human cytomegalovirus and map kinase pathways
| PAG Title | human cytomegalovirus and map kinase pathways |
| PAG ID | WAG000423 |
| Type | P |
| Source Link |  BioCarta |
| Publication Reference | NA |
| PAG Description | To replicate in the host cell, viruses commandeer cellular sigling pathways. Cytomegalovirus (CMV) is a D virus with that is widespread in the population but usually causes disease only in immunocompromised individuals and is also a viral cause of birth defects. One of the actions of CMV in the host cell is to stimulate MAP kise pathways. Both p38 and ERK kises are activated by CMV infection through activation map kise kises and inhibition of phosphatases. One result of Map kise activation by CMV is activation of transcription of viral genes, increasing the production of viral gene products. Both p38 and ERK kises contribute to the activation of viral genes by cellular transcription factors acting through the viral UL4 promoter at upstream and basal transcription elements. Another target of prolonged p38 activation during infection is Rb, contributing to viral replication. Activation of MKK1 and MKK2 leads to Erk1 and Erk2 activation, and phosphorylation of downstream targets. The MEKK1 kise regulates the immediate early promoter indirectly through downstream kise sigling and perhaps more directly through activation of NF-kB. Map kise pathways activated by CMV converge on increased transcription of viral genes and increased replication of the viral genome. Better understanding of the mechanisms involved in the interaction of CMV with cellular sigling machinery will provide improved ways to treat CMV-mediated disease. |
| Species | Homo sapiens |
| nCoCo Score | 3,011 |
| Base PAG ID | WAG000423 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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