consequence of these events is the induction of E2F activator complexes following HCMV infection [17].
n3:mentions
n2:7474079
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_:vb11107491
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noted that the cellular environment of HCMV infected cells is “G1/S-arrest”, yet these cells exhibit some biochemical properties of S and G2 phase, such as cyclin E and cyclin B kinase activation and pRb hyperphosphorylation [13], [>>14<<], [15], [16]. One consequence of these events is the induction of E2F activator complexes following HCMV infection [17].
n3:mentions
n2:12533700
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_:vb11107492
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n3:Context
rdf:value
that the cellular environment of HCMV infected cells is “G1/S-arrest”, yet these cells exhibit some biochemical properties of S and G2 phase, such as cyclin E and cyclin B kinase activation and pRb hyperphosphorylation [13], [14], [>>15<<], [16]. One consequence of these events is the induction of E2F activator complexes following HCMV infection [17].
n3:mentions
n2:18321963
Subject Item
_:vb11107493
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n3:Context
rdf:value
the cellular environment of HCMV infected cells is “G1/S-arrest”, yet these cells exhibit some biochemical properties of S and G2 phase, such as cyclin E and cyclin B kinase activation and pRb hyperphosphorylation [13], [14], [15], [>>16<<]. One consequence of these events is the induction of E2F activator complexes following HCMV infection [17].
n3:mentions
n2:18467589
Subject Item
_:vb11107494
rdf:type
n3:Context
rdf:value
One consequence of these events is the induction of E2F activator complexes following HCMV infection [>>17<<]. The RB-regulated activator class of proteins within the E2F family of transcription factors includes E2F1, E2F2, and E2F3a [18], [19]. These proteins regulate the transcription of many genes, such as those required for S-phase
n3:mentions
n2:1328853
Subject Item
_:vb11107495
rdf:type
n3:Context
rdf:value
The RB-regulated activator class of proteins within the E2F family of transcription factors includes E2F1, E2F2, and E2F3a [>>18<<], [19]. These proteins regulate the transcription of many genes, such as those required for S-phase progression and DNA repair [19]. In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads
n3:mentions
n2:18032011
Subject Item
_:vb11107496
rdf:type
n3:Context
rdf:value
The RB-regulated activator class of proteins within the E2F family of transcription factors includes E2F1, E2F2, and E2F3a [18], [>>19<<]. These proteins regulate the transcription of many genes, such as those required for S-phase progression and DNA repair [19]. In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads to DNA
n3:mentions
n2:11799067
Subject Item
_:vb11107497
rdf:type
n3:Context
rdf:value
These proteins regulate the transcription of many genes, such as those required for S-phase progression and DNA repair [>>19<<]. In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads to DNA double strand break (DSB) accumulation and cell cycle checkpoint signaling [20], [21], [22], [23]. Although it is well
n3:mentions
n2:11799067
Subject Item
_:vb11107498
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n3:Context
rdf:value
In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads to DNA double strand break (DSB) accumulation and cell cycle checkpoint signaling [>>20<<], [21], [22], [23].
n3:mentions
n2:15024084
Subject Item
_:vb11107499
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n3:Context
rdf:value
In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads to DNA double strand break (DSB) accumulation and cell cycle checkpoint signaling [20], [>>21<<], [22], [23].
n3:mentions
n2:16186801
Subject Item
_:vb11107500
rdf:type
n3:Context
rdf:value
In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads to DNA double strand break (DSB) accumulation and cell cycle checkpoint signaling [20], [21], [>>22<<], [23]. Although it is well established that one of the initial effects of HCMV infection is to inactivate the RB family of proteins, whether the consequential deregulation of the E2F proteins affects HCMV replication is unknown.
n3:mentions
n2:16434972
Subject Item
_:vb11107501
rdf:type
n3:Context
rdf:value
In addition, it has been shown that RB inactivation and deregulation of E2F1, but not E2F2 or E2F3, leads to DNA double strand break (DSB) accumulation and cell cycle checkpoint signaling [20], [21], [22], [>>23<<]. Although it is well established that one of the initial effects of HCMV infection is to inactivate the RB family of proteins, whether the consequential deregulation of the E2F proteins affects HCMV replication is unknown.
