ATR and ATRIP Are Recruited to Herpes Simplex Virus Type 1 Replication Compartments Even though ATR Signaling Is Disabled
نویسندگان
چکیده
منابع مشابه
Upstream-binding factor is sequestered into herpes simplex virus type 1 replication compartments
Previous reports have shown that adenovirus recruits nucleolar protein upstream-binding factor (UBF) into adenovirus DNA replication centres. Here, we report that despite having a different mode of viral DNA replication, herpes simplex virus type 1 (HSV-1) also recruits UBF into viral DNA replication centres. Moreover, as with adenovirus, enhanced green fluorescent protein-tagged fusion protein...
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Background and Aims: Several drugs are being used in treatment of HSV infection in human but still introducing an effective safe drug is desirable. Methods: We investigated the inhibitory effect of morphine on replication of HSV in vitro. Results: The results indicated that a concentration of up to 200 ug/ml morphine had a limited effect on Vero cell viability. At this concentration the growt...
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Herpes Simplex Virus type 1 (HSV-1) has evolved to disable the cellular DNA damage response kinase, ATR. We have previously shown that HSV-1-infected cells are unable to phosphorylate the ATR substrate Chk1, even under conditions in which replication forks are stalled. Here we report that the HSV-1 single stranded DNA binding protein (ICP8), and the helicase/primase complex (UL8/UL5/UL52) form ...
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متن کامل
Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection.
Like other DNA viruses, herpes simplex virus type 1 (HSV-1) interacts with components of the cellular response to DNA damage. For example, HSV-1 sequesters endogenous, uninduced, hyperphosphorylated RPA (replication protein A) away from viral replication compartments. RPA is a ssDNA-binding protein that signals genotoxic stress through the ATR (ataxia telangiectasia-mutated and Rad3-related) pa...
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ژورنال
عنوان ژورنال: Journal of Virology
سال: 2010
ISSN: 0022-538X,1098-5514
DOI: 10.1128/jvi.01643-10