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ELF4 (E74-like factor 4 (ets domain transcription factor))

Written2013-12Stephen D Nimer, Yan Liu
Sylvester Comprehensive Cancer Center Professor of Medicine, Biochemistry & Molecular Biology, University of Miami, USA (SDN); Indiana University School of Medicine, USA (YL)

(Note : for Links provided by Atlas : click)


HGNC (Hugo) ELF4
HGNC Alias symbMEF
HGNC Previous nameE74-like factor 4 (ets domain transcription factor)
LocusID (NCBI) 2000
Atlas_Id 42990
Location Xq26.1  [Link to chromosome band Xq26]
Location_base_pair Starts at 130063958 and ends at 130110497 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping ELF4.png]
Local_order The ELF4 gene maps on chomosome X at position +1805468958720.00 (interpolated), at Xq26 according to Entrez Gene. In AceView, it covers 46,69 kb, from 129244687 to 129197994, on the reverse strand.
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)
ELF4 (Xq26.1)::CREB5 (7p15.1)ELF4 (Xq26.1)::ERG (21q22.2)ERG (21q22.2)::ELF4 (Xq26.1)


  The ELF4 gene is located on the X-chromosome (Xq26) and is transcribed from telomere to centromere. The ELF4 gene contains 8 coding exons and 1 non-coding exon.
Description The gene encompasses 45 kb of DNA; 9 exons. The ELF4 gene contains 12 distinct gt-ag introns. Transcription produces 5 alternatively spliced mRNAs. There are 2 probable alternative promoters, 2 non overlapping alternative last exons and 2 validated alternative polyadenylation sites. The mRNAs appear to differ by truncation of the 3' end, presence or absence of 3 cassette exons, overlapping exons with different boundaries, splicing versus retention of 2 introns.
Transcription 4190 bp mRNA; 1991 bp open reading frame.
Pseudogene No observed pseudogenes.