n3:mentions
n2:15140942
Subject Item
_:vb11107502
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n6:Section
dc:title
materials and methods
n6:contains
_:vb11107508 _:vb11107504 _:vb11107505 _:vb11107506 _:vb11107507 _:vb11107503
Subject Item
_:vb11107503
rdf:type
n3:Context
rdf:value
Recombinant adenoviruses encoding HCMV IE1-72 (Ad-IE1), HCMV IE2-86 (Ad-IE2), β-galactosidase (Ad β-gal), and HPV16 E7 (Ad-E7) have been described [>>11<<], [20], [55], [56]. Recombinant adenovirus stocks were generated, purified and titered as described [20], [57].
n3:mentions
n2:12062798
Subject Item
_:vb11107504
rdf:type
n3:Context
rdf:value
Recombinant adenoviruses encoding HCMV IE1-72 (Ad-IE1), HCMV IE2-86 (Ad-IE2), β-galactosidase (Ad β-gal), and HPV16 E7 (Ad-E7) have been described [11], [>>20<<], [55], [56]. Recombinant adenovirus stocks were generated, purified and titered as described [20], [57].
n3:mentions
n2:15024084
Subject Item
_:vb11107505
rdf:type
n3:Context
rdf:value
Recombinant adenoviruses encoding HCMV IE1-72 (Ad-IE1), HCMV IE2-86 (Ad-IE2), β-galactosidase (Ad β-gal), and HPV16 E7 (Ad-E7) have been described [11], [20], [>>55<<], [56]. Recombinant adenovirus stocks were generated, purified and titered as described [20], [57].
n3:mentions
n2:1317548
Subject Item
_:vb11107506
rdf:type
n3:Context
rdf:value
Recombinant adenoviruses encoding HCMV IE1-72 (Ad-IE1), HCMV IE2-86 (Ad-IE2), β-galactosidase (Ad β-gal), and HPV16 E7 (Ad-E7) have been described [11], [20], [55], [>>56<<]. Recombinant adenovirus stocks were generated, purified and titered as described [20], [57].
n3:mentions
n2:9151854
Subject Item
_:vb11107507
rdf:type
n3:Context
rdf:value
Recombinant adenovirus stocks were generated, purified and titered as described [>>20<<], [57]. All recombinant adenovirus infections were done at a MOI of 250 unless otherwise noted.
n3:mentions
n2:15024084
Subject Item
_:vb11107508
rdf:type
n3:Context
rdf:value
Recombinant adenovirus stocks were generated, purified and titered as described [20], [>>57<<]. All recombinant adenovirus infections were done at a MOI of 250 unless otherwise noted.
n3:mentions
n2:10933712
Subject Item
_:vb11107509
rdf:type
n6:Section
dc:title
results
n6:contains
_:vb11107510 _:vb11107511 _:vb11107512 _:vb11107513 _:vb11107514 _:vb11107515 _:vb11107516 _:vb11107517 _:vb11107518 _:vb11107519 _:vb11107536 _:vb11107537 _:vb11107538 _:vb11107520 _:vb11107521 _:vb11107522 _:vb11107523 _:vb11107524 _:vb11107525 _:vb11107526 _:vb11107527 _:vb11107528 _:vb11107529 _:vb11107530 _:vb11107531 _:vb11107532 _:vb11107533 _:vb11107534 _:vb11107535
Subject Item
_:vb11107510
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n3:Context
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Many viruses require ATM activation for a fully permissive infection, and it has been reported that ATM is activated by IE1 expression or HCMV infection [>>8<<], [9], [10]. We asked whether HCMV replication is affected by functional changes in ATM.
