| 1992 |
ELF-1 (Elf-1) was identified as a novel Ets-related transcription factor that binds specifically to two Ets binding sites (EBS1 and EBS2) in the IL-2 enhancer; in vitro mutagenesis showed that these sites are required for inducible IL-2 enhancer function, and neither Ets-1 nor Ets-2 bound these sites. |
Electrophoretic mobility shift assay (EMSA), methylation interference analysis, in vitro mutagenesis, low-stringency cDNA library screen |
Molecular and cellular biology |
High |
1545787
|
| 1992 |
Elf-1 binds specifically to two purine-rich motifs in the HIV-2 enhancer, and mutagenesis of these Elf-1 binding sites abolishes inducible HIV-2 transcription following T-cell-receptor-mediated T-cell activation. |
EMSA, site-directed mutagenesis, transient transfection reporter assays |
Journal of virology |
High |
1527846
|
| 1993 |
Elf-1 binds to the underphosphorylated (but not phosphorylated) form of the retinoblastoma protein (Rb) via a sequence motif homologous to viral oncoprotein Rb-binding sites, interacting with Rb's pocket region both in vitro and in vivo. After T cell activation, Rb phosphorylation releases Elf-1, correlating temporally with activation of Elf-1-mediated transcription. Overexpression of a phosphorylation-defective Rb inhibited Elf-1-dependent transcription. |
Co-immunoprecipitation, in vitro binding assays, overexpression of phosphorylation-defective Rb mutant, transcriptional reporter assays |
Science |
High |
8493578
|
| 1993 |
A single amino acid substitution (Lys→Thr) in conserved region III (CRIII) of the Ets domain of Ets1 confers selective binding to GGAA core-containing sites (the specificity of Elf1/E74); the reciprocal mutation in Elf1 confers ability to bind GGAT core-containing EBS. CRIII plays a key role in Ets domain recognition of the GGAA/T core motif. |
Site-directed mutagenesis of Ets domain, DNA binding assays |
Nucleic acids research |
High |
8255775
|
| 1993 |
Elf-1 binds to adjacent AP-1 and Ets sites in the GM-CSF purine box 1 (PB1) element cooperatively with c-Fos and JunB; mutagenesis of either the Ets or AP-1 site abolishes binding of the inducible PB1 complex and transcriptional activation of the GM-CSF promoter in activated T cells. |
EMSA with specific antibodies, in vitro mutagenesis, transient transfection reporter assays |
Molecular and cellular biology |
High |
8289796
|
| 1993 |
Elf-1 binds to the purine-rich ets site in the HTLV-I enhancer (not Ets-1 as previously thought), and site-specific mutation of this site significantly diminishes inducible HTLV-I enhancer function in Jurkat T cells. |
EMSA, site-directed mutagenesis, transient transfection reporter assays |
Journal of virology |
Medium |
8350410
|
| 1994 |
ELF-1 was identified as a ligand for the Eph family receptor tyrosine kinases Mek4 and Sek; ELF-1 is membrane-bound via a phosphatidylinositol (GPI) tail, as demonstrated by its expression in cell lines and embryos. |
cDNA expression library screen with receptor-alkaline phosphatase fusion proteins (RAP in situ), sequence analysis, cell line expression studies |
Cell |
High |
7522971
|
| 1994 |
Elf-1 binds to the Ets consensus site in a second CD4 enhancer 24 kb upstream of the CD4 promoter; mutation of this Ets site abolishes enhancer activity in T cells. |
EMSA, in vitro mutagenesis, transient transfection reporter assays |
Molecular and cellular biology |
Medium |
7935370
|
| 1995 |
ELF-1 is expressed in a high-to-low gradient in the tectum while its receptor Mek4 is expressed in a complementary gradient in the retina; binding activity detected with alkaline phosphatase fusions of ELF-1 and Mek4 shows molecular complementarity of gradients in reciprocal fields, indicating roles in retinotectal map development. |
