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p(FPLX:AMPK)

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Entity

Name
AMPK
Namespace
FPLX
Namespace Version
20190217
Namespace URL
https://raw.githubusercontent.com/sorgerlab/famplex/d9ec0526c20795146a9a6aef17496efe1a36cac6/export/famplex.belns

Appears in Networks 3

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

Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. v1.0.0

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

In-Edges 11

a(CHEBI:"AICA ribonucleotide") increases act(p(FPLX:AMPK)) View Subject | View Object

The aminoimidazole derivative 5-aminoimidazole- 4-carboxamide ribonucleotide (AICAR) undergoes intra- cellular transformation to an AMP analogue that triggers AMPK-mediated autophagy 21,108 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"alpha,alpha-trehalose") increases act(p(FPLX:AMPK)) View Subject | View Object

The di-glucose derivative trehalose inhibits the sol- ute carrier 2A (SLC2A) family of glucose transporters to promote AMPK-induced autophagy and reduce neurotoxic protein load, although it also exerts other actions downstream in the ALN 4,120 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:"amyloid-beta polypeptide 42") decreases act(p(FPLX:AMPK)) View Subject | View Object

Sixth, Aβ42 compro- mises the function of AMPK to impede initiation of the ALN 67 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"methylene blue") increases act(p(FPLX:AMPK)) View Subject | View Object

Other compounds that act through AMPK acti- vation include the antiaggregant methylene blue (Supplementary Box 1), which elevated levels of beclin  1, p62 and LC3, induced autophagy and suppressed tau in organotypic neuronal cultures and a mouse model of FTD 101,102 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:calcitriol) increases act(p(FPLX:AMPK)) View Subject | View Object

In addition, calcitriol (the active metabolite of vitamin D 3 ) elicited AMPK-dependent autophagy in a neurochemical lesion-induced model of PD 129. PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
MeSH
Parkinson Disease

a(CHEBI:metformin) increases act(p(FPLX:AMPK)) View Subject | View Object

The antidiabetic drug metformin, a prototypical activator of AMPK, induced autophagy and increased longevity in mice 116 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(CHEBI:resveratrol) increases act(p(FPLX:AMPK)) View Subject | View Object

Resveratrol can stimulate SIRT1 via AMPK (see above), and it also possesses an AMPK-independent mode of SIRT1 recruitment that participates in blunting the neurotoxicity of Aβ25–35 fragments in PC12 cells 160 . PubMed:30116051

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

a(CHEBI:selenomethionine) increases act(p(FPLX:AMPK)) View Subject | View Object

Selenium deficits have been linked to AD, and thus it is interesting that seleno- methionine boosted ALN flux, from AMPK recruit- ment through autophagosome formation to lysosomal degradation, in the 3×Tg AD mouse model 112 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(PUBCHEM:54708532) increases act(p(FPLX:AMPK)) View Subject | View Object

Another direct facilitator of AMPK, A769662, elicited autophagy and reduced the burden of Htt in a striatal cell line derived from knock-in mice expressing a humanized form of mutant Htt (exon 1 containing seven polyglutamine repeats) 111 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

p(HGNC:SESN2) increases act(p(FPLX:AMPK)) View Subject | View Object

Supporting the relevance of sestrin 2, it has been shown to protect dopaminergic neurons from the neurotoxin rotenone via AMPK-transduced autophagy 247 . PubMed:30116051

Appears in Networks:

composite(p(FPLX:AMPK), p(HGNC:TSC2)) hasComponent p(FPLX:AMPK) View Subject | View Object

Appears in Networks:

Out-Edges 15

p(FPLX:AMPK) hasVariant p(FPLX:AMPK, pmod(Ph, Thr, 172)) View Subject | View Object

Appears in Networks:

p(FPLX:AMPK) hasVariant p(FPLX:AMPK, pmod(Ph, Tyr, 172)) View Subject | View Object

Appears in Networks:

p(FPLX:AMPK) increases bp(GO:macroautophagy) View Subject | View Object

The heterotrimeric serine/threonine kinase 5ʹ‑AMP‑ activated protein kinase (AMPK) and mammalian target of rapamycin complex 1 (mTORC1) trigger autophagy and repress mitophagy 3,10,20–23 (BOX 2; FIG. 3) . PubMed:30116051