n3:mentions
n2:16103197
Subject Item
_:vb11107511
rdf:type
n3:Context
rdf:value
Many viruses require ATM activation for a fully permissive infection, and it has been reported that ATM is activated by IE1 expression or HCMV infection [8], [>>9<<], [10]. We asked whether HCMV replication is affected by functional changes in ATM.
n3:mentions
n2:17151099
Subject Item
_:vb11107512
rdf:type
n3:Context
rdf:value
Many viruses require ATM activation for a fully permissive infection, and it has been reported that ATM is activated by IE1 expression or HCMV infection [8], [9], [>>10<<]. We asked whether HCMV replication is affected by functional changes in ATM. Initially, we examined the effects of caffeine, an inhibitor of PI3-like kinases including ATM, on HCMV replication.
n3:mentions
n2:15105295
Subject Item
_:vb11107513
rdf:type
n3:Context
rdf:value
Our observations suggesting a role for ATM in HCMV replication is contrary to another study [>>9<<]. Moreover, there is a concern with using AT fibroblasts as a model because the prolonged absence of functional ATM in cells from AT patients may have resulted in secondary genetic and/or biochemical changes that alter cellular
n3:mentions
n2:17151099
Subject Item
_:vb11107514
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n3:Context
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pUL44 is a virally encoded PCNA-like processivity factor of the viral DNA polymerase [>>24<<], [25]. In addition, dermal fibroblasts from normal and AT individuals were infected with virus, RC structures identified and scored. Under conditions of ATM depletion, the percentage of merged, “mature” RCs was reduced relative to control
n3:mentions
n2:1318399
Subject Item
_:vb11107515
rdf:type
n3:Context
rdf:value
pUL44 is a virally encoded PCNA-like processivity factor of the viral DNA polymerase [24], [>>25<<]. In addition, dermal fibroblasts from normal and AT individuals were infected with virus, RC structures identified and scored. Under conditions of ATM depletion, the percentage of merged, “mature” RCs was reduced relative to control cells
n3:mentions
n2:15260974
Subject Item
_:vb11107516
rdf:type
n3:Context
rdf:value
Because it was reported that HCMV infection or expression of IE1 or IE2 can activate ATM as measured by autophosphorylation on Ser1981 [>>8<<], [10], we asked whether HCMV could induce the formation of DNA damage sensing foci containing γH2AX, an event downstream of ATM activation and other DNA damage-activated kinases [26], [27], [28].
n3:mentions
n2:16103197
Subject Item
_:vb11107517
rdf:type
n3:Context
rdf:value
Because it was reported that HCMV infection or expression of IE1 or IE2 can activate ATM as measured by autophosphorylation on Ser1981 [8], [>>10<<], we asked whether HCMV could induce the formation of DNA damage sensing foci containing γH2AX, an event downstream of ATM activation and other DNA damage-activated kinases [26], [27], [28].
n3:mentions
n2:15105295
Subject Item
_:vb11107518
rdf:type
n3:Context
rdf:value
ATM as measured by autophosphorylation on Ser1981 [8], [10], we asked whether HCMV could induce the formation of DNA damage sensing foci containing γH2AX, an event downstream of ATM activation and other DNA damage-activated kinases [>>26<<], [27], [28]. γH2AX is the phosphorylated form of H2AX that is mediated by PI3-like kinases, including ATM.
n3:mentions
n2:14627815
Subject Item
_:vb11107519
rdf:type
n3:Context
rdf:value
as measured by autophosphorylation on Ser1981 [8], [10], we asked whether HCMV could induce the formation of DNA damage sensing foci containing γH2AX, an event downstream of ATM activation and other DNA damage-activated kinases [26], [>>27<<], [28]. γH2AX is the phosphorylated form of H2AX that is mediated by PI3-like kinases, including ATM.
n3:mentions
n2:11673449
Subject Item
_:vb11107520
rdf:type
n3:Context
rdf:value
by autophosphorylation on Ser1981 [8], [10], we asked whether HCMV could induce the formation of DNA damage sensing foci containing γH2AX, an event downstream of ATM activation and other DNA damage-activated kinases [26], [27], [>>28<<]. γH2AX is the phosphorylated form of H2AX that is mediated by PI3-like kinases, including ATM.