RNA in situ hybridization, receptor-alkaline phosphatase fusion binding assays |
Cell |
High |
7634327
|
| 1995 |
Elf-1 (ELF-1) activates autophosphorylation of the Cek7 receptor tyrosine kinase; high-affinity binding (Kd ~1.7 × 10⁻¹⁰ M) was demonstrated between Elf-1 and the MDK1 (Eph family) receptor, and Elf-1 binding leads to autophosphorylation of MDK1 and tyrosine phosphorylation of a 62 kDa substrate. |
Scatchard binding analysis, receptor autophosphorylation assay |
The Journal of biological chemistry |
Medium |
7876076
|
| 1996 |
ELF-1 acts as a repellent axon guidance factor in vitro for temporal but not nasal retinal axons; retroviral overexpression of ELF-1 in the tectum in vivo causes retinal axons to avoid ectopic ELF-1 patches and map abnormally, demonstrating topographically specific axon guidance. |
In vitro axon guidance assay, retroviral overexpression in vivo, retinal axon mapping |
Cell |
High |
8797822
|
| 1996 |
Elf-1 is constitutively localized in the nucleus, dependent on amino acids 86–265. The N-terminal 86 amino acids contain a transcriptional activation domain whose activity is attenuated by an internal repression domain. Elf-1 stimulates transcription via E74 target sequences independently of mitogenic signaling. |
Subcellular fractionation, deletion mutagenesis of Elf-1 fused to Gal4 DNA binding domain, reporter assays |
FEBS letters |
Medium |
9180266
|
| 1996 |
Elf-1 binds to a conserved Ets site (site III) in the mouse IL-2 receptor alpha IL-2-responsive enhancer (IL-2rE) and participates in IL-2 responsiveness; mutations in site III that reduce Elf-1 binding in vitro reduce IL-2rE activity in vivo, suggesting Elf-1 can act as a transcriptional repressor at the PRRIII element of the human IL-2Rα gene. |
EMSA with recombinant Elf-1, supershift with anti-Elf-1 antibody, biotinylated probe precipitation, in vivo footprinting, transient transfection reporter assays, mutagenesis |
Molecular and cellular biology / The EMBO journal |
High |
8943338 9104808
|
| 1996 |
Elf-1 is expressed in an increasing gradient in the septum and selectively allows neurite growth from topographically appropriate lateral hippocampal neurons while inhibiting medial hippocampal neurite outgrowth; Elf-1 specifically binds the Bsk Eph receptor and elicits its tyrosine kinase activity. |
In vitro neurite outgrowth assay, receptor binding assay, kinase activity assay |
Proceedings of the National Academy of Sciences |
Medium |
8855326
|
| 1996 |
ELF-1 (RAGS and ELF-1) acts as a repellent factor for temporal retinal axons in two in vitro assays; RAGS is repellent for both temporal and nasal axons while ELF-1 is repellent only for temporal axons, correlating with strength of receptor interaction. |
Stripe assay and growth cone collapse assay in vitro |
The EMBO journal |
Medium |
9135142
|
| 1997 |
ELF-1 inhibits neurite outgrowth of Cek8-expressing motoneurons when presented in membrane-bound or clustered Fc chimeric form but not as unclustered soluble protein, and this inhibition correlates with receptor (Cek8) phosphorylation. |
Motoneuron neurite outgrowth assay, receptor phosphorylation assay, Fc-chimera clustering |
Mechanisms of development |
Medium |
9232603
|
| 1996 |
Elf-1 binds to the Ets consensus site in the IL-3 promoter; both the AP-1 and Elf-1 binding sites are required for T cell-specific IL-3 promoter activity, but unlike in the IL-2 gene, Elf-1 and AP-1 factors bind independently in the IL-3 promoter. |
DNase I footprinting, EMSA, in vitro translation of Elf-1, supershift with Elf-1 antisera, transient transfection with mutagenized reporter constructs |
The Journal of experimental medicine |
