PMC:7640975 / 58420-60881
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7640975","sourcedb":"PMC","sourceid":"7640975","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7640975","text":"Finally, we sought to uncover the hidden interaction networks among the DEPs using STRING analysis, and discovered three major functional networks consisting of the RIG-I-like receptor, PDK1-AKT2 and cell cycle signaling pathways. These findings are in accordance with the results of KEGG pathway analysis, thus further consolidating the credibility of these putative signaling pathways involved in PDCoV-infected IPEC-J2 cells. Given the former two signaling pathways have already been discussed earlier, we next focus on the cell cycle signaling pathway. As can be seen from the network diagram (Figure 6), three small networks with NUP37, SMARCA2, and CDK9 as the respective hub proteins together constitute the cell cycle signaling pathway. NUP37 is an important constituent of the nuclear pore Nup107–160 subcomplex, which controls the bidirectional trafficking of macromolecules that traverse the nuclear envelope.72 SMARCA2 is an important member of the SWI/SNF family with helicase and ATPase activities, and has been shown to regulate numerous biological processes such as cell proliferation and DNA repair.73 CDK9 paired with cyclin T1 forms the positive transcription elongation factor b (p-TEFb) complex and induces transcriptional activation by hyperphosphorylating RNA polymerase II, and thereby regulating numerous vital cellular functions including proliferation, differentiation, DNA repair and apoptosis.74,75 However, growing studies suggest that CDK9 is also related to many pathologic processes, such as cancer, cardiovascular diseases and viral replication.74 Currently, CDK9 has been demonstrated to be involved in the replication of multiple viruses, such as influenza A virus, dengue virus, human adenovirus, and human immunodeficiency virus.75 For example, CDK9 was found to interact with the viral RNA-dependent RNA polymerases of influenza A virus and facilitate its association with cellular RNA polymerase II, thereby promoting viral transcription.76 CDK9 was also shown to be critical for the transcription of viral early genes and the replication of human adenovirus. Treatment of host cells with the CDK9 inhibitor, FIT-039, which functions by suppressing mRNA transcription, can efficiently inhibits the replication of human adenovirus.77 In the present study, CDK9 was significantly downregulated in IPEC-J2 cells upon PDCoV infection; however, the biological functions hidden behind this change warrant further 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