p(HGNC:GSK3B) increases p(HGNC:NFE2L2, pmod(Ph))

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PubMed:29121589

The second mechanism is related to GSK-3, which phosphorylates NRF2 creating a recognition site for β-Transducin Repeat Containing E3 Ubiquitin Protein Ligase (β-TrCP). β-TrCP leads to Cullin-1/Rbx1-mediated NRF2 ubiquitination and its subsequent degradation [8]. Since GSK-3β is inhibited by phosphorylation at Ser9 by Ser/Thr protein kinases such as AKT, it has been suggested that NRF2 might be up-regulated through activation of AKT and permanent inactivation of GSK-3 [9], [10].

Related Edges 7

• complex(p(HGNC:BTRC), p(HGNC:CUL1), p(HGNC:NFE2L2, pmod(Ph))) increases p(HGNC:NFE2L2, pmod(UbPoly))
• p(HGNC:BTRC) increases complex(p(HGNC:BTRC), p(HGNC:CUL1), p(HGNC:NFE2L2, pmod(Ph)))
• p(HGNC:NFE2L2) positiveCorrelation p(FPLX:AKT)
• p(FPLX:AKT) increases p(HGNC:GSK3B, pmod(Ph, Ser, 9))
• p(FPLX:AKT) positiveCorrelation p(HGNC:NFE2L2)
• p(HGNC:GSK3B) decreases p(HGNC:NFE2L2)
• p(HGNC:GSK3B, pmod(Ph, Ser, 9)) decreases act(p(HGNC:GSK3B), ma(kin))

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