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. 2016 Apr 8;7(2):39–46. doi: 10.1080/21541248.2016.1161698

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© 2016 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License http://creativecommons.org/licenses/by-nc/3.0/, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — Intersection between the Ras and the SUMO pathway in cancer. Ras can be activated by multiple upstream signaling inputs including receptor tyrosine kinases (RTKs), G protein-coupled receptors (GPCRs), calcium influx (Ca²⁺) and the T-cell receptor (TCR) complex. Downstream of Ras, several members of MAPK pathway, including MEK kinases and the transcription factors Ets-1 and Elk-1, are SUMOylated. The SUMO pathway consists of a single E1 ligase (SAE1/SAE2 heterodimer), a single E2 ligase (Ubc9) and several E3 proteins. Through the regulation of KRAS-associated SUMOylated proteins (KASPs) such as KAP1, the SUMO pathway plays a supportive role in KRAS-driven transformation. SUMO modification is reversible by sentrin-specific proteases (SENPs).