| 1994 |
RFX1 belongs to a novel family of DNA-binding proteins (RFX1, RFX2, RFX3) that share five conserved regions including DNA-binding and dimerization domains; RFX proteins heterodimerize both in vitro and in vivo, and their DNA binding shows a peculiar dependence on methylated CpG dinucleotides at certain sites. |
Cloning, in vitro and in vivo heterodimerization assays, DNA-binding specificity assays |
Molecular and cellular biology |
High |
8289803
|
| 1993 |
RFX1 (identical to enhancer factor C, EF-C) is a transactivator of hepatitis B virus enhancer I; RFX1-specific antisense oligonucleotides inhibit EnhI-driven expression, and RFX1 transactivates EnhI in liver-derived but not non-liver cell lines, indicating cooperation with liver-specific factors. |
Antisense oligonucleotide inhibition, transfection assays |
Molecular and cellular biology |
High |
8413236
|
| 1989 |
EF-C (later identified as RFX1) binds to an inverted repeat (5'-GTTGCNNNGCAAC-3') in the HBV enhancer; diethyl pyrocarbonate interference and mutation analysis showed that EF-C contacts symmetrical nucleotides within the repeat, and spacer-length mutations demonstrated that binding is stabilized by dimerization. |
Diethyl pyrocarbonate interference binding assays, competition binding, site-directed mutagenesis, in vivo enhancer assays |
Molecular and cellular biology |
High |
2550788
|
| 1997 |
RFX1 contains an N-terminal glutamine-rich activation domain and a C-terminal repression domain overlapping the dimerization domain; these two activities mutually neutralize each other in the intact protein, producing a nearly inactive transcription factor that can be relieved of self-neutralization to act as a dual-function regulator. |
Deletion mutant analysis, chimeric protein assays, transfection reporter assays |
Nucleic acids research |
High |
9278482
|
| 1998 |
RFX1 possesses a split, extended dimerization domain composed of multiple conserved boxes; this domain mediates formation of two alternative homodimeric DNA-protein complexes (a standard complex and a novel extremely low-mobility complex formed only with palindromic DNA), and formation of the low-mobility complex correlates with transcriptional repression. |
Deletion analysis, electrophoretic mobility shift assays, transfection reporter assays |
The Journal of biological chemistry |
High |
9733744
|
| 1995 |
MIBP1 and RFX1 are distinct molecules that associate in vivo and form complexes at the c-myc intron I (MIF-1) element and MHC class II X-box; the MIF-1/EP element can function as a silencer in HepG2 and HeLa cells. |
Co-immunoprecipitation, supershift EMSA, silencer assays |
Molecular and cellular biology |
High |
7760800
|
| 1995 |
Purified EF-C/RFX1 requires an intact inverted repeat for stable binding and functional activity at viral enhancers; at the MHC class II DRA promoter, RFX1 binds only a half-site, which is unstable, suggesting an additional stabilizing activity is needed at MHC class II promoters. |
Chemical footprinting, modification interference assays, EMSA with purified protein, enhancer functional assays |
The Journal of biological chemistry |
High |
7713944
|
| 1999 |
RFX1 binding inversely correlates with PCNA promoter transcriptional activity; mutations within the RFX1 consensus site reduce RFX1 binding and increase promoter activity, indicating RFX1 plays an inhibitory role in PCNA gene regulation. |
EMSA, site-directed mutagenesis, transfection reporter assays (CAT) |
The Journal of biological chemistry |
High |
10336433
|
| 2000 |
Protein kinase C (PKC) activation induces nuclear translocation of RFX1 in HL-60 cells; increased nuclear RFX1 binds the c-myc intron 1 X box (MIE1), and this binding is required for PMA-induced down-regulation of c-myc expression. |
EMSA with supershift, subcellular fractionation, PKC inhibitor, transfection with myc reporter constructs, RFX1 antiserum |
The Journal of biological chemistry |
High |
10918054
|
| 2001 |
RFX1 contains a nonclassical nuclear localization signal (NLS) at its extreme C-terminus; an adjacent acidic region potentiates the NLS but also inhibits DNA-binding activity (autoinhibitory mechanism); the dimerization domain enhances nuclear association, while the acidic region inhibits it, coordinating nuclear import and DNA binding potentially via PKC-mediated phosphorylation. |
