Jul 10, 2019 · In this study, we discovered that the Wnt/β-catenin signaling destabilizes IRF1 through the ubiquitination-proteasome pathway, and that reduced expression of IRF1 is involved in the...

Feb 19, 2003 · The strong inhibition of soft-agar growth in the cells expressing c-myc and c-Ha-ras looks like a complete reversal of the oncogenic phenotype by IRF-1 expression.

May 26, 2015 · Interferon Regulatory Factor (IRF)-1, originally identified as a transcription factor of the human interferon (IFN)-β gene, mediates tumor suppression and may inhibit oncogenesis.

Aug 15, 1994 · Here we report that c-myc- or fosB-transformed rat embryonic fibroblast cells can be reverted by the introduction of the IRF-1 gene. Thus, the anti-oncogenic function of IRF-1 is not limited to only IRF-2 overexpressing cells, suggesting the broad role of IRF-1 …

MYC directly occupies IRF7 promoter to repress its expression. MYC is a well-known transcription factor that regulates the expression of many genes either as an enhancer or repressor by binding to consensus sequences (E-boxes).

IRF-1 regulates expression of target genes by binding to an interferon stimulated response element (ISRE) in their promoters. The IRF-1 protein binds to the ISRE via an N-terminal helix-turn-helix DNA binding domain, [7] which is highly conserved among all IRF proteins.

Apr 1, 2007 · IFN regulatory factor-1 (IRF-1) is a major target gene of IFNs. It inhibits cell proliferation and oncogenic transformation. Here, we show that 60% of all mRNAs deregulated by oncogenic transformation mediated by c-myc and H-ras are reverted to the expression levels of nontransformed cells by IRF-1.

Aug 15, 1994 · Here we report that c-myc- or fosB-transformed rat embryonic fibroblast cells can be reverted by the introduction of the IRF-1 gene. Thus, the anti-oncogenic function of IRF-1 is not limited to only IRF-2 overexpressing cells, suggesting the broad role of IRF-1 …

Oct 1, 2021 · Myc overexpression in IRF4-deficient cells was sufficient to overcome the cell growth defect. Together, these data reveal an IRF4-MYC-mTORC1 relationship critical for controlling cell growth and the proliferative response during B cell differentiation.

Fine-tuning of these ancient IRF1-mediated host defenses, and countering strategies by pathogens to disarm IRF1, play crucial roles in pathogenesis and determining the outcome of infection. Innate immunity provides a critical biological barrier protecting the …