Key result
A Raf-induced, MEK-independent signaling pathway activates atrial natriuretic factor gene expression in cardiac myocytes, whereas the MEK-ERK pathway inhibits it.
Why the study?
Does Raf-induced signaling regulate ANF gene expression in cardiac myocytes?
Does Raf-induced signaling regulate ANF gene expression in cardiac myocytes?
Answers are grounded in this paper and cite their sources.
Raf activates ANF gene expression in cardiac myocytes via a MEK-independent pathway, while the MEK-ERK pathway inhibits it, providing a mechanism for regulating ANF in response to hypertrophic stimuli.
The atrial natriuretic factor (ANF) gene is activated in cardiac myocytes by Ras and its effector Raf. However, MEK, the best-characterized Raf substrate, cannot efficiently activate ANF suggesting that Raf uses a MEK-independent pathway to activate ANF. By manipulating MEK and Raf activities so that they are equally effective at activating ERK, we now demonstrate that Raf activates at least two signaling pathways in cardiac myocytes that regulate the ANF promoter; the MEK-->ERK pathway inhibits ANF gene expression while a Raf-induced, MEK-independent pathway activates expression. This mechanism may provide increased ability to regulate ANF expression in response to hypertrophic stimuli.
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Jette et al. (2000) studied this question. Raf and MEK pathway manipulation was evaluated on Atrial natriuretic factor (ANF) gene expression. A Raf-induced, MEK-independent signaling pathway activates atrial natriuretic factor gene expression in cardiac myocytes, whereas the MEK-ERK pathway inhibits it.
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