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p(HGNC:NFKBIA, pmod(Ph, Tyr, 42))

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
NFKBIA
Namespace
hgnc
Namespace Version
20190224
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/c328ad964c08967a0417a887510b97b965a62fa5/external/hgnc-names.belns

Appears in Networks 2

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

In-Edges 5

act(p(HGNC:LCK)) increases p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) View Subject | View Object

The mechanism underlying the effect of BDNF and CNTF on NF-κB activation has been attributed to the activation of Src and Lck non-receptor tyrosine kinases which phosphorylate IκBα on Tyr42 resulting in subsequent NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:NFKBIA) hasVariant p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) View Subject | View Object

Appears in Networks:

act(p(HGNC:SRC)) increases p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) View Subject | View Object

The mechanism underlying the effect of BDNF and CNTF on NF-κB activation has been attributed to the activation of Src and Lck non-receptor tyrosine kinases which phosphorylate IκBα on Tyr42 resulting in subsequent NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:melatonin) decreases p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) View Subject | View Object

The antioxidants LY231617, and melatonin pro- tect the neurons against the insult and prevented the Tyr42 phosphorylation of IκBα, which acts to protect the neurons against physiological injury by repressing the insult-induced oxidative stress activation of transcription factor NF-κB [86]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(PUBCHEM:3968) decreases p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) View Subject | View Object

The antioxidants LY231617, and melatonin pro- tect the neurons against the insult and prevented the Tyr42 phosphorylation of IκBα, which acts to protect the neurons against physiological injury by repressing the insult-induced oxidative stress activation of transcription factor NF-κB [86]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

Out-Edges 1

p(HGNC:NFKBIA, pmod(Ph, Tyr, 42)) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

The mechanism underlying the effect of BDNF and CNTF on NF-κB activation has been attributed to the activation of Src and Lck non-receptor tyrosine kinases which phosphorylate IκBα on Tyr42 resulting in subsequent NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.