tetano
Editor, Senior Moderator
Virology. 2018 Sep 18;525:40-47. doi: 10.1016/j.virol.2018.09.005. [Epub ahead of print]
[h=1]CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein.[/h] Cui L[SUP]1[/SUP], Mahesutihan M[SUP]1[/SUP], Zheng W[SUP]2[/SUP], Meng L[SUP]3[/SUP], Fan W[SUP]2[/SUP], Li J[SUP]1[/SUP], Ye X[SUP]1[/SUP], Liu W[SUP]4[/SUP], Sun L[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Cell division cycle 25 B (CDC25B) is a member of the CDC25 phosphatase family. It can dephosphorylate cyclin-dependent kinases and regulate the cell division cycle. Moreover, siRNA knockdown of CDC25B impairs influenza A virus (IAV) replication. Here, to further understand the regulatory mechanism of CDC25B for IAV replication, a CDC25B-knockout (KO) 293T cell line was constructed using CRISPR/Cas9. The present data indicated that the replication of IAV was decreased in CDC25B-KO cells. Additionally, CDC25B deficiency damaged viral polymerase activity, nucleoprotein (NP) self-oligomerization, and NP nuclear export. Most importantly, we found that the NP phosphorylation levels were significantly increased in CDC25B-KO cells. These findings indicate that CDC25B facilitates the dephosphorylation of NP, which is vital for regulating NP functions and the life cycle of IAV.
[h=4]KEYWORDS:[/h] CDC25B; Influenza A virus; Nuclear export; Nucleoprotein; Phosphorylation; Self-oligomerization
PMID: 30240957 DOI: 10.1016/j.virol.2018.09.005
[h=1]CDC25B promotes influenza A virus replication by regulating the phosphorylation of nucleoprotein.[/h] Cui L[SUP]1[/SUP], Mahesutihan M[SUP]1[/SUP], Zheng W[SUP]2[/SUP], Meng L[SUP]3[/SUP], Fan W[SUP]2[/SUP], Li J[SUP]1[/SUP], Ye X[SUP]1[/SUP], Liu W[SUP]4[/SUP], Sun L[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Cell division cycle 25 B (CDC25B) is a member of the CDC25 phosphatase family. It can dephosphorylate cyclin-dependent kinases and regulate the cell division cycle. Moreover, siRNA knockdown of CDC25B impairs influenza A virus (IAV) replication. Here, to further understand the regulatory mechanism of CDC25B for IAV replication, a CDC25B-knockout (KO) 293T cell line was constructed using CRISPR/Cas9. The present data indicated that the replication of IAV was decreased in CDC25B-KO cells. Additionally, CDC25B deficiency damaged viral polymerase activity, nucleoprotein (NP) self-oligomerization, and NP nuclear export. Most importantly, we found that the NP phosphorylation levels were significantly increased in CDC25B-KO cells. These findings indicate that CDC25B facilitates the dephosphorylation of NP, which is vital for regulating NP functions and the life cycle of IAV.
[h=4]KEYWORDS:[/h] CDC25B; Influenza A virus; Nuclear export; Nucleoprotein; Phosphorylation; Self-oligomerization
PMID: 30240957 DOI: 10.1016/j.virol.2018.09.005