First-pass extracted concept

mTORC1

Candidate: concept label2 source documents5 linked claims

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Aliases

mammalian target of rapamycin complex 1

Evidence Snippets

Primary anchor verification confirms the seed paper is PMID 31924757 / DOI 10.1038/s41467-019-13889-6, a 2020 Nature Communications article showing that PHD1/EGLN2 regulates leucine-induced mTORC1 signaling in skeletal muscle by stabilizing leucyl-tRNA synthetase (LRS/LARS1) in a hydroxylation-independent manner.

Evidence 1Source 1DOI PubMedprovenance

the mammalian target of rapamycin complex 1 (mTORC1)

Evidence 2Source 2DOI PubMedprovenance

Supporting Sources

Source 1primary paper2020Nature CommunicationsDOI PubMed

1 evidence snippet 2 linked claims Claim 1 Claim 2

Source 2primary paper2012Frontiers in PharmacologyDOI PubMed

1 evidence snippet 3 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1mechanistic regulationsupports2020Source 1DOI PubMed

PHD1 controls muscle mTORC1 in a hydroxylation-independent manner by stabilizing leucyl tRNA synthetase.

Quoted textsource-backed

PHD1 controls muscle mTORC1 in a hydroxylation-independent manner by stabilizing leucyl tRNA synthetase

Claim 2pathway regulationsupports2020Source 1DOI PubMed

PHD1/EGLN2 regulates leucine-induced mTORC1 signaling in skeletal muscle by stabilizing leucyl-tRNA synthetase.

Quoted textsource-backed

Primary anchor verification confirms the seed paper is PMID 31924757 / DOI 10.1038/s41467-019-13889-6, a 2020 Nature Communications article showing that PHD1/EGLN2 regulates leucine-induced mTORC1 signaling in skeletal muscle by stabilizing leucyl-tRNA synthetase (LRS/LARS1) in a hydroxylation-independent manner.

Claim 3disease relevancesupports2012Source 2DOI PubMed

mTORC1 is presented as a potential critical link in neurobiological processes that drive addiction and relapse behavior.

Quoted textsource-backed

mTORC1 functions to regulate synaptic protein translation and is a potential critical link in our understanding of the neurobiological processes that drive addiction and relapse behavior.

Claim 4functional rolesupports2012Source 2DOI PubMed

mTORC1 regulates synaptic protein translation.

Quoted textsource-backed

mTORC1 functions to regulate synaptic protein translation

Claim 5pathway dysregulationsupports2012Source 2DOI PubMed

Drug exposure may dysregulate mTORC1 signaling and contribute to aberrant translation of synaptic proteins including AMPARs that are relevant to relapse vulnerability.

Quoted textsource-backed

we aim to highlight evidence that mTORC1 signaling may be dysregulated by drug exposure and that these changes may contribute to aberrant translation of synaptic proteins that appear critical to increased relapse vulnerability, including AMPARs.