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a(CHEBI:"NAD(+)")

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

Entity

Name
NAD(+)
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 2

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

In-Edges 4

bp(GO:aging) decreases a(CHEBI:"NAD(+)") View Subject | View Object

Activity of the deacetylase SIRT1 declines with age, partially owing to limited availability of its co fac- tor, nicotinamide 24,56,156 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Machado-Joseph Disease

p(FPLX:AMPK) increases a(CHEBI:"NAD(+)") View Subject | View Object

SIRT1 is activated by AMPK- mediated increases in nicotinamide, and it drives the ALN by inhibiting mTORC1, inducing FOXO1 and FOXO3 and activating key regulatory proteins such as ATG5, ATG7 and LC3. PubMed:30116051

Appears in Networks:

rxn(reactants(a(CHEBI:"NAD(+)"), a(PUBCHEM:9543037)), products(a(CHEBI:"3-oxo-fatty acyl-CoA(4-)"), a(CHEBI:NADH), a(PUBCHEM:1038))) hasReactant a(CHEBI:"NAD(+)") View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"NAD(+)"), p(HGNC:HSD17B10)) hasComponent a(CHEBI:"NAD(+)") View Subject | View Object

Appears in Networks:

Out-Edges 2

a(CHEBI:"NAD(+)") increases act(p(HGNC:SIRT1)) View Subject | View Object

Because the class III deacetylase NAD- dependent protein deacetylase sirtuin 1 (SIRT1) requires nicotinamide adenine dinucleotide (NAD) to sustain its activity, this positive regulator of autophagy may also be considered a sensor 24 . PubMed:30116051

Appears in Networks:

a(CHEBI:"NAD(+)") increases act(p(HGNC:SIRT1)) View Subject | View Object

SIRT1 is activated by AMPK- mediated increases in nicotinamide, and it drives the ALN by inhibiting mTORC1, inducing FOXO1 and FOXO3 and activating key regulatory proteins such as ATG5, ATG7 and LC3. PubMed:30116051

Appears in Networks:

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.