Skip to main content
Fig. 6 | Epigenetics & Chromatin

Fig. 6

From: Distinctive epigenomic alterations in NF1-deficient cutaneous and plexiform neurofibromas drive differential MKK/p38 signaling

Fig. 6

Proposed differential signaling schema comparing PNFs and CNFs. Although both RAS/MEK/ERK and RAS/MKK3/P38 signaling occurs in both tumor types, RAS activation results in differential signaling strength and fidelity through RAS/MEK in PNFs (left panel) and, alternatively, RAS/MKK3/P38 in CNFs (right panel). CNFs divert RAS activation through MKK3 thereby enhancing the cellular response to stress and inflammation that is mediated by MKK3/p38, whereas the downstream impact in RAS/MEK dependent PNFs is unchecked growth and proliferation (left). CNFs still maintain growth and proliferation signaling through RAS/ERK or p38/ERK, but strongly exhibit a pro-inflammatory phenotype and are characterized by broad chromatin remodeling (right)

Back to article page
\