Medium |
8228815
|
| 1998 |
Elf-1 is the primary Ets factor binding to the Ets binding sites (zEBS1 and zEBS2) in the TCR zeta-chain promoter; mutagenesis of these sites markedly reduces transcription, and ectopic Elf-1 expression increases TCR zeta-chain promoter activity mapping to zEBS1 and zEBS2. A GAL4-Elf-1 fusion also trans-activates TCR zeta-chain promoter constructs containing GAL4 sites. |
EMSA, in vitro mutagenesis, ectopic expression in COS-7 cells, GAL4 fusion trans-activation assay |
Journal of immunology |
High |
9510181
|
| 1998 |
PU.1 and Elf-1 both bind to the SCL (tal-1) promoter 1b Ets motifs and transactivate the promoter in mast cells; transcription factors PU.1, Elf-1, Sp1, and Sp3 are present in mast cell extracts and bind promoter 1b. |
Gel shift assay, reporter transactivation, ChIP (not explicitly stated but implied by promoter binding), transient transfection |
The Journal of biological chemistry |
Medium |
9786909
|
| 1999 |
Elf-1 binds to the Ets site in the FcεRI alpha-chain promoter and is one of the factors (with GATA-1) essential for promoter activity; Elf-1 binding is required for alpha-chain-producing cell specificity. |
EMSA with nuclear extracts and in vitro-translated proteins, transient transfection reporter assays with mutagenized promoter |
Journal of immunology |
Medium |
10395650
|
| 1999 |
Elf-1 binds to the P4 Ets site in the CD4 promoter and specifically activates CD4 promoter activity; no other tested Ets family members bound this site in T cells. |
EMSA, transient transfection reporter assays |
The Journal of biological chemistry |
Medium |
10347164
|
| 1999 |
Elf-1 and PU.1 both bind to a promoter element mutated in chronic granulomatous disease (CGD) patients (-57 to -52 bp) and transactivate the gp91(phox) promoter; CGD-associated point mutations at -57 and -55 significantly reduce Elf-1 and PU.1 binding and transactivation, but no synergy occurs between Elf-1 and PU.1 on this promoter. |
EMSA, transient transfection reporter assays with CGD mutations, overexpression in HeLa and PLB985 cells |
Blood |
Medium |
10233904
|
| 1999 |
Elf-1 does not cooperate with GATA3 to activate the human IL-5 promoter (unlike Ets1 and Ets2), demonstrating specificity among closely related Ets factors in this context. |
Transient transfection reporter assays in Jurkat T-cells and Kasumi myeloid cells |
The Journal of biological chemistry |
Medium |
10212281
|
| 2001 |
Elf-1 is a transcriptional regulator of the Tie2 gene in endothelial cells; chicken Elf-1 (cELF-1) is expressed in developing blood vessels, binds conserved Ets sites in Tie1 and Tie2 promoters, and strongly transactivates these genes. Elf-1-containing complexes in CAM blood vessel extracts are recognized by anti-cELF-1 antibody. |
In situ hybridization, immunohistochemistry, RT-PCR, EMSA with antibody supershift, transient transfection reporter assays |
Circulation research |
Medium |
11157678
|
| 2002 |
Elf-1 exists as an 80-kDa form in the cytoplasm and as a 98-kDa form in the nucleus; phosphorylation and O-linked glycosylation contribute to the increased molecular mass. The 98-kDa nuclear form is released from cytoplasmic retinoblastoma protein tethering and moves to the nucleus to bind the TCR zeta-chain promoter; the cytoplasmic 98-kDa form undergoes proteasomal degradation. |
Subcellular fractionation, Western blot, phosphatase and glycosidase treatment, immunoprecipitation, DNA binding assay, proteasome inhibitor experiments |
Journal of immunology |
High |
11884456
|
| 2002 |
