Evidence map›Paper›PMID 24857657›Full record

ArticleCell reports2014

HuD regulates coding and noncoding RNA to induce APP→Aβ processing.

Min-Ju Kang, Kotb Abdelmohsen, Emmette R Hutchison, Sarah J Mitchell, Ioannis Grammatikakis, Rong Guo, Ji Heon Noh, Jennifer L Martindale, Xiaoling Yang, Eun Kyung Lee and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 6% 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

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.

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  16. Roles of lncRNAs in brain development and pathogenesis: Emerging therapeutic opportunities.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 1 country.

Min-Ju KangLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Kotb AbdelmohsenLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Emmette R HutchisonLaboratory of Neurosciences, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Sarah J MitchellTranslational Gerontology Branch, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Ioannis GrammatikakisLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Rong GuoLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Ji Heon NohLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Jennifer L MartindaleLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Xiaoling YangLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Eun Kyung LeeLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Mohammad A FaghihiCenter for Therapeutic Innovation, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
Claes WahlestedtCenter for Therapeutic Innovation, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
Juan C TroncosoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Olga PletnikovaDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Nora Perrone-BizzozeroDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
Susan M ResnickLaboratory of Behavioral Neuroscience, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Rafael de CaboTranslational Gerontology Branch, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Mark P MattsonLaboratory of Neurosciences, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
Myriam GorospeLaboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA. Electronic address: myriam-gorospe@nih.gov.
National Institute on Aging · USUniversity of Miami · USJohns Hopkins Medicine · USJohns Hopkins University · USNational Institutes of Health · USUniversity of New Mexico · US

Funding

'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1985 to 2019
$37.6M
Early Markers of Alzheimer DiseaseZIAAG000185 · NIA · NATIONAL INSTITUTE ON AGING · PI WALKER, KEENAN · 2009 to 2025
$20.4M
RNA-binding Factors Implicated in Neurogenesis, Alzheimer's Disease, and other Neurodegenerative PathologiesZIAAG000518 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$11.6M
Competing roles of microRNAs and RNA-binding proteins in drug addictionR01DA034097 · NIDA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI NEISEWANDER, JANET L, PERRONE-BIZZOZERO, NORA IRMA · 2012 to 2016
$2.2M
Intramural NIH HHS ZIA AG000518NIA NIH HHS P50 AG005146NIA NIH HHS P50AG05146NIDA NIH HHS R01 DA034097NIDA NIH HHS R01DA034097
6 · The paper itself

Abstract

The primarily neuronal RNA-binding protein HuD is implicated in learning and memory. Here, we report the identification of several HuD target transcripts linked to Alzheimer's disease (AD) pathogenesis. HuD interacted with the 3' UTRs of APP mRNA (encoding amyloid precursor protein) and BACE1 mRNA (encoding β-site APP-cleaving enzyme 1) and increased the half-lives of these mRNAs. HuD also associated with and stabilized the long noncoding (lnc)RNA BACE1AS, which partly complements BACE1 mRNA and enhances BACE1 expression. Consistent with HuD promoting production of APP and APP-cleaving enzyme, the levels of APP, BACE1, BACE1AS, and Aβ were higher in the brain of HuD-overexpressing mice. Importantly, cortex (superior temporal gyrus) from patients with AD displayed significantly higher levels of HuD and, accordingly, elevated APP, BACE1, BACE1AS, and Aβ than did cortical tissue from healthy age-matched individuals. We propose that HuD jointly promotes the production of APP and the cleavage of its amyloidogenic fragment, Aβ.

Indexed as

3' Untranslated RegionsAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesCase-Control StudiesCell Line, TumorCerebral CortexELAV ProteinsFemaleHumansMaleMice3' Untranslated RegionsAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanBace1 protein, mouseELAV ProteinsRNA, Long Noncoding

Identifiers

PMID24857657
PMCPMC4074355
OpenAlexW2094430125

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.