+ |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
EBNA1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266803 |
|
|
Homo sapiens |
|
pmid |
sentence |
29659505 |
We found that EBV-encoded Qp-EBNA1 can be upregulated by NF-κB, while EBNA1 protein expression has been shown to negatively regulate NF-κB activation by inhibiting IKKα/β phosphorylation |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | EBV infection |
+ |
EBNA1 | up-regulates quantity by expression
transcriptional regulation
|
STAT1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267614 |
|
|
Homo sapiens |
AGS Cell, HONE-1 Cell |
pmid |
sentence |
17486072 |
EBNA1 enhances the expression and activity of STAT1. EBNA1 also induced STAT1 expression, with associated enhancement of IFNγ-induced activation. The ability of EBNA1 to enhance IFNγ-induced STAT1 signaling was observed at the protein level by enhanced nuclear translocation of STAT1 (Figure 3b) and at the transcriptional level. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | EBV infection |
+ |
EBNA1 | down-regulates quantity
destabilization
|
SMAD2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-267615 |
|
|
Homo sapiens |
Nasopharyngeal Carcinoma Cell |
pmid |
sentence |
17486072 |
The studies described above show that SMAD2 protein levels are reduced by EBNA1 with consequent attenuation of SMAD2 activation in response to TGFβ1. This analysis confirmed the stability of the EBNA1 protein and revealed that the SMAD2 protein is more rapidly degraded in Ad/AH cells expressing EBNA1 as compared to the control cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | EBV infection |
+ |
EBNA1 | down-regulates activity
|
IKK-complex |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266802 |
|
|
Homo sapiens |
|
pmid |
sentence |
29659505 |
EBNA1 has been reported to block p65 activation by inhibiting IKKα/β through an unknown mechanism, we suggest that, in NPC, NF-κB signaling and EBNA1 may form a regulatory loop which supports EBV latent gene expression, while also limiting NF-κB activity |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | EBV infection |