|
Kidney: Vero cells
|
HSV-1 strain 17
|
–
|
c-Rel
|
As a novel cause of HSE disease susceptibility.
|
[31]
|
|
Hematological: Jurkat cells
|
HSV-1
|
–
|
p65/c-Rel
|
the p65/c-Rel heterodimer is responsible for the NF-kB-dependent induction of HIV-1 LTR in HSV- 1-infected cells.
|
[32]
|
|
Embryonic: WT and dOct MEF cells
|
HSV-1 strain F
|
Oct-1
|
–
|
Oct-1 is required for the formation of HSV replication factories and late gene expression.
|
[33]
|
|
Digestive: Hep2 cells
|
HSV-1 strain KOS
|
Oct-1
|
–
|
Oct-1 directly recognizes TAATGARAT elements in promoters of IE genes.
|
[34]
|
|
Urinary: COS-7 cells
|
HSV-1 strain KOS
|
Oct-1
|
–
|
Distinct conformations of Oct-1 on the BHV IE1 sites and on the HSV IE110 sites.
|
[35]
|
|
Genital: HeLa cells
|
HSV-1 strain F
|
Oct-1
|
–
|
late in infection Oct-1 is posttranslationally modified and exhibits a reduced capacity to bind to its cognate sites.
|
[36]
|
|
Genital: HeLa cells
|
HSV-1 strain KOS
|
Oct-1
|
–
|
Ser375 is important for the interaction of VP16 with Oct-1, and that the interaction is required to enable both proteins to bind to IE promoters.
|
[28]
|
|
Genital: HFF
|
HSV-1 strain KOS
|
Oct-1
|
–
|
forms a transactivation complex with the cellular proteins HCF-1 and HSV-1 VP16 tegument protein.
|
[29]
|
|
Genital: HeLa cells
|
HSV-2 strain 333
|
Oct-1
|
–
|
the HSV-2 protein forms a transcriptional complex with the cellular Oct-1 protein and target TAATGARAT elements from immediate-early promoters.
|
[37]
|