Confocal fluorescence microscopy, subcellular fractionation, deletion mutant analysis |
European journal of biochemistry |
High |
11358531
|
| 1993 |
RFX1 antisense oligonucleotides specifically inhibit IFN-γ-inducible but not constitutive expression of MHC class II genes (HLA-DR, -DQ, -DP) in monocytic cells, revealing distinct roles for RFX1 in the inducible versus constitutive modes of MHC class II regulation. |
Antisense oligonucleotide inhibition, flow cytometry for HLA class II expression |
European journal of immunology |
Medium |
8223867
|
| 1999 |
The C-terminal dimerization/repression domain of RFX1 mediates formation of two alternative homodimeric complexes conserved across yeast (Crt1, Sak1) and human RFX1; this domain independently mediates complex formation and transcriptional repression; the dimerization capacity is conserved but repression strength differs between species. |
Domain-swap chimeras with yeast orthologs, Gal4-fusion assays, EMSA |
Journal of molecular biology |
Medium |
10556033
|
| 2010 |
RFX1 recruits co-repressors DNMT1 and HDAC1 to the CD11a and CD70 promoters in CD4+ T cells, maintaining DNA methylation and histone deacetylation; decreased RFX1 in SLE T cells causes DNA demethylation and histone hyperacetylation at these loci, leading to overexpression of CD11a and CD70 and lupus-like autoimmunity. |
ChIP, overexpression/knockdown experiments, co-immunoprecipitation, reporter assays |
Journal of autoimmunity |
High |
20223637
|
| 2010 |
RFX1 interacts with histone methyltransferase SUV39H1 and recruits it to the CD11a and CD70 promoters in CD4+ T cells, regulating H3K9 tri-methylation; RFX1 overexpression increases and knockdown decreases H3K9me3 at these loci, correlating with CD11a and CD70 expression. |
ChIP, co-immunoprecipitation, Western blot, immunofluorescence, overexpression/knockdown |
Arthritis research & therapy |
High |
21192791
|
| 1993 |
RFX1 binds to the alpha element of the mouse rpL30 promoter; mutation of the alpha element that abolishes RFX1 binding reduces rpL30 promoter activity to ~43% of wild-type, indicating RFX1 is an important transactivator of this ribosomal protein gene. |
EMSA competition, antibody supershift, promoter mutagenesis and reporter assay |
Gene |
Medium |
8224874
|
| 2010 |
RFX1 binds the 18-bp cis-element of the FGF1 1B promoter and represses FGF1-1B transcription; RFX1 overexpression reduces FGF1-1B mRNA and neurosphere formation, while RFX1 knockdown has the opposite effect in glioblastoma stem cells. |
Yeast one-hybrid, EMSA, ChIP, gain/loss-of-function assays, neurosphere assays |
The Journal of biological chemistry |
High |
20189986
|
| 2016 |
RFX1 protein is targeted for polyubiquitination and proteasomal degradation by the E3 ligase STUB1; STUB1 is upregulated in SLE CD4+ T cells, and STUB1 overexpression increases CD70 and CD11a levels, providing a mechanism for RFX1 downregulation in SLE. |
Co-immunoprecipitation, ubiquitination assay, overexpression experiments, Western blot |
Clinical immunology |
Medium |
27283392
|
| 2018 |
RFX1 functions downstream of STAT3 in CD4+ T cells; phosphorylated STAT3 inhibits RFX1 expression, and RFX1 deficiency increases IL-17A expression by increasing histone H3 acetylation and decreasing DNA methylation and H3K9me3 at the IL-17A locus, promoting Th17 differentiation. |
Conditional Rfx1 knockout mice, in vitro differentiation assays, forced expression, ChIP, EAE and lupus-like syndrome models |
Nature communications |
High |
29422534
|
| 2003 |
RFX1 binds to the P sequence element (PSE-A) in the human GH locus in pituitary chromatin and co-immunoprecipitates with NF-1 family members; disruption of the RFX1 site within 263P blunts repressor activity, and both RFX1 and NF-1 are associated with P sequences in human pituitary tissue. |
ChIP, co-immunoprecipitation, site-directed mutagenesis, transfection assays |
Molecular endocrinology |
Medium |
12624117
|
| 2016 |
RFX1 directly activates transcription of Itga6 (integrin alpha-6) in Sertoli cells; conditional Rfx1 knockout mice (Rfx1flox/flox, Amh-Cre) show disrupted testis cord basal lamina, decreased integrin alpha-6, blocked spermatogenesis, and complete infertility. |
Conditional knockout, luciferase reporter assay, ChIP, Western blot |
Molecular reproduction and development |
High |
27228460
|
| 2019 |
