Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Varicella zoster virus glycoprotein I (VZV gpI; Mr 98,000) was phosphorylated in virus-infected human cell monolayers, while two other major VZV glycoproteins (gpII and gpIII) were not similarly modified. Phosphorylation of VZV gpI was not blocked by inhibitors of glycosylation, nor were the phosphoryl groups enzymatically removed by endoglycosidases. Phosphoamino acid analysis revealed the presence of phosphoserine and phosphothreonine residues on the polypeptide backbone. The selective nature of the phosphorylation event was further demonstrated in vitro by a protein kinase (Mr 50,000), which was present in virus-infected cells but absent from uninfected cells or purified virions. The enzyme catalyzed the transfer of 32Pi from [gamma-32P]ATP to gpI but not to gpII and gpIII. Like VZV gpI, this virus-induced protein kinase was also a constituent of the plasma membrane of live VZV-infected cells.
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PMID:Varicella zoster virus glycoprotein gpI is selectively phosphorylated by a virus-induced protein kinase. 302 58

Varicella zoster virus tegument components include the regulatory proteins IE4, IE62, IE63 and the ORFI0 protein, a protein kinase (ORF47) and an abundant protein encoded in ORF9 which is the homolog of HSV VP22. The kinase is able to phosphorylate IE62 and the ORF9 protein specifically in viral particles. We show that interactions among these proteins are, at least in part, dependent on the presence or absence of phosphate groups and we suggest models for tegument formation and for its dissolution in the infected cell.
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PMID:Interactions among structural proteins of varicella zoster virus. 1133 53

Varicella zoster virus (VZV) results in chicken pox and herpes zoster. Female rats show a higher level of herpes zoster associated pain than males, consistent with human studies. In this study, we addressed the novel hypothesis that sex difference in herpes zoster associated pain is due, in part, to estradiol modulating activity in the thalamus. To test this hypothesis a high and low physiological dose of estradiol was administered to castrated and ovariectomized rats and the affective pain response was measured after injection of VZV into the whisker pad. Thalamic infusion of the estrogen receptor antagonist ICI 182,780 concomitant with a high dose of estradiol addressed the role of estradiol binding to its receptor to effect pain. Phosphorylated extracellular signal-regulated protein kinase (pERK) positive cells were measured in excitatory (glutaminase positive) and inhibitory (glutamate decarboxylase 67 positive) cells of the lateral thalamic region. Our results show that a high dose of estradiol significantly reduced the pain response in both males and females. pERK significantly increased in excitatory cells after treatment with a low dose of estradiol and increased in inhibitory cells after treatment with a high dose of estradiol. Administration of ICI 182,780 significantly increased the pain response, reduced expression of GABA related genes in the thalamic region and significantly reduced the number of inhibitory cells expressing pERK. The results suggest that estradiol attenuates herpes zoster pain by increasing the activity of inhibitory neurons within the thalamus and that this reduction includes an estrogen receptor dependent mechanism.
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PMID:Estradiol Acts in Lateral Thalamic Region to Attenuate Varicella Zoster Virus Associated Affective Pain. 3127 31