Interferon regulatory factor-1 (IRF1) binds to the upstream cis elements of both the interferon-alpha and the interferon-beta genes.
It was found that IRF1 functions as a transcriptional activator for the type I IFN genes.
NCBI Summary:
IRF1 encodes interferon regulatory factor 1, a member of the interferon regulatory transcription factor (IRF) family. IRF1 serves as an activator of interferons alpha and beta transcription, and in mouse it has been shown to be required for double-stranded RNA induction of these genes. IRF1 also functions as a transcription activator of genes induced by interferons alpha, beta, and gamma. Further, IRF1 has been shown to play roles in regulating apoptosis and tumor-suppressoion.
General function
Nucleic acid binding, DNA binding, Transcription factor
Comment
Cellular localization
Nuclear
Comment
Ovarian function
Luteinization, Oocyte maturation
Comment
Expression of interferon regulatory factor-1 in the mouse cumulus-oocyte complex is negatively related with oocyte maturation. Kim YS et al. We found previously that interferon regulatory factor (Irf)-1 is a germinal vesicle (GV)-selective gene that highly expressed in GV as compared to metaphase II oocytes. To our knowledge, the function of Irf-1 in oocytes has yet to be examined. The present study was conducted to determine the relationship between retinoic acid (RA) and RA-mediated expression of Irf-1 and the mouse oocyte maturation.
Expression regulated by
Growth Factors/ cytokines
Comment
Ovarian localization
Oocyte, Cumulus, Luteal cells
Comment
Suter J, et al 2001 reported the mediators of interferon gamma-initiated signaling in bovine
luteal cells. Interferon gamma (IFN gamma) has been implicated as a mediator of luteal
steroidogenesis and cell fate. IFN gamma -initiated signaling events, although
implied by studies in cell lines, have yet to be described in primary luteal
cells. Dispersed bovine luteal cell
cultures were challenged with increasing levels of bovine recombinant IFN
gamma (0-1000 U) or IFN gamma (200 U) in the presence or absence of tumor
necrosis factor cu (TNF alpha, 10 ng/ml) over time (short term, 0-60 min; long
term, 0, 24, 48 h). Fractionated or total cell lysates were evaluated by the
Western blotting technique to determine the changes in the levels of signal
transducers and activators of transcription (STAT), interferon regulatory
factor 1 (IRF-1), and I kappa B alpha (I kappaB-alpha). Utilizing antibodies
that recognize the nonphosphorylated forms of STAT-1 and STAT-3, it was
determined that levels of STAT-1 and STAT-3 in total cell lysates were
constitutively expressed and did not change in response to treatment with IFN
gamma or TNFa. In contrast, nuclear levels of STAT-1 and phosphorylated STAT-3
were elevated in a time-dependent manner in response to IFN gamma treatment.
Furthermore, IFN gamma and TNF alpha treatment elevated levels of IRF-1 within
2 h. TNF alpha -induced increases in the levels of IRF-1 were transient,
whereas the levels of IRF-1 in response to IFN gamma treatment remained
elevated at 48 h.