  The ELF4 protein contains the following domains: (A) transactivation domain, (B) AML1 interacting domain, (C) ETS domain, (D) serine/threonine rich region and (E) proline rich region.
Description 663 amino acids; 70730 Da protein; numerous posttranslational modifications: phosphorylation, sumoylation and ubiquitination (Miyazaki et al., 2001; Liu et al., 2006; Suico et al., 2006). ELF4 contains, from N-term to C-term, transactivation domain (53-86), AML1 interacting domain (87-206), ETS domain (207-291), serine/threonine rich region (306-347) and proline rich region (477-517) (Miyazaki et al., 1996; Mao et al., 1999; Suico et al., 2002; Lacorazza and Nimer, 2003).
Expression Abundantly expressed in the placenta and in a variety of myeloid leukemia cell lines. Moderate levels of expression in heart, lung, spleen, thymus, peripheral blood lymphocytes, ovary and colon. Lower levels of expression in Jurkat T-cells and other T-cell lines and no expression in brain (Lacorazza and Nimer, 2003).
Localisation Nucleus, PML body. Accumulation into PML nuclear bodies is mediated by PML (Suico et al., 2004a; Suico et al., 2004b).
Function ELF4 is a member of the ETS family of transcription factors (TF) with transcription activating properties (Lacorazza and Nimer, 2003). ELF4 binds to DNA sequences containing the consensus 5'-WGGA-3' and transactivates promoters of the hematopoietic growth factor genes CSF2, IL3, IL8, and of the bovine lysozyme gene (Miyazaki et al., 1996; Mao et al., 1999; Hedvat et al., 2004; Suico et al., 2004). ELF4 acts synergistically with RUNX1 to transactivate the IL3 promoter (Mao et al., 1999). It also transactivates the PRF1 promoter in natural killer (NK) cells (Lacorazza et al., 2002). ELF4 has important molecular functions, including protein binding, transcription activator activity, sequence-specific DNA binding, transcription factor activity. ELF4 interacts with multiple proteins, including Cyclin A/CDK2 kinase complex, FBXO4, FBXO7, PML, RUNX1, SKP2 and UBB (Miyazaki et al., 1996; Mao et al., 1999; Miyazaki et al., 2001; Liu et al., 2006; Suico et al., 2006). ELF4 has been implicated in widely divergent physiological and pathological processes (such as development and oncogenesis). ELF4 plays an important role in the development and function of NK and NK T-cells and in innate immunity (Lacorazza et al., 2002). It controls the proliferation and homing of CD8+ T-cells via the Kruppel-like factors KLF4 and KLF2 (Yamada et al., 2009; Yamada et al., 2010). ELF4 regulates hematopoietic stem cell quiescence and self-renewal (Lacorazza et al., 2006; Liu et al., 2009). ELF4 also regulates self-renewal of brain-tumor stem cells (Bazzoli et al., 2012). In addition, ELF4 plays an important role in osteogenic differentiation and bone development (Kim et al., 2007; Seul et al., 2011; Baek et al., 2012). It mediates DNA damage response (Morales et al., 2008; Sashida et al., 2011). ELF4 controls cell senescence in a p53-dependent manner and can also promote cellular transformation through inhibition of the p16 pathway as well (Sashida et al., 2009). ELF4, a member of the ETS transcription factors, can function as an oncogene in murine cancer models and is overexpressed in various human cancers (Lacorazza and Nimer, 2003; Sashida et al., 2010). In addition to its oncogenic potential, ELF4 has been proposed to be a candidate tumor suppressor gene on the X chromosome (Seki et al., 2002).
  ELF4 interacts with multiple proteins and plays important role in development and oncogenesis.
Homology The transcription factor ELF4 belongs to the ETS family of transcription factors, named after the E26 (E twenty six) leukemogenic chicken virus which contains a gag-myb-ets fusion. These proteins are characterized by the presence of the ETS domain (a conserved 84 amino acid domain) that binds to a DNA consensus sequence containing a GGAA central core via a winged helix-turn-helix motif. Based on the homology of the ETS domain, these proteins have been classified in different subfamilies (e.g., Elf, Spi, and Yan). The ETS domain is highly conserved among family members with the greatest homology of ELF4 with other proteins in the Elf subfamily, which also includes ELF1, NERF1a, and NERF1b. ELF4 does not contain an HLH or pointed protein-protein interaction domain, which is present in members of the ETS, ERG, GABP, and Yan subfamilies (Lacorazza and Nimer, 2003).


Note No known mutations. Fused in hepatocellular carcinoma with the BCORL1 gene.