Defective production of the functional 98-kDa nuclear form of Elf-1 in SLE T cells results from abnormal posttranslational modifications; two distinct defects were identified: decreased 98-kDa levels OR normal apparent levels but abnormal isoelectric focusing pattern. This defect causes reduced TCR zeta-chain transcription. |
Subcellular fractionation, Western blot, isoelectric focusing, transcription/translation analysis, reporter assays |
Journal of immunology |
Medium |
12421992
|
| 2004 |
Elf-1 binds to conserved Ets sites in the scl/tal-1 5' (-3.8) bifunctional enhancer in hematopoietic progenitors and endothelial cells in vivo, as demonstrated by ChIP; the -3.8 enhancer (but not the +18/19 enhancer) is required for scl transcription. |
ChIP, comparative genomics, transgenic mice, knockout approach |
Molecular and cellular biology |
Medium |
14966269
|
| 2005 |
Elf-1 was identified via DNA affinity chromatography as the Ets protein with highest affinity for the TdT promoter D' element; a D' mutation that selectively reduces Elf-1 binding greatly reduces TdT promoter activity in immature T and B cells. |
DNA affinity chromatography, peptide microsequencing, immunoblot, transient transfection reporter assays |
Molecular and cellular biology |
Medium |
8887642
|
| 2005 |
Elf-1, Fli-1, and Ets1 bind in vivo to conserved Ets sites in the LMO2 proximal promoter in hematopoietic and endothelial cells, and these sites are required for promoter activity; transgenic analysis confirmed the proximal promoter drives endothelial expression in vivo. |
ChIP, EMSA, transient/stable transfection reporter assays, transgenic mice |
Blood |
Medium |
15994290
|
| 2005 |
A 34-amino-acid peptide corresponding to the terminal ETS domain of ELF-1 blocks ELF-1 function; a TAT-fused version enters endothelial cell nuclei, reduces Tie2 and eNOS expression, inhibits angiopoietin-1-mediated endothelial cell migration, and systemically attenuates B16 melanoma tumor growth and tumor angiogenesis in nude mice. |
Cell-penetrating peptide delivery, reporter assays, endothelial cell migration assay, mouse tumor xenograft model |
Blood |
Medium |
16352813
|
| 2005 |
Elf1 (yeast) is a transcription elongation factor that associates co-transcriptionally with actively transcribed regions; synthetic lethality with mutations in Spt4, Spt5, Spt6, and Paf1 complex members identifies it as part of the elongation machinery. Association is partially dependent on Spt4 and Spt6. Elf1 is purified in association with casein kinase II. |
Genetic screen (synthetic lethality), ChIP genome-wide, protein purification/mass spectrometry |
Molecular and cellular biology |
High |
16260625
|
| 2006 |
Fli-1, Erg, and Elf-1 bind in vivo to conserved Ets sites in both the endoglin promoter and a -8 kb enhancer in endothelial cells; both elements depend on these Ets sites for activity. |
ChIP, comparative genomics, transient transfection reporter assays, transgenic mice |
Blood |
Medium |
16484587
|
| 2006 |
Elf-1 binds to two Ets binding sites in the LAT gene proximal promoter and overexpression of Elf-1 augments LAT promoter activity; a Runx-1 binding site adjacent to one Ets site has an inhibitory effect. |
EMSA, transient transfection reporter assays, Elf-1 overexpression |
BMC molecular biology |
Medium |
16464244
|
| 2006 |
Yeast Elf1 is phosphorylated by protein kinase CK2 at Ser95 and Ser117 in vitro; Elf1 co-immunoprecipitates with both catalytic (α, α') and regulatory (β, β') subunits of CK2. |
In vitro kinase assay, MALDI-MS phosphosite identification, co-immunoprecipitation |
Journal of biochemistry and molecular biology |
Medium |
16756761
|
| 2007 |
Elf-1 specifically binds to GGAA elements in the FcRγ promoter and represses FcRγ expression; forced Elf-1 expression suppresses FcRγ, while siRNA knockdown of Elf-1 increases FcRγ expression. |