n3:mentions
n2:11571274
Subject Item
_:vb11107521
rdf:type
n3:Context
rdf:value
The pattern of γH2AX immunostaining in Figure 3 is different from the punctate foci observed when cells are treated with DNA damaging agents that cause dsDNA breaks [>>28<<], [29]. In HCMV-infected cells, γH2AX appears to accumulate in larger “domains” of the nucleus and by 72 hpi, much of the nucleus appears to be reactive to the γH2AX antibody.
n3:mentions
n2:11571274
Subject Item
_:vb11107522
rdf:type
n3:Context
rdf:value
The pattern of γH2AX immunostaining in Figure 3 is different from the punctate foci observed when cells are treated with DNA damaging agents that cause dsDNA breaks [28], [>>29<<]. In HCMV-infected cells, γH2AX appears to accumulate in larger “domains” of the nucleus and by 72 hpi, much of the nucleus appears to be reactive to the γH2AX antibody.
n3:mentions
n2:15788728
Subject Item
_:vb11107523
rdf:type
n3:Context
rdf:value
We had previously shown that p53 is phosphorylated by ATM during HCMV infection [>>8<<] and others have shown that p53 contributes to HCMV replication [12].
n3:mentions
n2:16103197
Subject Item
_:vb11107524
rdf:type
n3:Context
rdf:value
We had previously shown that p53 is phosphorylated by ATM during HCMV infection [8] and others have shown that p53 contributes to HCMV replication [>>12<<].
n3:mentions
n2:16912290
Subject Item
_:vb11107525
rdf:type
n3:Context
rdf:value
Given the rapid formation of γH2AX foci and protein accumulation after HCMV infection (5 hpi; Figure 5A–B) and given that it has been previously reported that ectopic IE1 expression results in ATM autophosphorylation [>>8<<], we further examined the DDR associated with expression of IE gene products by monitoring the accumulation of γH2AX and p-ATM.
n3:mentions
n2:16103197
Subject Item
_:vb11107526
rdf:type
n3:Context
rdf:value
We previously reported that altering RB function or increasing E2F1 levels leads to an ATM-dependent DDR [>>20<<], [21], [22], [30].
n3:mentions
n2:15024084
Subject Item
_:vb11107527
rdf:type
n3:Context
rdf:value
We previously reported that altering RB function or increasing E2F1 levels leads to an ATM-dependent DDR [20], [>>21<<], [22], [30].
n3:mentions
n2:16186801
Subject Item
_:vb11107528
rdf:type
n3:Context
rdf:value
We previously reported that altering RB function or increasing E2F1 levels leads to an ATM-dependent DDR [20], [21], [>>22<<], [30]. Given that HCMV infection or ectopic expression of IE1 or IE2 leads to increased E2F activity [17], [31], [32], [33], we asked whether E2F1 or other RB-associated, activator E2Fs were responsible for the DDR following HCMV
n3:mentions
n2:16434972
Subject Item
_:vb11107529
rdf:type
n3:Context
rdf:value
We previously reported that altering RB function or increasing E2F1 levels leads to an ATM-dependent DDR [20], [21], [22], [>>30<<]. Given that HCMV infection or ectopic expression of IE1 or IE2 leads to increased E2F activity [17], [31], [32], [33], we asked whether E2F1 or other RB-associated, activator E2Fs were responsible for the DDR following HCMV infection or
n3:mentions
n2:18836483
Subject Item
_:vb11107530
rdf:type
n3:Context
rdf:value
Given that HCMV infection or ectopic expression of IE1 or IE2 leads to increased E2F activity [>>17<<], [31], [32], [33], we asked whether E2F1 or other RB-associated, activator E2Fs were responsible for the DDR following HCMV infection or IE cDNA transduction.