Implicated in

Entity Acute myeloid leukemia
Disease Acute myeloid leukemia (AML) is the most common acute leukemia in adults. It usually occurs around age 60 with no identifiable cause and it carries a very poor prognosis, with most patients living less than 18 months. AML is a devastating illness with over 13000 new diagnoses and 10000 patients dying annually in the United States. Although select molecular subpopulations of patients are long-term survivors, the overall five-year survival for adults is only 25%. ETS proteins (such as PU.1, Fli-1 and ETS-1) have been shown to play important roles in normal and abnormal hematopoiesis (Lacorazza and Nimer, 2003). ELF1 and ELF4 were expressed in all AML samples, whereas NERF was not. The relative expression of ELF4, but not ELF1, was significantly lower (P<0.0001) in AML with t(8;21) and t(15;17) compared with AML with normal karyotype (Fukushima et al., 2003; Ando et al., 2013).
Prognosis The low relative expression of ELF4, might be part of a gene expression profile characterizing AML with a good prognosis (Fukushima et al., 2003; Ando et al., 2013).
Cytogenetics A chromosomal translocation has been reported in AML, , that generates a fusion transcript between two ETS family members, ELF4 (at Xq26) and ERG (at 21q22). The translocation occurs within intron 1 of ERG isoform 1 (ERG-1) and intron 2 of ELF4 resulting in an in-frame fusion joining exon 2 from ELF4 with exon 2 of ERG (Moore et al., 2006).
Hybrid/Mutated Gene ELF4-ERG. The fusion sequence includes exon 2 of ELF4 and exon 2 of ERG1, with the breakpoint occurring after exon 2 in ELF4 (intron 2) and before exon 2 of ERG1 (intron 1) (Moore et al., 2006).
Abnormal Protein ELF4-ERG (495 amino acids).
Horizontal lines represent amino acid residues for ELF4 and ERG-1. Numbers above each line indicate the number of amino acids at the corresponding position. Boxes below indicate locations of the conserved domains within both protein sequences. The predicted fusion protein would include the first 25 amino acid residues from ELF4 encoded by exon 2 and the last 470 amino acid residues encoded by ERG exons 2-10 resulting in a protein of 495 amino acids. The conserved SAM-PNT and ETS domains from ERG would be included in the fusion while the ETS domain from ELF4 would be excluded.
Oncogenesis ERG has been associated with other fusion partners, specifically FUS and EWSR1, and implicated in both AML and Ewing's sarcoma. The ELF4-ERG fusion suggests a new role for ELF4 in leukemogenesis and human cancer (Moore et al., 2006), as it provides a strong promoter to express ERG. In addition, wild-type nucleophosmin (NPM1) inhibits the DNA binding and transcriptional activity of ELF4 on the HDM2 promoter, while a common, leukemia-associated NPM1 mutant protein (Mt-NPM1) enhances these activities of ELF4 (Ando et al., 2013). Moreover, clinical leukemia samples with NPM1 mutations have higher human MDM2 (HDM2) mRNA expression. These data suggest that enhanced HDM2 expression induced by mutant NPM1 may have a role in ELF4-dependent leukemogenesis (Ando et al., 2013).
Entity Ovarian cancer
Disease Ovarian cancer is the seventh most common cancer in women worldwide and the second leading cause of death among the gynecological malignancies. ELF4 is expressed in a significant proportion of ovarian carcinomas, and in the CAOV3 and SKOV3 ovarian cancer cell lines, but not in normal ovarian surface epithelium (Yao et al., 2007).
Prognosis High levels of ELF4 expression in ovarian cancer are associated with a poor prognosis (Yao et al., 2007).
Oncogenesis Manipulating MEF levels in ovarian cancer cell lines alters their behavior; reducing ELF4 levels, using short hairpin RNA expressing vectors, significantly inhibited the proliferation of SKOV3 and CAOV3 cells in culture, and impaired the anchorage-independent growth of CAOV3 cells. Overexpression of ELF4 in SKOV3 cells significantly increased their growth rate, enhanced colony formation in soft agar and promoted tumor formation in nude mice. The oncogenic activity of MEF was further shown by the ability of ELF4 to transform NIH3T3 cells, and induce their tumor formation in nude mice (Yao et al., 2007). Thus, ELF4 is an important regulator of the tumorigenic properties of ovarian cancer cells and could be used a therapeutic target in ovarian cancer (Yao et al., 2007).
Entity Gliomas
Disease Malignant gliomas represent the most prevalent primary brain tumor in adults and inevitably have a poor prognosis. Despite the implementation of new therapeutic strategies, the median survival of patients with glioblastoma multiforme (GBM), the most aggressive glioma variant, is only 14-16 months and these tumors remain rapidly and uniformly fatal. High-grade gliomas are composed of a heterogeneous population of cells that include many with stem-cell-like properties. The acquisition of stem-like traits might contribute to glioma initiation, growth, and recurrence. ELF4 is highly expressed in both human and mouse glioblastomas and its absence impairs gliomagenesis in a PDGF-driven glioma mouse model (Bazzoli et al., 2012).
Prognosis High levels of ELF4 expression in gliomas are associated with a poor prognosis (Bazzoli et al., 2012).
Oncogenesis Modulation of ELF4 levels in both mouse neural stem cells and human glioblastoma cells has a significant impact on neurosphere formation. Thus, ELF4 is a gatekeeper gene that promotes stemness in the pathogenesis of gliomas (Bazzoli et al., 2012).