In CD14+ monocytes, RFX1 recruits DNMT1, HDAC1, and SUV39H1 to the TLR4 promoter, maintaining DNA methylation, H3K9me3, and histone deacetylation; RFX1 knockdown causes TLR4 overexpression with decreased DNA methylation and H3K9me3 and increased H3/H4 acetylation at the TLR4 promoter. |
ChIP, knockdown/overexpression, co-immunoprecipitation, Western blot |
Clinical epigenetics |
Medium |
30857550
|
| 2019 |
The C-terminal repression domain of RFX1 interacts with protein phosphatase PP1c, and this interaction can target PP1c to specific genomic loci, suggesting PP1c recruitment as a mechanism of RFX1-mediated transcriptional repression. |
Co-immunoprecipitation, chromatin recruitment assays |
Biochemical and biophysical research communications |
Medium |
30654936
|
| 2018 |
RFX1 homodimers and RFX1/RFX3 heterodimers bind specifically to the double-stranded D sequence of the AAV inverted terminal repeat, and RFX proteins interact with AAV genomes in the nucleus following transduction, acting as regulators of AAV-mediated transgene expression. |
EMSA, supershift assays, DNA pulldown from transduced cells |
Scientific reports |
Medium |
29317724
|
| 2005 |
Alpha-adducin specifically interacts with RFX1 in a yeast two-hybrid screen; the interaction was confirmed by co-immunoprecipitation and nuclear co-localization in cells, suggesting adducin may modulate RFX1 transcriptional regulatory activity. |
Yeast two-hybrid, co-immunoprecipitation, co-localization |
FEBS letters |
Low |
16289097
|
| 1997 |
RFX1 and MIBP1 bind simultaneously (likely as a heterodimer) to the NRE gamma element of the HBV core promoter; RFX1 can transactivate the core promoter through NRE gamma, and mutations abolishing gene suppression prevent RFX1 binding, suggesting RFX1 and MIBP1 cooperate to negatively regulate core promoter activity. |
EMSA, mutagenesis, transfection reporter assays |
Virology |
Medium |
9018153
|
| 2018 |
Doxorubicin promotes HBV replication by increasing RFX1 expression and enhancing RFX1 binding to HBV enhancer I; RFX1 knockdown and EP element mutation in the HBV enhancer I attenuate doxorubicin-induced HBV replication. |
RFX1 knockdown, ChIP, EP element mutation, HBV replication assay |
Cancer medicine |
Medium |
29601674
|
| 2025 |
NgBR deficiency suppresses KAT7 expression, which impairs KAT7-mediated acetylation of RFX1; loss of acetylation stabilizes RFX1 by blocking proteasomal degradation, causing RFX1 to suppress FGF1 transcription and inactivate PI3K/AKT signaling, leading to neuronal damage. |
RNA sequencing, knockdown/overexpression, Western blot, rescue experiments |
Cellular and molecular life sciences |
Medium |
40192836
|
| 2024 |
RFX1 inhibits CD36 expression by directly binding to the CD36 promoter in macrophages; myeloid-specific Rfx1 knockout (ApoE-/-Rfx1f/f Lyz2-Cre) mice show aggravated atherosclerotic lesions and increased foam cell formation. |
Dual luciferase reporter assays, myeloid-specific knockout mice, ox-LDL stimulation, lipid uptake assays |
International immunopharmacology |
Medium |
38402833
|
| 2025 |
The splicing factor RBM39 binds RFX1 pre-mRNA and promotes skipping of exon 2, producing an N-terminal truncated RFX1 that lacks transcriptional repression activity on collagen genes, thereby activating the FAK/PI3K/AKT signaling pathway and promoting HCC malignancy. |
RIP-seq, alternative splicing analysis, knockdown/overexpression, FAK/PI3K/AKT pathway assays |
Oncogene |
Medium |
40033026
|
| 2009 |
RFX1 binds to the PNRC promoter and represses PNRC gene transcription in a dose-dependent manner, as demonstrated by gel shift, ChIP, and co-transfection experiments. |
EMSA (gel shift), ChIP, co-transfection reporter assay |
Molekuliarnaia biologiia |
Low |
19334528
|
| 2025 |
miR-320 suppresses RFX1 expression in hepatocytes; reduced RFX1 enhances FGF1 production; Rfx1 knockdown in hepatocytes mitigates MASH by enhancing FGF1-mediated AMPK activation. |
Hepatocyte-specific miR-320 knockout mice, AAV-mediated restoration, Rfx1 knockdown, AMPK pathway assays |
Acta pharmaceutica sinica B |
Medium |
40893671
|
| 1991 |
EF-C (RFX1) binds to certain DNA sites only when CpG dinucleotides are methylated (m5C), while binding to other sites is methylation-independent; EF-C likely corresponds to the methylated DNA-binding protein (MDBP). |
In vitro DNA binding assays with methylated and unmethylated substrates |
Virology |
Medium |
1850932
|