Evidence map›Paper›PMID 38183387›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

SHMT2 Mediates Small-Molecule-Induced Alleviation of Alzheimer Pathology Via the 5'UTR-dependent ADAM10 Translation Initiation.

Li Song, Qiu-Ling Pan, Gui-Feng Zhou, Sheng-Wei Liu, Bing-Lin Zhu, Pei-Jia Lin, Xiao-Tong Hu, Jing-Si Zha, Yan Long, Biao Luo and 7 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 6 institutions in 1 country.

Li SongDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.ORCID 0009-0009-2148-970X
Qiu-Ling PanDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Gui-Feng ZhouDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Sheng-Wei LiuDepartment of Pharmacy, Yongchuan Hospital of Chongqing Medical University, Chongqing, 402160, China.
Bing-Lin ZhuDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Pei-Jia LinDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiao-Tong HuDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Jing-Si ZhaDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yan LongDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Biao LuoDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Jian ChenDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Ying TangDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Jing TangDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiao-Jiao XiangDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiao-Yong XieDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiao-Juan DengDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Guo-Jun ChenDepartment of Neurology, Chongqing Key Laboratory of Major Neurological and Mental Disorders, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNDaping Hospital · CNChongqing Medical University · CNDalian Medical University · CNSichuan University · CNSouthwest University · CN

Funding

Chongqing Education Commission KJZD-K201900404National Key R&D Program of China 2018YFC1314702NSFC 81971030NSFC 82201578NSFC 82271461Postgraduate Research and Innovation Project of Chongqing CYB19146
6 · The paper itself

Abstract

It is long been suggested that one-carbon metabolism (OCM) is associated with Alzheimer's disease (AD), whereas the potential mechanisms remain poorly understood. Taking advantage of chemical biology, that mitochondrial serine hydroxymethyltransferase (SHMT2) directly regulated the translation of ADAM metallopeptidase domain 10 (ADAM10), a therapeutic target for AD is reported. That the small-molecule kenpaullone (KEN) promoted ADAM10 translation via the 5' untranslated region (5'UTR) and improved cognitive functions in APP/PS1 mice is found. SHMT2, which is identified as a target gene of KEN and the 5'UTR-interacting RNA binding protein (RBP), mediated KEN-induced ADAM10 translation in vitro and in vivo. SHMT2 controls AD signaling pathways through binding to a large number of RNAs and enhances the 5'UTR activity of ADAM10 by direct interaction with GAGGG motif, whereas this motif affected ribosomal scanning of eukaryotic initiation factor 2 (eIF2) in the 5'UTR. Together, KEN exhibits therapeutic potential for AD by linking OCM with RNA processing, in which the metabolic enzyme SHMT2 "moonlighted" as RBP by binding to GAGGG motif and promoting the 5'UTR-dependent ADAM10 translation initiation.

Indexed as

Alzheimer DiseaseGlycine Hydroxymethyltransferase5' Untranslated RegionsADAM10 ProteinAmyloid Precursor Protein SecretasesAnimalsHydroxymethyl and Formyl TransferasesMembrane ProteinsMiceRNA, Messenger5' Untranslated RegionsADAM10 ProteinAdam10 protein, mouseAmyloid Precursor Protein SecretasesGlycine HydroxymethyltransferaseHydroxymethyl and Formyl TransferasesMembrane ProteinsRNA, MessengerShmt2 protein, mouse5′UTRADAM10Alzheimer's diseaseKenpaulloneRNA binding proteinSHMT2translation inhibitory element

Identifiers

PMID38183387
PMCPMC10953581
OpenAlexW4390639700

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.