Mutations in the nucleolar phosphoprotein, nucleophosmin, promote the expression of the oncogenic transcription factor MEF/ELF4 in leukemia cells and potentiates transformation.
Ando K, Tsushima H, Matsuo E, Horio K, Tominaga-Sato S, Imanishi D, Imaizumi Y, Iwanaga M, Itonaga H, Yoshida S, Hata T, Moriuchi R, Kiyoi H, Nimer S, Mano H, Naoe T, Tomonaga M, Miyazaki Y.
J Biol Chem. 2013 Mar 29;288(13):9457-67. doi: 10.1074/jbc.M112.415703. Epub 2013 Feb 7.
PMID 23393136
Myeloid Elf-1-like factor stimulates adipogenic differentiation through the induction of peroxisome proliferator-activated receptor gamma expression in bone marrow.
Baek K, Cho JY, Hwang HR, Kwon A, Lee HL, Park HJ, Qadir AS, Ryoo HM, Woo KM, Baek JH.
J Cell Physiol. 2012 Nov;227(11):3603-12. doi: 10.1002/jcp.24064.
PMID 22307523
MEF promotes stemness in the pathogenesis of gliomas.
Bazzoli E, Pulvirenti T, Oberstadt MC, Perna F, Wee B, Schultz N, Huse JT, Fomchenko EI, Voza F, Tabar V, Brennan CW, DeAngelis LM, Nimer SD, Holland EC, Squatrito M.
Cell Stem Cell. 2012 Dec 7;11(6):836-44. doi: 10.1016/j.stem.2012.09.012.
PMID 23217424
The level of MEF but not ELF-1 correlates with FAB subtype of acute myeloid leukemia and is low in good prognosis cases.
Fukushima T, Miyazaki Y, Tsushima H, Tsutsumi C, Taguchi J, Yoshida S, Kuriyama K, Scadden D, Nimer S, Tomonaga M.
Leuk Res. 2003 May;27(5):387-92.
PMID 12620289
Myeloid ELF1-like factor is a potent activator of interleukin-8 expression in hematopoietic cells.
Hedvat CV, Yao J, Sokolic RA, Nimer SD.
J Biol Chem. 2004 Feb 20;279(8):6395-400. Epub 2003 Nov 17.
PMID 14625302
The suppressive effect of myeloid Elf-1-like factor (MEF) in osteogenic differentiation.
Kim YJ, Kim BG, Lee SJ, Lee HK, Lee SH, Ryoo HM, Cho JY.
J Cell Physiol. 2007 Apr;211(1):253-60.
PMID 17167770
The transcription factor MEF/ELF4 regulates the quiescence of primitive hematopoietic cells.
Lacorazza HD, Yamada T, Liu Y, Miyata Y, Sivina M, Nunes J, Nimer SD.
Cancer Cell. 2006 Mar;9(3):175-87.
PMID 16530702
p53 regulates hematopoietic stem cell quiescence.
Liu Y, Elf SE, Miyata Y, Sashida G, Liu Y, Huang G, Di Giandomenico S, Lee JM, Deblasio A, Menendez S, Antipin J, Reva B, Koff A, Nimer SD.
Cell Stem Cell. 2009 Jan 9;4(1):37-48. doi: 10.1016/j.stem.2008.11.006.
PMID 19128791
The ETS protein MEF is regulated by phosphorylation-dependent proteolysis via the protein-ubiquitin ligase SCFSkp2.
Liu Y, Hedvat CV, Mao S, Zhu XH, Yao J, Nguyen H, Koff A, Nimer SD.
Mol Cell Biol. 2006 Apr;26(8):3114-23.
PMID 16581786
Functional and physical interactions between AML1 proteins and an ETS protein, MEF: implications for the pathogenesis of t(8;21)-positive leukemias.
Mao S, Frank RC, Zhang J, Miyazaki Y, Nimer SD.
Mol Cell Biol. 1999 May;19(5):3635-44.
PMID 10207087
Cyclin A-dependent phosphorylation of the ETS-related protein, MEF, restricts its activity to the G1 phase of the cell cycle.
Miyazaki Y, Boccuni P, Mao S, Zhang J, Erdjument-Bromage H, Tempst P, Kiyokawa H, Nimer SD.
J Biol Chem. 2001 Nov 2;276(44):40528-36. Epub 2001 Aug 14.
PMID 11504716
ELF4 is fused to ERG in a case of acute myeloid leukemia with a t(X;21)(q25-26;q22).
Moore SD, Offor O, Ferry JA, Amrein PC, Morton CC, Dal Cin P.
