Neuronal sprouting in mouse sensory ganglia infected with herpes simplex virus type 2 (HSV-2): Induction of growth-associated protein (GAP-43) and ultrastructural evidence

Henken, Deborah B.; Goldstein, Murray; Zhang, Qian-Lin; Curtis, Rory

doi:10.3109/13550289509113962

Cited by 5 publications

(2 citation statements)

References 36 publications

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“…Acyl protein thioesterases are involved in cellular fatty acid metabolism process. Acyl-protein thioesterase 2 catalyzes the deacylation of peripheral membrane-associated GAP-43, which is induced in Herpes simplex virus infection . Platelet activating factor acetylhydrolase (PAF-AH) beta and gamma subunits were down-regulated in A549 cells.…”

Section: Discussionmentioning

confidence: 99%

“…Acyl-protein thioesterase 2 catalyzes the deacylation of peripheral membrane-associated GAP-43, which is induced in Herpes simplex virus infection. 79 Platelet activating factor acetylhydrolase (PAF-AH) beta and gamma subunits were down-regulated in A549 cells. PAF-AH activity is found to be significantly lower in HCV patients.…”

Section: Proteasomal Subunits Are Affected By Iav Infectionmentioning

confidence: 99%

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Proteasomal Serine Hydrolases Are Up-Regulated by and Required for Influenza Virus Infection

Shahiduzzaman

Ezatti²,

et al. 2014

J. Proteome Res.

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Interactions between viruses and their host cells are important determinants of virus replication and of immune responses to the virus. However, these interactions and resulting consequences of these interactions remain poorly defined. Numerous recent quantitative proteomic approaches have measured host proteins affected by virus infection. Here, we used activity-based protein profiling (ABPP) to measure functional alterations in host serine hydrolases after influenza A virus infection of Madin-Darby canine kidney and human A549 lung cells. We identified 62 serine proteases. We then combined the ABPP approach with stable isotope labeling to directly measure how serine hydrolase activities were affected by virus infection. Differentially regulated SHs mapped into a few key cellular pathway systems, most notably the proteasomal system. The specific serine protease inhibitors Aprotinin and Pefablock and specific proteasomal inhibitors Bortezomib and MG132 significantly inhibited influenza virus growth. Some inhibitors also down-regulated activities of several proteasomal proteins, including PSMA1, PSMA2, and PMSB3. Genetic knockdown of PMSA2 also attenuated influenza virus replication. These findings further our understanding of enzymatic cellular processes affected by influenza virus and may be beneficial in the search for additional antiviral therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

Section: Proteasomal Subunits Are Affected By Iav Infectionmentioning

confidence: 99%

Proteasomal Serine Hydrolases Are Up-Regulated by and Required for Influenza Virus Infection

Shahiduzzaman

Ezatti²,

et al. 2014

J. Proteome Res.

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Viral Persistent Infection Affects both Transcriptional and Posttranscriptional Regulation of Neuron-Specific Molecule GAP43

Cao¹,

Oldstone

Torre

1997

Virology

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Recently, we reported that in vitro and in vivo persistent infection of neurons by lymphocytic choriomeningitis virus (LCMV) downregulated GAP43 expression, a protein involved in neuronal plasticity associated with learning and memory. Here, we investigated the transcriptional and posttranscriptional events involved. Persistent LCMV infection of PC12 cells (PC12Pi) caused reduced levels of GAP43 steady-state mRNA when compared to uninfected PC12 cells. In addition, an increase in the steady-state levels of GAP43 mRNA observed in PC12 cells in response to nerve growth factor (NGF) was abrogated in PC12Pi cells. Nuclear run-on analysis revealed that the rate of GAP43 transcription was reduced threefold in PC12Pi cells compared to uninfected PC12 cells. Moreover, analysis of the half-life of GAP43 mRNA indicated that NGF-mediated stabilization of GAP43 transcripts was significantly diminished in PC12Pi cells. Treatment of PC12Pi cells with basic fibroblast growth factor, dibutyryl cyclic AMP, and 12-o-tetradecanoyl-phorbol-13-acetate, a potent activator of protein kinase C, did not increase the GAP43 mRNA steady-state level, suggesting that LCMV infection interferes with a step downstream from protein kinases A and C in the NGF signal transduction pathway.

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Molecular circuitry regulating herpes simplex virus type 1 latency in neurons

Millhouse¹,

Wigdahl²

2000

J Neurovirol

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Neuronal sprouting in mouse sensory ganglia infected with herpes simplex virus type 2 (HSV-2): Induction of growth-associated protein (GAP-43) and ultrastructural evidence

Cited by 5 publications

References 36 publications

Proteasomal Serine Hydrolases Are Up-Regulated by and Required for Influenza Virus Infection

Proteasomal Serine Hydrolases Are Up-Regulated by and Required for Influenza Virus Infection

Viral Persistent Infection Affects both Transcriptional and Posttranscriptional Regulation of Neuron-Specific Molecule GAP43

Molecular circuitry regulating herpes simplex virus type 1 latency in neurons

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