Evidence map›Paper›PMID 42491662›Full record

ArticleiScience2026

Phospholipid flippases ATP8A1 and ATP8A2 regulate GABA

Muneyuki Kawase, Shu Tokunaga, Yuta Umemura, Hossam H Shawki, Jumpei Omi, Ayana Hoshiai, Tomoha Ohshima, Tsuzumi Nakajima, Takao Kohno, Takashi Sakurai and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 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
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Muneyuki KawaseDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Shu TokunagaDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Yuta UmemuraDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Hossam H ShawkiDepartment of Comparative and Experimental Medicine, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-0002, Japan.
Jumpei OmiDepartment of Health Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Ayana HoshiaiDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Tomoha OhshimaDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Tsuzumi NakajimaDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Takao KohnoDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
Takashi SakuraiDepartment of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Junken AokiDepartment of Health Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan.
Hisashi OishiDepartment of Comparative and Experimental Medicine, Graduate School of Medical Sciences, Nagoya City University, 1 Kawasumi Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-0002, Japan.
Mitsuharu HattoriDepartment of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phospholipid asymmetry in cellular membranes is maintained by flippases. ATP8A1 and ATP8A2 are the principal flippases of phosphatidylserine (PS) in the mammalian nervous system; however, their specific physiological roles and potential functional redundancy remain incompletely characterized. Here, we show that ATP8A1/ATP8A2 double-knockout mice displayed more severe growth retardation than ATP8A2 knockout mice, indicating that ATP8A1 and ATP8A2 play redundant roles. In hippocampal neurons, ATP8A2 was highly enriched at inhibitory post-synapses. Surface biotinylation assays revealed increased surface GABA

Indexed as

dynaminGABAA receptorinhibitory synapsephosphatidylserinePhospholipid flippase

Identifiers

PMID42491662
PMCPMC13378359

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.