n3:mentions
n2:1328853
Subject Item
_:vb11107531
rdf:type
n3:Context
rdf:value
Given that HCMV infection or ectopic expression of IE1 or IE2 leads to increased E2F activity [17], [>>31<<], [32], [33], we asked whether E2F1 or other RB-associated, activator E2Fs were responsible for the DDR following HCMV infection or IE cDNA transduction.
n3:mentions
n2:10756032
Subject Item
_:vb11107532
rdf:type
n3:Context
rdf:value
Given that HCMV infection or ectopic expression of IE1 or IE2 leads to increased E2F activity [17], [31], [>>32<<], [33], we asked whether E2F1 or other RB-associated, activator E2Fs were responsible for the DDR following HCMV infection or IE cDNA transduction.
n3:mentions
n2:8392623
Subject Item
_:vb11107533
rdf:type
n3:Context
rdf:value
Given that HCMV infection or ectopic expression of IE1 or IE2 leads to increased E2F activity [17], [31], [32], [>>33<<], we asked whether E2F1 or other RB-associated, activator E2Fs were responsible for the DDR following HCMV infection or IE cDNA transduction.
n3:mentions
n2:8892909
Subject Item
_:vb11107534
rdf:type
n3:Context
rdf:value
This level of γH2AX immunostaining most likely represents DNA damage signaling that normally occurs in human fibroblasts replicating their own DNA [>>30<<]. Depletion of individual E2Fs did not affect this background staining (Figure 6A). Infection with HCMV resulted in increased γH2AX immunostaining, with ∼35% of the cells positive for γH2AX (Figure 6A). This percentage dropped to ∼16% when
n3:mentions
n2:18836483
Subject Item
_:vb11107535
rdf:type
n3:Context
rdf:value
Ad-E7, which encodes HPV type 16 E7, was included as a positive control for E2F1-mediated DDR [>>20<<], [21]. Therefore, HCMV infection and IE1 or IE2 expression activate an E2F1-mediated DNA damage response.
n3:mentions
n2:15024084
Subject Item
_:vb11107536
rdf:type
n3:Context
rdf:value
Ad-E7, which encodes HPV type 16 E7, was included as a positive control for E2F1-mediated DDR [20], [>>21<<]. Therefore, HCMV infection and IE1 or IE2 expression activate an E2F1-mediated DNA damage response.
n3:mentions
n2:16186801
Subject Item
_:vb11107537
rdf:type
n3:Context
rdf:value
E2Fs are generally thought to function as transcription factors with E2F1 having additional, less well-characterized roles in DNA damage accumulation and apoptosis [>>34<<]. To begin to differentiate whether the effects of E2F1 depletion on virus replication were due to reduced levels of an “activator E2F” (i.e., E2F1, E2F2, and E2F3a) or due to unique functions of E2F1, we determined whether depletion of
n3:mentions
n2:18805009
Subject Item
_:vb11107538
rdf:type
n3:Context
rdf:value
Depletion of E2F2, E2F3a, E2F3b (an E2F3 isoform that does not contribute to proliferation [>>35<<]), or a combination of E2F3a and E2F3b reduced the levels of the targeted protein to approximately that observed in mock-infected samples (Figures S4A–B).
n3:mentions
n2:18663357
Subject Item
_:vb11107539
rdf:type
n6:Section
dc:title
discussion
n6:contains
_:vb11107560 _:vb11107561 _:vb11107562 _:vb11107563 _:vb11107564 _:vb11107565 _:vb11107566 _:vb11107567 _:vb11107552 _:vb11107553 _:vb11107554 _:vb11107555 _:vb11107556 _:vb11107557 _:vb11107558 _:vb11107559 _:vb11107568 _:vb11107569 _:vb11107570 _:vb11107544 _:vb11107545 _:vb11107546 _:vb11107547 _:vb11107548 _:vb11107549 _:vb11107550 _:vb11107551 _:vb11107540 _:vb11107541 _:vb11107542 _:vb11107543
Subject Item
_:vb11107540
rdf:type
n3:Context
rdf:value
Our results are consistent with ATM contributing to the replication of other viruses (for review, see [>>36<<]). This conclusion contrasts with what has been previously reported for HCMV infection [9], where it was determined that ATM is not required for the progression of HCMV infection. It is unclear why there is a discrepancy between these
n3:mentions
n2:19473887
Subject Item
_:vb11107541
rdf:type
n3:Context
rdf:value
This conclusion contrasts with what has been previously reported for HCMV infection [>>9<<], where it was determined that ATM is not required for the progression of HCMV infection.
