Jun 23, 2020 · The ERK-activated transcription factors MYC and hypoxia-inducible factor 1α (HIF1α) jointly stimulate the expression of glucose transporters and glycolysis enzymes, thus increasing...

We discovered that c-Myc, a master transcription factor controlling central metabolism, is an effector protein downstream of MEK–ERK and that disruption of the MEK–ERK–c-Myc bioenergetic axis in tumor ECs may be an efficient strategy to inhibit tumor growth.

May 15, 2012 · Here we show that ADI-PEG20 activates Ras signaling and the effector extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/AKT/GSK-3β kinase cascades, resulting in phosphorylation and stabilization of c-Myc by attenuation of its ubiquitin-mediated protein degradation mechanism.

Jul 18, 2023 · Expression of nuclear-localized ERK2 constructs in serum-starved cells revealed that ERK2 in the nucleus—regardless of its kinase activity—increased MYC mRNA expression and MYC protein abundance.

Aug 9, 2006 · We demonstrate that, in all the tumor cell lines used, the MEK/ERK inhibitor U0126 rapidly induces c-Myc de-phosphorylation, which is followed by a marked reduction in its expression level, by inhibition of proliferation and by reversion of anchorage-independent growth.

Here we show that ADI-PEG20 activates Ras signaling and the effector ERK and PI3K/AKT/GSK-3β kinase cascades, resulting in phosphorylation and stabilization of c-Myc by attenuation of its ubiquitin-mediated protein degradation mechanism.

Western blotting and DNA-binding assays confirmed the inhibition of c-MYC expression and transcriptional activity by shikonins. Reduction of c-MYC expression was closely associated with deregulated ERK, JNK MAPK and AKT activity, indicating their involvement in shikonin-triggered c-MYC inactivation.

Aug 3, 2012 · We show that endoglin impedes cell growth through sustained inhibition of ERK-induced c-Myc and cyclinD1 expression in a TGF-β-independent manner. The down-regulation of c-Myc and cyclinD1, along with growth-inhibition, are reversed when the endoglin/β-arrestin2 interaction is disrupted.

Feb 29, 2008 · Our results suggest that Myc integrates Erk and PI3K signals to result in various cellular responses by differential stability control of Myc protein isoforms. Such signal integration confers a flexible dynamic range for the system output, governed by stability change.

The MAPK/ERK pathway (also known as the Ras-Raf-MEK-ERK pathway) is a chain of proteins in the cell that communicates a signal from a receptor on the surface of the cell to the DNA in the nucleus of the cell.