Evidence map›Paper›PMID 42004027›Full record

ArticleiScience2026

NSF is required for diverse endocytic modes by promoting fusion and fission pore closure in secretory cells.

Xin-Sheng Wu, Tao Sun, Bo Shi, Sunghoon Lee, Zheng Zhang, Lisi Wei, Xin Wang, Maryam Molakarimi, Sue Han, Aaron Uy and 2 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

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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

5 · Who and what money

Authors and funding

12 authors.

Xin-Sheng WuNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Tao SunNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Bo ShiNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Sunghoon LeeNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Zheng ZhangNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Lisi WeiNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Xin WangNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Maryam MolakarimiNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Sue HanNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Aaron UyNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.
Lin GanFlaum Eye Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York, NY 14642, USA.
Ling-Gang WuNational Institute of Neurological Disorders and Stroke, 35 Convent Dr, Bldg. 35, Rm. 2B-1012, Bethesda, MD 20892, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ATPase N-ethylmaleimide-sensitive factor (NSF), known for disassembling SNARE complexes, plays key roles in neurotransmitter release, neurotransmitter (AMPA, GABA, and dopamine) receptor trafficking, and synaptic plasticity, and its dysfunction or mutation is linked to neurological disorders. These roles are largely attributed to SNARE-mediated exocytosis. Here, we reveal an unexpected role for NSF: mediating diverse modes of endocytosis-including slow, fast, ultrafast, overshoot, and bulk-by driving closure of both fusion and fission pores. This function was consistently observed across large calyx nerve terminals, small hippocampal boutons, and chromaffin cells using capacitance recordings, synapto-pHluorin imaging, electron microscopy, and multi-color pore-closure imaging. Results were robust across four NSF inhibitors, gene knockout, knockdown, and mutations. Furthermore, NSF facilitates content release. These findings establish NSF as a central regulator of membrane fission, kiss-and-run fusion, endocytosis, and exo-endocytosis coupling, providing a mechanistic basis for its diverse roles in synaptic transmission, receptor trafficking, and disease.

Indexed as

Cellular neuroscienceNeuroscience

Identifiers

PMID42004027
PMCPMC13091539

What Socratic holds

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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 Socratic graph.