Title : ROS-independent Nrf2 activation in prostate cancer.

Pub. Date : 2017 Sep 15

PMID : 28978049






4 Functional Relationships(s)
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1 We showed GRP78/BiP translocation to PC3 cell surface in the presence of tunicamycin, an ER stress inductor, and demonstrated the existence of a GRP78/BiP-dependent non-canonical Nrf2 activation, responsible for increased resistance to ER-stress induced apoptosis. Tunicamycin heat shock protein family A (Hsp70) member 5 Homo sapiens
2 We showed GRP78/BiP translocation to PC3 cell surface in the presence of tunicamycin, an ER stress inductor, and demonstrated the existence of a GRP78/BiP-dependent non-canonical Nrf2 activation, responsible for increased resistance to ER-stress induced apoptosis. Tunicamycin heat shock protein family A (Hsp70) member 5 Homo sapiens
3 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin heat shock protein family A (Hsp70) member 5 Homo sapiens
4 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin heat shock protein family A (Hsp70) member 5 Homo sapiens