Appears in Networks:

p(FPLX:AMPK) decreases bp(GO:mitophagy) View Subject | View Object

The heterotrimeric serine/threonine kinase 5ʹ‑AMP‑ activated protein kinase (AMPK) and mammalian target of rapamycin complex 1 (mTORC1) trigger autophagy and repress mitophagy 3,10,20–23 (BOX 2; FIG. 3) . PubMed:30116051

Appears in Networks:

p(FPLX:AMPK) increases p(HGNC:ULK1, pmod(Ph, Ser, 317)) View Subject | View Object

AMPK is central to several mechanisms that trigger autophagy — most importantly, activating phosphoryla- tion of ULK1 (Ser317 and Ser777) and inhibitory phos- phorylation of mTORC1 (REFS21,31) . PubMed:30116051

Appears in Networks:

p(FPLX:AMPK) increases p(HGNC:ULK1, pmod(Ph, Ser, 777)) View Subject | View Object

AMPK is central to several mechanisms that trigger autophagy — most importantly, activating phosphoryla- tion of ULK1 (Ser317 and Ser777) and inhibitory phos- phorylation of mTORC1 (REFS21,31) . PubMed:30116051

Appears in Networks:

p(FPLX:AMPK) increases p(FPLX:mTORC1, pmod(Ph)) View Subject | View Object

AMPK is central to several mechanisms that trigger autophagy — most importantly, activating phosphoryla- tion of ULK1 (Ser317 and Ser777) and inhibitory phos- phorylation of mTORC1 (REFS21,31) . PubMed:30116051

Appears in Networks:

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:

act(p(FPLX:AMPK)) increases bp(GO:autophagy) View Subject | View Object

The aminoimidazole derivative 5-aminoimidazole- 4-carboxamide ribonucleotide (AICAR) undergoes intra- cellular transformation to an AMP analogue that triggers AMPK-mediated autophagy 21,108 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

act(p(FPLX:AMPK)) increases bp(GO:autophagy) View Subject | View Object

The di-glucose derivative trehalose inhibits the sol- ute carrier 2A (SLC2A) family of glucose transporters to promote AMPK-induced autophagy and reduce neurotoxic protein load, although it also exerts other actions downstream in the ALN 4,120 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

act(p(FPLX:AMPK)) increases act(p(HGNC:SIRT1)) View Subject | View Object

Resveratrol can stimulate SIRT1 via AMPK (see above), and it also possesses an AMPK-independent mode of SIRT1 recruitment that participates in blunting the neurotoxicity of Aβ25–35 fragments in PC12 cells 160 . PubMed:30116051

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

p(FPLX:AMPK) increases bp(GO:autophagy) View Subject | View Object

The mammalian target of rapamycin (mTOR) kinase negatively modulates autophagy by phosphorylating Atg1, an autophagy initiating factor, while adenosine monophosphate-activated protein kinase (AMPK), a major sensor for the cellular energy status, activates autophagy through inhibiting mTOR signaling as well as by direct phosphorylation of Atg1 (Egan et al., 2011; Kim et al., 2011). Increased mTOR activity results in autophagy downregulation and tau accumulation. PubMed:23528736

Appears in Networks:

p(FPLX:AMPK) decreases act(p(FPLX:mTORC1)) View Subject | View Object

The mammalian target of rapamycin (mTOR) kinase negatively modulates autophagy by phosphorylating Atg1, an autophagy initiating factor, while adenosine monophosphate-activated protein kinase (AMPK), a major sensor for the cellular energy status, activates autophagy through inhibiting mTOR signaling as well as by direct phosphorylation of Atg1 (Egan et al., 2011; Kim et al., 2011). Increased mTOR activity results in autophagy downregulation and tau accumulation. PubMed:23528736

Appears in Networks:

p(FPLX:AMPK) increases p(HGNC:ULK1, pmod(Ph)) View Subject | View Object

The mammalian target of rapamycin (mTOR) kinase negatively modulates autophagy by phosphorylating Atg1, an autophagy initiating factor, while adenosine monophosphate-activated protein kinase (AMPK), a major sensor for the cellular energy status, activates autophagy through inhibiting mTOR signaling as well as by direct phosphorylation of Atg1 (Egan et al., 2011; Kim et al., 2011). Increased mTOR activity results in autophagy downregulation and tau accumulation. PubMed:23528736

Appears in Networks:

p(FPLX:AMPK) increases p(HGNC:ULK1, pmod(Ph)) View Subject | View Object

For instance, adenosine monophosphate- activated protein kinase (AMPK) phosphorylates ULK1 and inactivates mTOR through the raptor and tuberous sclerosis complex (TSC2). PubMed:29758300

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.