Disease relevance of Elf4

• Furthermore, neither MCA/129 fibrosarcoma nor B16 melanoma tumors showed differences in growth or radioresponsiveness when implanted into mutant mouse models (Rag(-/-) and MEF(-/-)) lacking functional immune cell [natural killer (NK), NK-T, T, and B cells] populations [1].
• We report that the transcription factor known as MEF (or ELF4), which is targeted by the t(X;21)(q26;q22) in acute myelogenous leukemia, regulates the proliferation of primitive hematopoietic progenitor cells at steady state, controlling their quiescence [2].
• This abrogation of SV40 transformation in vitro by cytotoxic T-lymphocyte clone K11 was specific, since transformation of B6/MEF cells by adenovirus type 5 DNA was not affected [3].
• Primary mouse embryo fibroblasts of C57BL/6 origin (B6/MEF) were transformed in vitro by transfection with simian virus 40 (SV40) DNA [3].
• Mouse embryonic fibroblast (MEF/3T3) and rat schwannoma (RT4) cell lines were generated to provide regulatable schwannomin expression [4].

High impact information on Elf4

• Promoter studies and chromatin immunoprecipitation analyses demonstrate that MEF and not ETS-1 directly regulates transcription of the perforin gene in NK cells [5].
• Our results uncover a specific role of MEF in the development and function of NK cells and in innate immunity [5].
• We utilized gene targeting by homologous recombination to define the role that MEF, a transcriptional activating member of the ETS family of transcription factors, plays in lymphopoiesis [5].
• The ETS protein MEF plays a critical role in perforin gene expression and the development of natural killer and NK-T cells [5].
• Mouse embryo fibroblasts deficient for the c-Jun proto-oncogene (c-Jun-/- MEF) undergo p53-dependent premature senescence in conventional culture [6].

Chemical compound and disease context of Elf4

• The effect of mild hyperthermia on cisplatin sensitization was examined in two cell line pairs, CHO parental AA8 and irsISF, an XRCC3 mutant (deficient in homologous recombination repair), and mouse parental MEF and knockout Ku80 mutants (deficient in non-homologous endjoining repair) [7].

Biological context of Elf4

• Thus, MEF plays an important role in the decision of stem/primitive progenitor cells to divide or remain quiescent by regulating their entry to the cell cycle [2].
• This accumulation may be attributable, at least in part, to inefficient repair, since DNA damage induced by gamma ionizing radiation and H2O2 persists for longer in c-Jun-/- MEF than in wild-type MEF [6].
• Hence, in oncogene-expressing MEF p53 induces apoptosis by BH3 protein-dependent caspase activation [8].
• Three cis-elements (i.e., the E box, myocyte enhancer factor [MEF] 2, and MEF3 sites) in the proximal myogenin promoter in response to these three pathways are defined [9].
• However, Peri Adelta1-6 failed to enhance PKA-stimulated lipolysis in either MEF adipocytes or differentiated brown adipocytes [10].

Anatomical context of Elf4

• MEF-/- mice have a profound reduction in the number of NK-T and NK cells [5].
• We compared FPR internalization and recycling kinetics in these cells to congenic wild type MEF cell lines [11].
• HSL-/- MEF differentiated into mature adipocytes in a manner indistinguishable from that of wild-type mice [12].
• When SGV 1w or TCV were treated with trypsin the infectivity for macrophages was unaltered as long as the inoculum was adjusted to contain the same number of p.f.u. as assayed in MEF [13].
• The feeders used were a continuous cell line of murine embryonic fibroblasts (STO), primary mouse (MEF) or primary rat (REF) embryonic fibroblasts, and a continuous cell line of rat uterine epithelial cells (RUCs) [14].

Associations of Elf4 with chemical compounds

• Mef null HSCs display increased residence in G0 with reduced 5-bromodeoxyuridine incorporation in vivo and impaired cytokine-driven proliferation in vitro [2].
• Extracts from HSL-/- MEF adipocytes hydrolyzed triacylglycerol (TG) but not cholesterol ester, indicating that the residual lipolytic activity was mediated by another TG-specific lipase [12].
• Similarly, these GlcNAc-containing residues blocked the binding of purified IgM monoclonal antibodies (MAbs) to MEF [15].
• In cells labelled for 1, 3, 6, 12 and 24 h fractional inositol-d(6) incorporation into whole-cell PtdIns species was consistently higher in PITPalpha(-/-) MEF implying greater flux through its biosynthetic pathway [16].
• Treatment of wt MEF with heat resulted in temperature- and heating duration-dependent tyrosine phosphorylation of PLC-gamma1 [17].

Analytical, diagnostic and therapeutic context of Elf4

• Due to their increased HSC quiescence, Mef null mice are relatively resistant to the myelosuppressive effects of chemotherapy and radiation [2].
• IFN-gamma inhibited MCMV replication in a signal transducer and activator of transcription (STAT)-1alpha-dependent manner much more effectively in BMMphi (approximately 100-fold) than MEF (5-10-fold) [18].
• Although initial STAT-1alpha activation by IFN-gamma was equivalent in MEF and BMMphi, microarray analysis demonstrated that IFN-gamma regulates different sets of genes in BMMphi compared with MEFs [18].
• One of the genes that was expressed at a higher level in a scratching group than in the control group was myocyte-specific enhancer binding factor (MEF) 2C, in the cerebral cortex [19].

References