n3:mentions
n2:17151099
Subject Item
_:vb11107542
rdf:type
n3:Context
rdf:value
Indeed, activation of the host DDR is an obstacle for the replication of at least one DNA virus, adenovirus, which blocks the host DDR during infection [>>37<<]. One reason for infection-associated ATM activation may be to utilize the consequential stimulation of cellular DNA repair and recombination enzymes [38] to benefit viral replication [3], [39], [40]. Perhaps, in the case of HCMV, repair
n3:mentions
n2:12124628
Subject Item
_:vb11107543
rdf:type
n3:Context
rdf:value
One reason for infection-associated ATM activation may be to utilize the consequential stimulation of cellular DNA repair and recombination enzymes [>>38<<] to benefit viral replication [3], [39], [40].
n3:mentions
n2:12612651
Subject Item
_:vb11107544
rdf:type
n3:Context
rdf:value
One reason for infection-associated ATM activation may be to utilize the consequential stimulation of cellular DNA repair and recombination enzymes [38] to benefit viral replication [>>3<<], [39], [40].
n3:mentions
n2:15824307
Subject Item
_:vb11107545
rdf:type
n3:Context
rdf:value
One reason for infection-associated ATM activation may be to utilize the consequential stimulation of cellular DNA repair and recombination enzymes [38] to benefit viral replication [3], [>>39<<], [40]. Perhaps, in the case of HCMV, repair and recombination enzymes may aid in circularizing the viral DNA after it has entered the cell and/or facilitate the maturation of nascent viral genomes. A DNA repair complex of DNA ligase IV
n3:mentions
n2:19386720
Subject Item
_:vb11107546
rdf:type
n3:Context
rdf:value
One reason for infection-associated ATM activation may be to utilize the consequential stimulation of cellular DNA repair and recombination enzymes [38] to benefit viral replication [3], [39], [>>40<<]. Perhaps, in the case of HCMV, repair and recombination enzymes may aid in circularizing the viral DNA after it has entered the cell and/or facilitate the maturation of nascent viral genomes. A DNA repair complex of DNA ligase IV and
n3:mentions
n2:19656881
Subject Item
_:vb11107547
rdf:type
n3:Context
rdf:value
A DNA repair complex of DNA ligase IV and XRCC4 circularizes herpes simplex virus genomes early in infection [>>41<<]. If correct, one would predict that γH2AX, as well as other DDR factors would be bound to virion-delivered HCMV DNA once uncoated in the nucleus. However, others have concluded that parental viral DNA and γH2AX do not co-localize [9]. It
n3:mentions
n2:17296606
Subject Item
_:vb11107548
rdf:type
n3:Context
rdf:value
However, others have concluded that parental viral DNA and γH2AX do not co-localize [>>9<<]. It remains an open question as to whether there is a contribution of the host DDR to very early events in HCMV replication.
n3:mentions
n2:17151099
Subject Item
_:vb11107549
rdf:type
n3:Context
rdf:value
Upon HIV infection, ATM activation requires the viral integrase and it is proposed that ATM functions in post integration DNA repair [>>41<<]. For polyomaviruses like SV40, it is thought that the onset of viral DNA replication activates ATM, which then phosphorylates an essential serine residue on large T antigen [42]. HPV genome replication appears to switch from theta to
n3:mentions
n2:17296606
Subject Item
_:vb11107550
rdf:type
n3:Context
rdf:value
For polyomaviruses like SV40, it is thought that the onset of viral DNA replication activates ATM, which then phosphorylates an essential serine residue on large T antigen [>>42<<]. HPV genome replication appears to switch from theta to rolling circle replication [43], which may activate ATM. Alternately, infection by DNA viruses may cause damage to host chromosomes, which would stimulate a host DDR. In this
n3:mentions
n2:16221684
Subject Item
_:vb11107551
rdf:type
n3:Context
rdf:value
HPV genome replication appears to switch from theta to rolling circle replication [>>43<<], which may activate ATM.
