Evidence map›Paper›PMID 32493979›Full record

ArticleNature communications2020

Polyamine regulation of ion channel assembly and implications for nicotinic acetylcholine receptor pharmacology.

Madhurima Dhara, Jose A Matta, Min Lei, Daniel Knowland, Hong Yu, Shenyan Gu, David S Bredt

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  11. The telencephalon is a neuronal substrate for systemic inflammatory responses in teleosts via polyamine metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

7 authors at 1 institution in 1 country.

Madhurima DharaNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA.
Jose A MattaNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA.
Min LeiNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA.
Daniel KnowlandNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA.
Hong YuNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA.
Shenyan GuNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA.
David S BredtNeuroscience Discovery, Janssen Pharmaceutical Companies of Johnson and Johnson, 3210 Merryfield Row, San Diego, CA, 92121, USA. dbredt@its.jnj.com.ORCID http://orcid.org/0000-0003-4985-0164
Johnson & Johnson (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small molecule polyamines are abundant in all life forms and participate in diverse aspects of cell growth and differentiation. Spermidine/spermine acetyltransferase (SAT1) is the rate-limiting enzyme in polyamine catabolism and a primary genetic risk factor for suicidality. Here, using genome-wide screening, we find that SAT1 selectively controls nicotinic acetylcholine receptor (nAChR) biogenesis. SAT1 specifically augments assembly of nAChRs containing α7 or α4β2, but not α6 subunits. Polyamines are classically studied as regulators of ion channel gating that engage the nAChR channel pore. In contrast, we find polyamine effects on assembly involve the nAChR cytosolic loop. Neurological studies link brain polyamines with neurodegenerative conditions. Our pharmacological and transgenic animal studies find that reducing polyamines enhances cortical neuron nAChR expression and augments nicotine-mediated neuroprotection. Taken together, we describe a most unexpected role for polyamines in regulating ion channel assembly, which provides a new avenue for nAChR neuropharmacology.

Indexed as

AcetyltransferasesAnimalsBiocatalysisDiamine N-AcetyltransferaseDNA, ComplementaryEnhancer Elements, GeneticFluorescenceGenome, HumanHEK293 CellsHumansIon Channel GatingIon ChannelsMiceNeuronsNeuroprotectionPolyaminesAcetyltransferasesDiamine N-AcetyltransferaseDNA, ComplementaryIon ChannelsPolyaminesProtein SubunitsReceptors, Nicotinic

Identifiers

PMID32493979
PMCPMC7271128
OpenAlexW3030096839

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.