EMSA, overexpression and siRNA knockdown, reporter assays |
Journal of immunology |
Medium |
17878388
|
| 2008 |
PP2A dephosphorylates Elf-1 at Thr-231, resulting in limited nuclear 98-kDa Elf-1 form and decreased binding to CD3ζ and FcRγ promoters. Aberrantly increased PP2A in lupus T cells causes this dephosphorylation. Suppression of PP2A expression increases CD3ζ and decreases FcRγ expression, correcting early signaling defects. |
Phosphatase activity assays, phosphosite-specific analysis, ChIP, siRNA knockdown of PP2A, Western blot |
Journal of immunology |
High |
18714041
|
| 2008 |
Elf-1 negatively regulates FcεRI alpha-chain expression in primary mast cells (BMMC) by suppressing PU.1-mediated transcription; Elf-1 siRNA knockdown increases alpha-chain transcription and increases PU.1 occupancy at the promoter (by ChIP), while Elf-1 overexpression suppresses alpha-chain promoter activity. |
siRNA knockdown, overexpression, transient reporter assay, ChIP |
Immunogenetics |
Medium |
18629488
|
| 2009 |
O-GlcNAc modification inhibits a physical interaction between Sp1 and Elf-1 transcription factors, negatively regulating transcription of the Pem gene. |
Co-immunoprecipitation, O-GlcNAc modification analysis, reporter assays |
Biochemical and biophysical research communications |
Medium |
19285002
|
| 2010 |
Elf-1-deficient mice exhibit a partial, cell-intrinsic block in NKT cell development affecting selection, survival, and maturation, with residual NKT cells producing less cytokine upon antigen stimulation; NK cell proportions are normal, demonstrating selective requirement for Elf-1 in NKT but not NK cell development. |
Knockout mouse model (Elf-1⁻/⁻), flow cytometry, bone marrow chimera (cell-intrinsic defect), cytokine stimulation assay |
Blood |
High |
21148815
|
| 2010 |
PU.1 is a major upstream transcriptional regulator of Elf-1 (identified by ChIP-chip); Elf-1 downregulation is necessary for terminal erythroid differentiation (overexpression of Elf-1 inhibits erythroid maturation). |
ChIP-chip (locus-wide), comparative genomics, overexpression in primary murine fetal liver erythroid differentiation assay |
Nucleic acids research |
Medium |
20525788
|
| 2010 |
ELF1 binds to a conserved ETS site in the MEIS1 promoter and is enriched there by ChIP; siRNA-mediated knockdown of ELF1 decreases MEIS1 expression in K562 cells and primary human samples, identifying ELF1 as a positive transcriptional regulator of MEIS1. |
EMSA, ChIP, siRNA knockdown with mRNA quantification |
Experimental hematology |
Medium |
20600580
|
| 2011 |
O-GlcNAc modification of Elf-1 promotes its nuclear localization; in intestinal epithelial cells (IECs), O-GlcNAc modification of Elf-1 is significantly lower than in monocytes, preventing nuclear translocation of Elf-1 and thereby relieving Elf-1-mediated repression of the Tollip gene, which explains elevated Tollip expression in IECs. |
Subcellular fractionation, Western blot for O-GlcNAc modification, comparison of Caco-2 (IEC) vs. THP-1 (monocyte) cells |
Biochemical and biophysical research communications |
Medium |
21867680
|
| 2018 |
ELF1 has two distinct tumor-suppressive roles in prostate cancer: (1) inhibiting cell migration and EMT by interfering with oncogenic ETS factors at ETS/AP-1 cis-regulatory sequences, and (2) activating genes promoting senescence at unique ELF1-targeted sites. ELF1 knockdown increases docetaxel resistance. |
Genome-wide chromatin mapping (ChIP-seq), cell migration assay, EMT marker analysis, senescence assay, siRNA knockdown, drug resistance assay |
Genes & cancer |
Medium |
30603056
|
| 2019 |
