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. 2009 Oct;23(10):1933-5.
doi: 10.1038/leu.2009.118. Epub 2009 Jun 4.

Src family kinase gene targets during myeloid differentiation: identification of the EGR-1 gene as a direct target

J E Jones, L Wang, P L Kropf, R Duan, D E Johnson

Src family kinase gene targets during myeloid differentiation: identification of the EGR-1 gene as a direct target

J E Jones et al. Leukemia. 2009 Oct.
No abstract available

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Figures

Figure 1
Figure 1
Inhibition of Src family kinases (SFKs) results in Egr-1 induction. NB4 cells were treated for 2 h with vehicle alone, 0.01 µm all-trans retinoic acid (ATRA) alone, 10 µm PP2 alone, or ATRA plus PP2. Following treatment, whole-cell lysates were prepared and proteins (20 µg per lane) were electrophoresed on a 10% SDS-PAGE gel, transferred to nitrocellulose, and probed with anti-Egr-1 monoclonal antibody (Cell Signaling Technology). The filter was stripped and reprobed with anti-β-actin to demonstrate equal protein loading. The experiment was performed three times, with similar results each time.
Figure 2
Figure 2
Time course of Egr-1 induction following Src family kinase (SFK) inhibition. NB4 cells were left untreated for 48 h, or were treated for varying lengths of time with 10 µm PP2 to inhibit SFKs. Following treatment, whole-cell lysates were subjected to immunoblotting for Egr-1 or β-actin as described for Figure 1. The experiment was performed twice, with similar results.
Figure 3
Figure 3
The gene encoding Egr-1 is a direct target of Src family kinases (SFKs). (a) NB4 cells were treated for 1 h with vehicle alone, 10 µm PP2, 10 µm cycloheximide (CHX) or cycloheximide plus PP2. After the preparation of total RNA, reverse transcription-polymerase chain reaction (RT-PCR) was carried out using primers specific for Egr-1 mRNA (forward primer: 5′-AGCCCTACGAGCACCTGAC-3′; reverse primer: 5′-TGGGTTGGTCATGCTCACTA-3′). The RT-PCR products were electrophoresed on a 2% agarose gel and stained with ethidium bromide. β-Actin was used as an internal control. (b) NB4 cells were treated as in (a), followed by immunoblotting for Egr-1 or β-actin. The experiment was performed three times with similar results.
See this image and copyright information in PMC

References

    1. Tallman MS, Nabhan C, Feusner JH, Rowe JM. Acute promyelocytic leukemia: evolving therapeutic strategies. Blood. 2002;99:759–767. - PubMed
    1. Miranda MB, Johnson DE. Signal transduction pathways that contribute to myeloid differentiation. Leukemia. 2007;21:1363–1377. - PubMed
    1. Miranda MB, Redner RL, Johnson DE. Inhibition of Src family kinases enhances retinoic acid-induced gene expression and myeloid differentiation. Mol Cancer Ther. 2007;6:3081–3090. - PubMed
    1. Yang L, Zhao H, Li S, Ahrens K, Collins C, Eckenrode S, et al. Gene expression profiling during all-trans retinoic acid-induced cell differentiation of acute promyelocytic leukemia cells. J Mol Diagn. 2003;5:212–221. - PMC - PubMed
    1. Kharbanda S, Nakamura T, Stone R, Hass R, Bernstein S, Datta R, et al. Expression of the early growth response 1 and 2 zinc finger genes during induction of monocytic differentiation. J Clin Invest. 1991;88:571–577. - PMC - PubMed

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