C, ChIP assay was used to test the binding of exogenous IRF - 9 to RIG -
G gene promoter.
This notion was sustained by the fact that IRF - 1 could activate the RIG -
G gene promoter in IRF - 9 — deficient U2A cells and by our ChIP assay, confirming the ability of IRF - 1 to bind the RIG -
G gene promoter (Fig. 4D).
Besides, some other potential cis - acting elements for transcription factors [such as CAAT / enhancer binding protein (C / EBP) and PU.1] have been also noted in the RIG -
G gene promoter.
Not exact matches
Published in
Genes Chromosomes Cancer Harland M, Holland EA, Ghiorzo P, Mantelli M, Bianchi - ScarrĂ
G, Goldstein AM, Tucker MA, Ponder BA, Mann GJ, Bishop DT, Newton Bishop J. Mutation screening of the CDKN2A
promoter in melanoma families.
It was noteworthy that IRF - 1 alone could significantly induce the expression of the reporter
gene containing RIG -
G promoter (Fig. 1C).
Because both IRF - 1 and the complex IRF - 9 / STAT2 could bind the RIG -
G gene, we therefore conducted a detailed functional analysis on RIG -
G promoter to precise the molecular basis for RIG -
G expression.
In this study, we provide the first evidence that in STAT1 - deficient U3A cells, STAT2 forms a complex with IRF - 9 on the ISRE regions of RIG -
G promoter and effectively mediates the transcription of RIG -
G gene, even without the tyrosine phosphorylation.
Several IFN signaling pathway — related key regulators, including STAT1, STAT2, IRF - 1, and IRF - 9, were transfected individually or in combination into STAT1 - deficient U3A cells, together with a luciferase reporter
gene containing RIG -
G promoter.
C, schematic representation of the wt or mutant RIG -
G promoter - luciferase reporter
gene constructs.
In addition, IRF - 1 itself can also recognize the ISRE sequences and directly bind RIG -
G promoter to induce RIG -
G gene expression.
These observations clearly indicated that the two ISRE sequences in RIG -
G promoter were the molecular basis for RIG -
G gene expression.