ELF1 inhibits replication of eight diverse RNA and DNA viruses (independent of type I interferons) in a broadly antiviral transcriptional program distinct from interferon signatures; Elf1-deficient mice show enhanced susceptibility to influenza A virus. ELF1's antiviral effect is independent of STAT1 and JAK phosphorylation. |
Microscopy-based viral infection quantification, Elf1-knockout mouse infection, RNA-seq comparative expression analysis, JAK inhibitor and STAT1-KO experiments |
PLoS pathogens |
High |
31682641
|
| 2021 |
In yeast, elongation factor Elf1 inhibits RNA Pol II transcriptional bypass of CTG and CAG trinucleotide repeat slip-out structures (individually and cooperatively with Spt4/5), while Spt4/5 promotes Pol II transcription through B-form CTG•CAG duplex DNA—opposite roles depending on DNA template structure. |
In vitro reconstituted yeast transcription system with defined DNA templates |
Nucleic acids research |
High |
33877330
|
| 2024 |
Yeast Elf1 promotes TC-NER by enhancing Rad26 (CSB ortholog) interactions with lesion-arrested RNA Pol II; cryo-EM structures of Pol II-Rad26 stalled at different obstacles show Rad26 uses a common mechanism to recognize stalled Pol II with additional interactions at lesion-arrested Pol II, and Elf1 further stabilizes Rad26–Pol II interactions specifically at lesions. Biochemical and genetic data support the Elf1–Rad26 interplay in TC-NER initiation. |
Cryo-EM structural determination, biochemical assays, genetic epistasis in yeast |
Proceedings of the National Academy of Sciences |
High |
38194460
|
| 2024 |
The C-terminal domain (CTD) of yeast Elf1 is required for efficient TC-NER genome-wide; the Elf1 CTD binds the pleckstrin homology (PH) domain of the p62 subunit of TFIIH in vitro, and a conserved TFIIH-interaction region (TIR) in the CTD is necessary for this binding and for TC-NER—functionally analogous to the TIR in mammalian UVSSA that recruits TFIIH. |
CPD-seq (genome-wide repair mapping), in vitro binding assay, CTD deletion/mutation analysis, structural/sequence comparison |
Nature communications |
High |
39043658
|
| 2025 |
In zebrafish, Elf1 is a cell-autonomous regulator of macrophage development with minimal effect on neutrophil differentiation; CRISPR/Cas9 knockout and dominant-negative overexpression demonstrate Elf1 is required for macrophage infiltration to tissue injury. Overexpression of cxcr4b (a downstream Elf1 target essential for cell migration) rescues the macrophage defect, placing cxcr4b downstream of Elf1. |
Morpholino knockdown, CRISPR/Cas9 knockout, dominant-negative overexpression in macrophages, rescue with cxcr4b overexpression, tissue injury model |
International journal of molecular sciences |
Medium |
40141178
|
| 2025 |
ELF1 binds to promoters of METTL3 and YTHDF2 and transactivates their expression; elevated ELF1 in nucleus pulposus cells promotes m6A methylation of E2F3 mRNA via METTL3, which is then recognized and destabilized by YTHDF2, causing E2F3 mRNA degradation, G1/S cell cycle arrest, and NPC senescence. |
ChIP-seq, ChIP, proteomic/RNA-seq, MeRIP-qPCR, RNA pull-down, luciferase reporter assay, AAV5 overexpression and KO mice, small molecule targeting |
Cell death discovery |
Medium |
40467575
|
| 2025 |
ELF-1 deficiency in non-hematopoietic (epithelial) cells intrinsically worsens DSS-induced colitis in mice; ELF-1 directly regulates Rack1 gene expression in colonic epithelial tissue and its absence enhances pro-inflammatory chemokine production, leading to neutrophil and immune cell infiltration. |
Conditional/global ELF-1 KO mouse, bone marrow transfer experiments (confirming non-hematopoietic cell-intrinsic defect), DSS colitis model, ChIP, chemokine quantification |
Communications biology |
Medium |
40057592
|