Leuk Res. 2006 Aug;30(8):1037-42. Epub 2005 Nov 21.
PMID 16303180
DNA damage signaling in hematopoietic cells: a role for Mre11 complex repair of topoisomerase lesions.
Morales M, Liu Y, Laiakis EC, Morgan WF, Nimer SD, Petrini JH.
Cancer Res. 2008 Apr 1;68(7):2186-93. doi: 10.1158/0008-5472.CAN-07-2355.
PMID 18381424
The mef/elf4 transcription factor fine tunes the DNA damage response.
Sashida G, Bae N, Di Giandomenico S, Asai T, Gurvich N, Bazzoli E, Liu Y, Huang G, Zhao X, Menendez S, Nimer SD.
Cancer Res. 2011 Jul 15;71(14):4857-65. doi: 10.1158/0008-5472.CAN-11-0455. Epub 2011 May 26.
PMID 21616937
ELF4/MEF activates MDM2 expression and blocks oncogene-induced p16 activation to promote transformation.
Sashida G, Liu Y, Elf S, Miyata Y, Ohyashiki K, Izumi M, Menendez S, Nimer SD.
Mol Cell Biol. 2009 Jul;29(13):3687-99. doi: 10.1128/MCB.01551-08. Epub 2009 Apr 20.
PMID 19380490
The ETS transcription factor MEF is a candidate tumor suppressor gene on the X chromosome.
Seki Y, Suico MA, Uto A, Hisatsune A, Shuto T, Isohama Y, Kai H.
Cancer Res. 2002 Nov 15;62(22):6579-86.
PMID 12438253
Osteoblast-specific expression of MEF induces osteopenia through downregulation of osteoblastogenesis and upregulation of osteoclastogenesis.
Seul KJ, Cho HS, Heo SH, Baek WY, Kim JE, Park EK, Choi JY, Ryoo HM, Cho JY.
J Bone Miner Res. 2011 Feb;26(2):341-50. doi: 10.1002/jbmr.208.
PMID 20715187
Functional dissection of the ETS transcription factor MEF.
Suico MA, Koyanagi T, Ise S, Lu Z, Hisatsune A, Seki Y, Shuto T, Isohama Y, Miyata T, Kai H.
Biochim Biophys Acta. 2002 Aug 19;1577(1):113-20.
PMID 12151102
The regulation of human beta-defensin 2 by the ETS transcription factor MEF (myeloid Elf-1-like factor) is enhanced by promyelocytic leukemia protein.
Suico MA, Lu Z, Shuto T, Koga T, Uchikawa T, Yoshida H, Matsuzaki K, Nakao M, Li JD, Kai H.
J Pharmacol Sci. 2004a Aug;95(4):466-70. Epub 2004 Jul 31.
PMID 15286431
SUMO down-regulates the activity of Elf4/myeloid Elf-1-like factor.
Suico MA, Nakamura H, Lu Z, Saitoh H, Shuto T, Nakao M, Kai H.
Biochem Biophys Res Commun. 2006 Sep 29;348(3):880-8. Epub 2006 Aug 1.
PMID 16904644
Myeloid Elf-1-like factor, an ETS transcription factor, up-regulates lysozyme transcription in epithelial cells through interaction with promyelocytic leukemia protein.
Suico MA, Yoshida H, Seki Y, Uchikawa T, Lu Z, Shuto T, Matsuzaki K, Nakao M, Li JD, Kai H.
J Biol Chem. 2004b Apr 30;279(18):19091-8. Epub 2004 Feb 19.
PMID 14976184
Cutting edge: Expression of the transcription factor E74-like factor 4 is regulated by the mammalian target of rapamycin pathway in CD8+ T cells.
Yamada T, Gierach K, Lee PH, Wang X, Lacorazza HD.
J Immunol. 2010 Oct 1;185(7):3824-8. doi: 10.4049/jimmunol.1000718. Epub 2010 Aug 27.
PMID 20802152
Transcription factor ELF4 controls the proliferation and homing of CD8+ T cells via the Kruppel-like factors KLF4 and KLF2.
Yamada T1, Park CS, Mamonkin M, Lacorazza HD.
Nat Immunol. 2009 Jun;10(6):618-26. doi: 10.1038/ni.1730. Epub 2009 May 3.
PMID 19412182
Tumor promoting properties of the ETS protein MEF in ovarian cancer.
Yao JJ, Liu Y, Lacorazza HD, Soslow RA, Scandura JM, Nimer SD, Hedvat CV.
Oncogene. 2007 Jun 7;26(27):4032-7. Epub 2007 Jan 8.
PMID 17213815


