Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Cesari, F. et al.

Mice deficient for the ets transcription factor elk-1 show normal immune responses and mildly impaired neuronal gene activation.

The transcription factor Elk-1 belongs to the ternary complex factor (TCF) subfamily of Ets proteins. TCFs interact with serum response factor to bind jointly to serum response elements in the promoters of immediate-early genes (IEGs). TCFs mediate the rapid transcriptional response of IEGs to various extracellular stimuli which activate mitogen-activated protein kinase signaling. To investigate physiological functions of Elk-1 in vivo, we generated Elk-1-deficient mice by homologous recombination in embryonic stem cells. These animals were found to be phenotypically indistinguishable from their wild-type littermates. Histological analysis of various tissues failed to reveal any differences between Elk-1 mutant and wild-type mice. Elk-1 deficiency caused no changes in the proteomic displays of brain or spleen extracts. Also, no immunological defects could be detected in mice lacking Elk-1, even upon infection with coxsackievirus B3. In mouse embryonic fibroblasts, Elk-1 was dispensable for c-fos and Egr-1 transcriptional activation upon stimulation with serum, lysophosphatidic acid, or tetradecanoyl phorbol acetate. However, in brains of Elk-1-deficient mice, cortical and hippocampal CA1 expression of c-fos, but not Egr-1 or c-Jun, was markedly reduced 4 h following kainate-induced seizures. This was not accompanied by altered patterns of neuronal apoptosis. Collectively, our data indicate that Elk-1 is essential neither for mouse development nor for adult life, suggesting compensatory activities by other TCFs.[1]

References

Mice deficient for the ets transcription factor elk-1 show normal immune responses and mildly impaired neuronal gene activation. Cesari, F., Brecht, S., Vintersten, K., Vuong, L.G., Hofmann, M., Klingel, K., Schnorr, J.J., Arsenian, S., Schild, H., Herdegen, T., Wiebel, F.F., Nordheim, A. Mol. Cell. Biol. (2004) [Pubmed]

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