n3:mentions
n2:9311789
Subject Item
_:vb11107552
rdf:type
n3:Context
rdf:value
Both H2AX (Figure 3) and p53 [>>8<<] are substrates of the ATM kinase during HCMV infection and both H2AX (Figure 4) and p53 [12] contribute to HCMV replication.
n3:mentions
n2:16103197
Subject Item
_:vb11107553
rdf:type
n3:Context
rdf:value
Both H2AX (Figure 3) and p53 [8] are substrates of the ATM kinase during HCMV infection and both H2AX (Figure 4) and p53 [>>12<<] contribute to HCMV replication. While the mechanism by which H2AX contributes to HCMV replication is unknown, p53 is found in RCs, binds viral DNA and evidence suggests that p53 influences the expression of viral genes [44].
n3:mentions
n2:16912290
Subject Item
_:vb11107554
rdf:type
n3:Context
rdf:value
While the mechanism by which H2AX contributes to HCMV replication is unknown, p53 is found in RCs, binds viral DNA and evidence suggests that p53 influences the expression of viral genes [>>44<<]. However, the roles of ATM-mediated phosphorylation of H2AX or p53 to productive replication are not known at this point.
n3:mentions
n2:19224996
Subject Item
_:vb11107555
rdf:type
n3:Context
rdf:value
The kinase(s) responsible for phosphorylating H2AX in the absence of ATM at these later times is unknown but it is possible that another PI3-like kinase, perhaps ATR [>>45<<], is responsible for H2AX phosphorylation.
n3:mentions
n2:11100718
Subject Item
_:vb11107556
rdf:type
n3:Context
rdf:value
DNA PKcs, another PI3-like kinase, is known to phosphorylate H2AX in response to DNA damage signaling, but it has been shown that DNA PKcs does not localize to HCMV RCs [>>9<<]. However, even though H2AX can be phosphorylated by other kinases later during infection, activated ATM is mostly located in HCMV RCs at these times pi, leaving open the possibility that ATM is influencing activities in these nuclear
n3:mentions
n2:17151099
Subject Item
_:vb11107557
rdf:type
n3:Context
rdf:value
ATM is required for efficient H2AX phosphorylation in MHV68-infected primary marcrophages and ATM is relocalized to sites of viral genome deposition, although a viral kinase also contributes to H2AX phosphorylation [>>46<<]. ATM is also rapidly relocalized to replication compartments during HSV infection [3].
n3:mentions
n2:18005708
Subject Item
_:vb11107558
rdf:type
n3:Context
rdf:value
ATM is also rapidly relocalized to replication compartments during HSV infection [>>3<<]. It will be interesting to determine whether ATM is only transiently responsible for host DDR signaling (and viral replication) during infections with herpesviruses.
n3:mentions
n2:15824307
Subject Item
_:vb11107559
rdf:type
n3:Context
rdf:value
HCMV infection and expression of its major IE proteins, particular IE1 and IE2, have been shown to inactivate RB family members and induce the expression of E2F regulated genes [>>17<<], [33], [47], [48] possibly by providing host factors that contribute to virus replication.
n3:mentions
n2:1328853
Subject Item
_:vb11107560
rdf:type
n3:Context
rdf:value
HCMV infection and expression of its major IE proteins, particular IE1 and IE2, have been shown to inactivate RB family members and induce the expression of E2F regulated genes [17], [>>33<<], [47], [48] possibly by providing host factors that contribute to virus replication.
n3:mentions
n2:8892909
Subject Item
_:vb11107561
rdf:type
n3:Context
rdf:value
HCMV infection and expression of its major IE proteins, particular IE1 and IE2, have been shown to inactivate RB family members and induce the expression of E2F regulated genes [17], [33], [>>47<<], [48] possibly by providing host factors that contribute to virus replication.
