Evidence map›Paper›PMID 40310720›Full record

ArticleCell reports2025

Activity-dependent degradation of Kv4.2 contributes to synaptic plasticity and behavior in Angelman syndrome model mice.

Jia-Hua Hu, Cole Malloy, Ying Liu, Jung M Park, Ashley Pratt, Meghyn Welch, Jonathan G Murphy, Daniel Abebe, Rose-Marie Karlsson, Heather A Cameron and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
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

11 authors.

Jia-Hua HuMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA. Electronic address: huj8@mail.nih.gov.
Cole MalloyMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Ying LiuMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Jung M ParkMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Ashley PrattMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Meghyn WelchMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Jonathan G MurphyMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Daniel AbebeMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Rose-Marie KarlssonSection on Neuroplasticity, National Institute of Mental Health, Bethesda, MD 20892, USA.
Heather A CameronSection on Neuroplasticity, National Institute of Mental Health, Bethesda, MD 20892, USA.
Dax A HoffmanMolecular Neurophysiology and Biophysics Section, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA. Electronic address: hoffmand@mail.nih.gov.

Funding

Neurogenesis In The Adult BrainZIAMH002784 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI CAMERON, HEATHER A · 2009 to 2025
$29.7M
Potassium Channels and Dendritic Function in Hippocampal Pyramidal NeuronsZ01HD008755 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI HOFFMAN, DAX A · 2003 to 2008
$1.6M
Intramural NIH HHS Z01 HD008755Intramural NIH HHS ZIA MH002784
6 · The paper itself

Abstract

Angelman syndrome (AS) is a severe neurological disorder characterized by intellectual disability, absence of speech, spontaneous seizure, and motor dysfunction. The absence of functional maternally derived UBE3A protein is considered the primary cause of AS, yet the downstream signaling pathways remain elusive. Here, we show the voltage-gated K

Indexed as

Angelman SyndromeBehavior, AnimalNeuronal PlasticityProteolysisShal Potassium ChannelsAnimalsDisease Models, AnimalHumansLong-Term PotentiationMaleMiceMice, Inbred C57BLMice, KnockoutUbiquitin-Protein LigasesShal Potassium ChannelsUbe3a protein, mouseUbiquitin-Protein LigasesAngelman syndromecognitive flexibilityCP: Molecular biologyCP: NeuroscienceDPP6Kv4.2LTPUBE3Aubiquitination

Identifiers

PMID40310720
PMCPMC12232208

What OpenQuestion holds

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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.