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Table 3 The TRFs c-Rel and Oct-1 are functional during HSV infection

From: Novel transcription regulatory sequences and factors of the immune evasion protein ICP47 (US12) of herpes simplex viruses

Tissue type HSV strain Oct-1 c-Rel Function Ref.
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]
  1. HSE Herpes simplex encephalitis, HIV human immunodeficiency virus, LTR long terminal repeat