Evidence map›Paper›PMID 42392996›Full record

ArticleZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences2026

[DOT1L controls neuronal amyloid precursor protein expres-sion via the p38 MAPK-mediated mitochondrial dynamics homeostasis axis].

Yumin Zhang, Feiyu Zhu, Xiaotian Wu, Zhansong Li, Peng Huang, Yanpan Gao, Linghui Zeng

Abstract readEnglish Abstract
PubMed Full text at PMC Publisher
In one paragraph

Article in Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

7 authors.

Yumin ZhangSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China. 18363918879@163.com.
Feiyu ZhuSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China. zfy1391481156@163.com.
Xiaotian WuSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China.
Zhansong LiSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China.
Peng HuangSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China.
Yanpan GaoSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China. gaoyp@hzcu.edu.cn.
Linghui ZengSchool of Medicine, Hangzhou City University, Zhejiang Province Key Laboratory of Novel Target and Drug Study for Neural Repair, Hangzhou 310015, China. zenglh@hzcu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the regulatory role of epigenetic regulator disruptor of telomeric silencing 1-like (DOT1L) and its mediated histone H3 lysine 79 (H3K79) methylation in modulating neuronal amyloid precursor protein (APP) expression, and to elucidate the underlying mechanisms involving mitochondrial dynamics homeo-stasis and the upstream p38 mitogen-activated protein kinase (p38 MAPK).

methodsAlzheimer's disease (AD) models were established using APP/presenilin-1 (APP/PS1) double-transgenic mice and N2a cells overexpressing the human Swedish mutant APP (N2a-APPswe). Immunofluorescence staining was employed to assess DOT1L expression and localization in mouse brain tissues. N2a-APPswe cells were treated with the DOT1L-specific inhibitor EPZ5676 and divided into four groups: blank control, solvent control, DOT1L inhibitor, and DOT1L inhibitor plus p38 agonist (

resultsDOT1L expression was significantly reduced in neurons of APP/PS1 mice compared to wild-type controls. DOT1L inhibition led to decreased H3K79 dimethylation levels (

conclusionsDOT1L maintains normal mitochondrial fission and functional homeostasis through regulation of the p38 MAPK mediated signaling pathway, thereby modulating APP expression.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorHistone-Lysine N-MethyltransferaseMitochondrial Dynamicsp38 Mitogen-Activated Protein KinasesAnimalsDynaminsHomeostasisHumansMiceMice, TransgenicMitochondriaNeuronsAmyloid beta-Protein PrecursorDynaminsHistone-Lysine N-Methyltransferasep38 Mitogen-Activated Protein KinasesAlzheimer’s diseaseAmyloid precursor proteinAmyloid β-proteinDisruptor of telomeric silencing 1-likeEpigenetic regulationMitochondrial fissionMitochondrial fusionp38 mitogen-activated protein kinase

Identifiers

PMID42392996
PMCPMC13439450

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.