Abstract: Pseudotyped HIV-1 with Tat S16E mutation replicated well, and HIV-1 Tat S46E-poorly, but no live viruses were obtained with Tat S16A or Tat S46A mutations.
Abstract: TAR RNA binding was affected by Tat Ser-16 alanine mutation.
Figure: 293T cells were co-transfected with pCI-His-hUbi pla
Figure: b, c Replication of VSVg pseudotyped pNL4-3.Luc.R-E-vectors with WT and mutant Tat S16A, S16E, S46A and S46E sequences.
Uncoating of human immunodeficiency virus type 1 requires prolyl isomerase Pin1.
PMID: 20529865
2010
The Journal of biological chemistry
Result: The S16A
Result: The viral entry assay indicated that the entry levels of S16A/P17A and WT were the same because the amounts of S16A/P17A CA protein in subcellular fractions were very similar to that of WT CA protein.
Result: These results suggest that the infectivity defect of the S16A/P17A variant is linked to a dysfunction of the uncoating process.
Result: To study the role of the phosphorylated Ser16 that precedes Pro, we replaced Ser16 with glutamic acid (S16E) or alanine (S16A) to mimic phosphorylated or unphosphorylated Ser, respectively.
Phosphorylation of HIV-1 Tat by CDK2 in HIV-1 transcription.