ELF5: E74 Like ETS Transcription Factor 5
A key regulator of epithelial cell differentiation and tumor suppression
Gene Information Card
| Symbol | ELF5 |
|---|---|
| Full Name | E74 Like ETS Transcription Factor 5 |
| Gene Type | Protein coding |
| Chromosomal Location | 11p13 |
| NCBI Gene ID | 2001 ncbi.nlm.nih.gov/gene/2001 |
| Ensembl ID | ENSG00000135318 |
| UniProt ID | Q9UKW6 |
| OMIM ID | 604526 |
| HGNC ID | 3320 |
| Aliases | ESE-2, ESE2, EPR-1 |
Description
ELF5 (E74 Like ETS Transcription Factor 5) is a member of the ETS family of transcription factors. It acts as a master regulator of epithelial cell differentiation, particularly in mammary gland, prostate, and lung. ELF5 is involved in cell proliferation, apoptosis, and tumor suppression. Loss of ELF5 expression is associated with aggressive breast cancer and prostate cancer progression.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Breast Cancer | Loss of ELF5 expression promotes epithelial-mesenchymal transition and metastasis | PMID: 22955915, COSMIC |
| Prostate Cancer | ELF5 suppresses androgen receptor signaling; loss leads to castration-resistant prostate cancer | PMID: 23934149, COSMIC |
| Lung Cancer | Downregulation of ELF5 correlates with poor prognosis in non-small cell lung cancer | PMID: 25636800 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Mammary gland | 15.2 | Medium |
| Prostate | 12.8 | Medium |
| Lung | 8.5 | Low |
| Salivary gland | 10.1 | Low |
| Kidney | 6.3 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| MCF7 (breast cancer) | 18.4 | High expression |
| PC3 (prostate cancer) | 2.1 | Low expression |
| A549 (lung cancer) | 7.8 | Moderate expression |
| HEK293 (embryonic kidney) | 0.5 | Very low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1A>G (p.Met1?) | Missense | 0.01% | Loss of start codon, likely loss of function |
| c.202C>T (p.Arg68*) | Nonsense | 0.005% | Premature stop, loss of function |
| c.350G>A (p.Arg117Gln) | Missense | 0.02% | Reduced DNA binding affinity |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations leading to truncated protein or loss of DNA-binding domain; associated with cancer progression.
Gain of Function (GOF)
Not reported in literature or curated databases.
Dominant Negative (DN)
Missense mutations in the ETS domain that impair DNA binding but retain dimerization capacity; rare.
View complete mutation data：
Gene Ontology (GO)
Pathways
• ETS family transcription factor pathway
• Epithelial-mesenchymal transition (EMT) regulation
• Androgen receptor signaling (negative regulation)
Protein Summary
ELF5 is a 265-amino acid transcription factor containing a conserved ETS DNA-binding domain. It binds to ETS recognition sites (GGAA/T) in target gene promoters. ELF5 is essential for mammary gland development and luminal epithelial differentiation. In cancer, ELF5 acts as a tumor suppressor by repressing EMT and inhibiting androgen receptor signaling. Protein structure includes an N-terminal transactivation domain and a C-terminal ETS domain.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ELF5 Knockout HEK293 Cell Line | EDJ-KQ4520 | Human | 2001 | Details Get a Quote |
| CELF5 Knockout HEK293 Cell Line | EDJ-KQ12856 | Human | 60680 | Details Get a Quote |
| CELF5 Knockout HCT 116 Cell Line | EDJ-KQ42019 | Human | 60680 | Details Get a Quote |
| ELF5 Knockout HeLa Cell Line | EDJ-KQ53155 | Human | 2001 | Details Get a Quote |
| CELF5 Knockout HeLa Cell Line | EDJ-KQ56989 | Human | 60680 | Details Get a Quote |
| ELF5 Knockout A-549 Cell Line | EDJ-KQ61629 | Human | 2001 | Details Get a Quote |
| CELF5 Knockout A-549 Cell Line | EDJ-KQ65492 | Human | 60680 | Details Get a Quote |
| ELF5 Knockout HCT 116 Cell Line | EDJ-KQ70114 | Human | 2001 | Details Get a Quote |
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