Evidence map›Paper›PMID 33571596›Full record

ArticleNeuroscience2021

HCN Channel Phosphorylation Sites Mapped by Mass Spectrometry in Human Epilepsy Patients and in an Animal Model of Temporal Lobe Epilepsy.

F A Concepcion, M N Khan, J-D Ju Wang, A D Wei, J G Ojemann, A L Ko, Y Shi, J K Eng, J-M Ramirez, N P Poolos

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 25% 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, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Inspiratory rhythm generation is stabilized byJournal of neurophysiology · 2022
    Article
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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

10 authors at 2 institutions in 1 country.

F A ConcepcionDepartment of Neurology and Regional Epilepsy Center, University of Washington, Seattle, WA, United States.
M N KhanDepartment of Neurology and Regional Epilepsy Center, University of Washington, Seattle, WA, United States.
J-D Ju WangSeattle Children's Research Institute, Center for Integrative Brain Research, Seattle, WA, United States.
A D WeiSeattle Children's Research Institute, Center for Integrative Brain Research, Seattle, WA, United States.
J G OjemannSeattle Children's Research Institute, Center for Integrative Brain Research, Seattle, WA, United States; Department of Neurological Surgery, University of Washington, Seattle, WA, United States.
A L KoDepartment of Neurological Surgery, University of Washington, Seattle, WA, United States.
Y ShiDepartment of Electrical and Computer Engineering, University of Washington, Seattle, WA, United States.
J K EngProteomics Resource, University of Washington, Seattle, WA, United States.
J-M RamirezSeattle Children's Research Institute, Center for Integrative Brain Research, Seattle, WA, United States; Department of Neurological Surgery, University of Washington, Seattle, WA, United States.
N P PoolosDepartment of Neurology and Regional Epilepsy Center, University of Washington, Seattle, WA, United States. Electronic address: npoolos@uw.edu.
University of Washington · USNeurological Surgery · US

Funding

Epilepsy and dendritic excitabilityR01NS050229 · NINDS · UNIVERSITY OF WASHINGTON · PI POOLOS, NICHOLAS P · 2005 to 2020
$4.1M
NINDS NIH HHS R01 NS050229
6 · The paper itself

Abstract

Because hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channels modulate the excitability of cortical and hippocampal principal neurons, these channels play a key role in the hyperexcitability that occurs during the development of epilepsy after a brain insult, or epileptogenesis. In epileptic rats generated by pilocarpine-induced status epilepticus, HCN channel activity is downregulated by two main mechanisms: a hyperpolarizing shift in gating and a decrease in amplitude of the current mediated by HCN channels, I

Indexed as

EpilepsyEpilepsy, Temporal LobeAnimalsCyclic Nucleotide-Gated Cation ChannelsHumansHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMaleMass SpectrometryPhosphorylationPotassium ChannelsRatsRats, Sprague-DawleyCyclic Nucleotide-Gated Cation ChannelsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsPotassium Channelsepilepsyepileptogenesishyperpolarization-activated cyclic nucleotide-gated ion channels (HCN channels)phosphorylationphosphositestatus epilepticus

Identifiers

PMID33571596
PMCPMC8009864
OpenAlexW3126674487

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.