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p(HGNC:NFE2L2, pmod(UbPoly))

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Entity

Name
NFE2L2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 1

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 3

complex(p(HGNC:BTRC), p(HGNC:CUL1), p(HGNC:NFE2L2, pmod(Ph))) increases p(HGNC:NFE2L2, pmod(UbPoly)) View Subject | View Object

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]. PubMed:29121589

Appears in Networks:

p(HGNC:NFE2L2) hasVariant p(HGNC:NFE2L2, pmod(UbPoly)) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CUL3), p(HGNC:KEAP1), p(HGNC:NFE2L2)) increases p(HGNC:NFE2L2, pmod(UbPoly)) View Subject | View Object

NRF2 is regulated principally by two different mechanisms. The best established mechanism is the control of protein stability by Kelch-like ECH-associated protein 1 (KEAP1). KEAP1 is an ubiquitin E3 ligase substrate adapter for a Cullin3/Rbx1-dependent E3 ubiquitin ligase complex; henceforth binding of KEAP1 to NRF2 mediates ubiquitination and subsequent proteasomal degradation of NRF2 [7]. PubMed:29121589

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Out-Edges 1

p(HGNC:NFE2L2, pmod(UbPoly)) increases deg(p(HGNC:NFE2L2)) View Subject | View Object

NRF2 is regulated principally by two different mechanisms. The best established mechanism is the control of protein stability by Kelch-like ECH-associated protein 1 (KEAP1). KEAP1 is an ubiquitin E3 ligase substrate adapter for a Cullin3/Rbx1-dependent E3 ubiquitin ligase complex; henceforth binding of KEAP1 to NRF2 mediates ubiquitination and subsequent proteasomal degradation of NRF2 [7]. PubMed:29121589

Appears in Networks:

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.