Herpes simplex virus 1 DNA polymerase processivity factor UL42 inhibits TNF-α-induced NF-κB activation by interacting with p65/RelA and p50/NF-κB1 (Q24339512)

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English	Herpes simplex virus 1 DNA polymerase processivity factor UL42 inhibits TNF-α-induced NF-κB activation by interacting with p65/RelA and p50/NF-κB1	scientific article

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Herpes simplex virus 1 DNA polymerase processivity factor UL42 inhibits TNF-α-induced NF-κB activation by interacting with p65/RelA and p50/NF-κB1 (English)

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object named as

Chunfu Zheng

4

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author name string

Jie Zhang

1

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Shuai Wang

2

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Kezhen Wang

3

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language of work or name

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publication date

August 2013

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Medical Microbiology and Immunology

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202

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4

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313-25

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Pathogen recognition and innate immunity

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Recognition of microorganisms and activation of the immune response

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Innate immune response to viral infection

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The NF-kappaB family of transcription factors and its regulation

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NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses

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NF-kappaB regulation in the immune system

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The two NF-kappaB activation pathways and their role in innate and adaptive immunity

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Ubiquitin signalling in the NF-kappaB pathway

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Signaling to NF-kappaB

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Introduction to NF-kappaB: players, pathways, perspectives

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NF-kappa B: ten years after

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The NF-kappa B and I kappa B proteins: new discoveries and insights

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Mechanisms employed by herpes simplex virus 1 to inhibit the interferon response

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Herpes simplex virus immediate-early ICP0 protein inhibits Toll-like receptor 2-dependent inflammatory responses and NF-kappaB signaling

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HSV ICP0 recruits USP7 to modulate TLR-mediated innate response

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Activation of NF-κB in CD8+ dendritic cells Ex Vivo by the γ134.5 null mutant correlates with immunity against herpes simplex virus 1.

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The virion host shutoff protein of herpes simplex virus 1 blocks the replication-independent activation of NF-κB in dendritic cells in the absence of type I interferon signaling.

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Functional Interaction between the Herpes Simplex Virus Type 1 Polymerase Processivity Factor and Origin-Binding Proteins: Enhancement of UL9 Helicase Activity

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Evidence against a simple tethering model for enhancement of herpes simplex virus DNA polymerase processivity by accessory protein UL42.

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Effects of substitutions of arginine residues on the basic surface of herpes simplex virus UL42 support a role for DNA binding in processive DNA synthesis

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Mutations that decrease DNA binding of the processivity factor of the herpes simplex virus DNA polymerase reduce viral yield, alter the kinetics of viral DNA replication, and decrease the fidelity of DNA replication

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Herpes simplex virus mutants with multiple substitutions affecting DNA binding of UL42 are impaired for viral replication and DNA synthesis

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Characterization of the subcellular localization of herpes simplex virus type 1 proteins in living cells

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The NF-kappa B activation in lymphotoxin beta receptor signaling depends on the phosphorylation of p65 at serine 536.

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The measles virus V protein binds to p65 (RelA) to suppress NF-kappaB activity

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IKK-1 and IKK-2: Cytokine-Activated IκB Kinases Essential for NF-κB Activation

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Sustained activation of protein kinase C downregulates nuclear factor-kappaB signaling by dissociation of IKK-gamma and Hsp90 complex in human colonic epithelial cells

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Comprehensive characterization of interaction complexes of herpes simplex virus type 1 ICP22, UL3, UL4, and UL20.5.

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Rel/NF-kappa B and I kappa B proteins: an overview

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Herpes simplex type 1 induction of persistent NF-kappa B nuclear translocation increases the efficiency of virus replication

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Activation of I kappa b kinase by herpes simplex virus type 1. A novel target for anti-herpetic therapy

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The patterns of accumulation of cellular RNAs in cells infected with a wild-type and a mutant herpes simplex virus 1 lacking the virion host shutoff gene

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Efficient replication by herpes simplex virus type 1 involves activation of the IkappaB kinase-IkappaB-p65 pathway

1 reference

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Herpesvirus tegument protein activates NF-kappaB signaling through the TRAF6 adaptor protein

1 reference

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U L 31 of Herpes Simplex Virus 1 Is Necessary for Optimal NF-κB Activation and Expression of Viral Gene Products

1 reference

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Influenza A virus-encoded NS1 virulence factor protein inhibits innate immune response by targeting IKK.

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Counteraction of interferon-induced antiviral responses by herpes simplex viruses.

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