ELF1 (E74 Like ETS Transcription Factor 1)

ETS-family proteins from all major classes bind CPD-containing DNA sites.Engagement of CPD by ETS proteins inhibits DNA repair in a position-dependent manner.Structure and thermodynamics of ETS binding to damaged DNA differ from undamaged substrates.

Cancers with high co-expression of ELF3 and HNF4A were frequently chromosomally instability (CIN), intestinal-type adenocarcinomas, and harbored TP53 mutations and WWOX deletions. Expression of E74 like ETS transcription factor 3 (ELF3), an ETS transcription family member, correlates with expression of other key factors in gastric cancer and confers specific characteristics that may become exploited in targeted therapeutic interventions.

The ELF1/IGF2BP2/FAM111B cascade drives CRC progression and ferroptosis resistance. Targeting this cascade may provide a therapeutic avenue for CRC treatment.

Among the differences, the absence of MALAT1 and NEAT1 lncRNAs in lactocytes correlates with loss of six transcription factors (EP300, ELF1, E2F3, BDP1, HOXC10, and KLF6). These findings provide insights into breast cancer and suggest new therapeutic targets.

show that Elf1, a member of the large "Ets" (E26 transformation specific) transcription factor family with importance for normal and malignant hematopoiesis, participates in typical myeloid enhancer structures. Elf1 is involved in control of transcripts with a role in innate immunity and it is essential for the ability of myeloid cells to respond rapidly to immunologic stimuli.

Single-cell transcriptomes uncovered sNK cells undertaking a unique differentiation trajectory and turning on STAT1, JUN, BHLHE40, ELF1, MAX and MYC regulons essential for augmenting antitumour effector functions and proliferation, respectively. Both proteomic and single-cell transcriptomes revealed that an increase in Cathepsin C helped to augment the quantity and function of Granzyme B. These results support that this unique method produces potent NK cells for clinical utilisation and delineate the molecular mechanisms associated with this process.

Utilizing the bioUbiquitination approach, which is based on cellular biotinylation of ubiquitin, in HEK293FT cells derived from immortalized human embryonic kidney cells, followed by sequential immunoprecipitation coupled mass spectrometry analyses, we identified ubiquitinated lysine residues of CXXC5. We show in both MCF-7 and HEK293FT cells that the ubiquitinated lysine residues contribute to the degradation of CXXC5 through the ubiquitin-proteasome pathway.

GPD1L is overexpressed in human HCCs and associated with worse clinical outcomes. Aberrant GPD1L expression, driven by ELF1, facilitates conversion of DHAP to G3P conversion to support triacylglycerol synthesis in HCC, promoting tumor growth and metastasis.

Subsequent analysis of RNA-seq and CUT&Tag results identified MYB as a key direct target of ZNF217. Overall, our research highlights ZNF217 as a critical oncogene in AML and offers new insights into the transcriptional regulatory mechanisms at play in AML.

In summary, this study identified IRF1 as a novel core transcription factor involved in AML pathogenesis. IRF1 collaborates with ELF1, ETV6, RUNX2, and MEF2D to form a core transcriptional regulatory circuit that promotes AML progression. Furthermore, we demonstrated that IRF1 directly regulates the expression of key genes involved in lipid metabolism, influencing the synthesis of diverse lipid molecules crucial for AML survival.

In summary, our study provides compelling evidence that ELF1 up-regulates DCLK1 expression, thereby promoting the malignant progression and stemness of colorectal cancer. These findings significantly contribute to our understanding of the regulatory mechanisms in CRC and may have implications for future therapeutic strategies.

Mature microRNA-5099-3p (miR-5099-3p) inhibited the expression of E74 like ETS transcription factor 1 (ELF1), which transcriptionally regulated pyroptosis factors such as acysteinyl aspartate-specific proteinase 1 (caspase-1) and gasdermin D (GSDMD), ultimately leading to cardiomyocyte pyroptosis. This study reveals that myocardial infarction-induced miR-5099-3p excessive maturation via m6A modification promotes the development and progression of cardiomyocyte pyroptosis.