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NRF2 appears to be essential for prevention of tunicamycin-induced apoptotic cell death [31] and its activation under these conditions is driven by the autophagic degradation of KEAP1 [51]

however, JAM-2 and JAM-3 are specific to endothelial cells

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Dworkin RH, OConnor AB, Audette J et al (2010) Recommendations for the pharmacological management of neuropathic pain: an overview and literature update