This paper should be referenced as such :
Nimer, SD ; Liu, Y
ELF4 (E74-like factor 4 (ets domain transcription factor))
Atlas Genet Cytogenet Oncol Haematol. 2014;18(7):511-515.
Free journal version : [ pdf ]   [ DOI ]

Other Leukemias implicated (Data extracted from papers in the Atlas) [ 1 ]
  t(X;21)(q26;q22) ELF4::ERG

External links


HGNC (Hugo)ELF4   3319
LRG (Locus Reference Genomic)LRG_335
Atlas Explorer : (Salamanque)ELF4
Entrez_Gene (NCBI)ELF4    E74 like ETS transcription factor 4
AliasesELFR; MEF
GeneCards (Weizmann)ELF4
Ensembl hg19 (Hinxton)ENSG00000102034 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000102034 [Gene_View]  ENSG00000102034 [Sequence]  chrX:130063958-130110497 [Contig_View]  ELF4 [Vega]
ICGC DataPortalENSG00000102034
TCGA cBioPortalELF4
AceView (NCBI)ELF4
Genatlas (Paris)ELF4
SOURCE (Princeton)ELF4
Genetics Home Reference (NIH)ELF4
Genomic and cartography
GoldenPath hg38 (UCSC)ELF4  -     chrX:130063958-130110497 -  Xq26.1   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)ELF4  -     Xq26.1   [Description]    (hg19-Feb_2009)
GoldenPathELF4 - Xq26.1 [CytoView hg19]  ELF4 - Xq26.1 [CytoView hg38]
Genome Data Viewer NCBIELF4 [Mapview hg19]  
Gene and transcription
Genbank (Entrez)AF000670 AK314972 BC017194 BC114355 BC114356
RefSeq transcript (Entrez)NM_001127197 NM_001421
Consensus coding sequences : CCDS (NCBI)ELF4
Gene ExpressionELF4 [ NCBI-GEO ]   ELF4 [ EBI - ARRAY_EXPRESS ]   ELF4 [ SEEK ]   ELF4 [ MEM ]
Gene Expression Viewer (FireBrowse)ELF4 [ Firebrowse - Broad ]
GenevisibleExpression of ELF4 in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)2000
GTEX Portal (Tissue expression)ELF4
Human Protein AtlasENSG00000102034-ELF4 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtQ99607   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtQ99607  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProQ99607
Domaine pattern : Prosite (Expaxy)ETS_DOMAIN_1 (PS00345)    ETS_DOMAIN_2 (PS00346)    ETS_DOMAIN_3 (PS50061)   
Domains : Interpro (EBI)Elf4    Ets_dom    TF_Elf_N    WH-like_DNA-bd_sf    WH_DNA-bd_sf   
Domain families : Pfam (Sanger)Elf-1_N (PF12310)    Ets (PF00178)   
Domain families : Pfam (NCBI)pfam12310    pfam00178   
Domain families : Smart (EMBL)ETS (SM00413)  
Conserved Domain (NCBI)ELF4
AlphaFold pdb e-kbQ99607   
Human Protein Atlas [tissue]ENSG00000102034-ELF4 [tissue]
Protein Interaction databases
IntAct (EBI)Q99607
Ontologies - Pathways
Ontology : AmiGOchromatin  RNA polymerase II cis-regulatory region sequence-specific DNA binding  DNA-binding transcription factor activity, RNA polymerase II-specific  DNA-binding transcription factor activity, RNA polymerase II-specific  DNA-binding transcription activator activity, RNA polymerase II-specific  natural killer cell proliferation  NK T cell proliferation  protein binding  nucleus  nucleoplasm  regulation of transcription by RNA polymerase II  nuclear body  PML body  cell differentiation  innate immune response  positive regulation of transcription, DNA-templated  positive regulation of transcription by RNA polymerase II  sequence-specific double-stranded DNA binding  