n3:mentions
n2:11867723
Subject Item
_:vb11107562
rdf:type
n3:Context
rdf:value
HCMV infection and expression of its major IE proteins, particular IE1 and IE2, have been shown to inactivate RB family members and induce the expression of E2F regulated genes [17], [33], [47], [>>48<<] possibly by providing host factors that contribute to virus replication.
n3:mentions
n2:8026474
Subject Item
_:vb11107563
rdf:type
n3:Context
rdf:value
Inactivation of RB and the subsequent deregulation of E2F1—but not the related family members, E2F2 or E2F3, which also interact with RB—leads to an accumulation of DNA double-strand breaks in human fibroblasts [>>21<<]. Although it is not clear if HCMV infection causes extensive host DNA damage, infection can result in a DNA double strand break on chromosome 1 [49]. Whether this single DNA break is sufficient to initiate the observed host DDR is unclear.
n3:mentions
n2:16186801
Subject Item
_:vb11107564
rdf:type
n3:Context
rdf:value
Although it is not clear if HCMV infection causes extensive host DNA damage, infection can result in a DNA double strand break on chromosome 1 [>>49<<]. Whether this single DNA break is sufficient to initiate the observed host DDR is unclear. Alternately, it has been shown that activation of a DDR does not necessarily require DNA lesions. Rather, the physical interaction of DNA repair
n3:mentions
n2:10639169
Subject Item
_:vb11107565
rdf:type
n3:Context
rdf:value
Rather, the physical interaction of DNA repair factors with chromatin can be sufficient to activate the DDR signaling cascade [>>50<<]. Therefore, host chromosomal changes mediated by disruption of RB/E2F1 complexes or other mechanisms of E2F1 deregulation should also be considered as possible ATM activators during infection.
n3:mentions
n2:18483401
Subject Item
_:vb11107566
rdf:type
n3:Context
rdf:value
Most productive infections by DNA viruses result in deregulation of E2F activity through inactivation of RB and RB family members [>>51<<]. These viruses also activate an ATM-centric DDR, although some viruses, including MHV68, KSHV, and adenovirus, encode factors that can block signals from reaching ATM or its targets [37], [52], [53], [54].
n3:mentions
n2:11921304
Subject Item
_:vb11107567
rdf:type
n3:Context
rdf:value
These viruses also activate an ATM-centric DDR, although some viruses, including MHV68, KSHV, and adenovirus, encode factors that can block signals from reaching ATM or its targets [>>37<<], [52], [53], [54].
n3:mentions
n2:12124628
Subject Item
_:vb11107568
rdf:type
n3:Context
rdf:value
These viruses also activate an ATM-centric DDR, although some viruses, including MHV68, KSHV, and adenovirus, encode factors that can block signals from reaching ATM or its targets [37], [>>52<<], [53], [54].
n3:mentions
n2:16731925
Subject Item
_:vb11107569
rdf:type
n3:Context
rdf:value
These viruses also activate an ATM-centric DDR, although some viruses, including MHV68, KSHV, and adenovirus, encode factors that can block signals from reaching ATM or its targets [37], [52], [>>53<<], [54]. The herpesviral proteins responsible for this inhibition are often expressed during latency, which raises the possibility that the host DDR interferes with aspects of latency such as cell survival, proliferation or, perhaps, the
n3:mentions
n2:16474133
Subject Item
_:vb11107570
rdf:type
n3:Context
rdf:value
These viruses also activate an ATM-centric DDR, although some viruses, including MHV68, KSHV, and adenovirus, encode factors that can block signals from reaching ATM or its targets [37], [52], [53], [>>54<<]. The herpesviral proteins responsible for this inhibition are often expressed during latency, which raises the possibility that the host DDR interferes with aspects of latency such as cell survival, proliferation or, perhaps, the
n3:mentions
n2:14657032
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