Ontology : EGO-EBIchromatin  RNA polymerase II cis-regulatory region sequence-specific DNA binding  DNA-binding transcription factor activity, RNA polymerase II-specific  DNA-binding transcription factor activity, RNA polymerase II-specific  DNA-binding transcription activator activity, RNA polymerase II-specific  natural killer cell proliferation  NK T cell proliferation  protein binding  nucleus  nucleoplasm  regulation of transcription by RNA polymerase II  nuclear body  PML body  cell differentiation  innate immune response  positive regulation of transcription, DNA-templated  positive regulation of transcription by RNA polymerase II  sequence-specific double-stranded DNA binding  
NDEx NetworkELF4
Atlas of Cancer Signalling NetworkELF4
Wikipedia pathwaysELF4
Orthology - Evolution
GeneTree (enSembl)ENSG00000102034
Phylogenetic Trees/Animal Genes : TreeFamELF4
Homologs : HomoloGeneELF4
Homology/Alignments : Family Browser (UCSC)ELF4
Gene fusions - Rearrangements
Fusion : MitelmanELF4::ERG [Xq26.1/21q22.2]  
Fusion : FusionHubEIF3E--ELF4    ELF4--C11ORF54    ELF4--CREB5    ELF4--ERG    ELF4--FUS    ELF4--HERPUD1    ELF4--MEF    ELF4--MFAP4    ELF4--NDRG1    ELF4--PDGFA   
ELF4--TJAP1    ERG--ELF4   
Fusion : QuiverELF4
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerELF4 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)ELF4
Exome Variant ServerELF4
GNOMAD BrowserENSG00000102034
Varsome BrowserELF4
ACMGELF4 variants
Genomic Variants (DGV)ELF4 [DGVbeta]
DECIPHERELF4 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisELF4 
ICGC Data PortalELF4 
TCGA Data PortalELF4 
Broad Tumor PortalELF4
OASIS PortalELF4 [ Somatic mutations - Copy number]
Cancer Gene: CensusELF4 
Somatic Mutations in Cancer : COSMICELF4  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DELF4
Mutations and Diseases : HGMDELF4
intOGen PortalELF4
LOVD (Leiden Open Variation Database)[gene] [transcripts] [variants]
DgiDB (Drug Gene Interaction Database)ELF4
DoCM (Curated mutations)ELF4
CIViC (Clinical Interpretations of Variants in Cancer)ELF4
NCG (London)ELF4
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Genetic Testing Registry ELF4
NextProtQ99607 [Medical]
Target ValidationELF4
Huge Navigator ELF4 [HugePedia]
Clinical trials, drugs, therapy
Protein Interactions : CTDELF4
Pharm GKB GenePA27747
Clinical trialELF4
DataMed IndexELF4
PubMed39 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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