Evidence map›Paper›PMID 41708645›Full record

ArticleNature communications2026

Molecular insights into fungal inositol phosphorylceramide synthesis and its inhibition by antifungal aureobasidin A.

Jiehui Chen, Yan Ke, Min Zhang, Xinyuan Lin, Zhengkang Hua, Di Zhang, Xinlin Hu, Xuyang Ding, Jiameng Li, Ping Yang and 1 more

Abstract read
In one paragraph

Article in Nature communications, 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

11 authors.

Jiehui Chen *Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Yan Ke *Department of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Min Zhang *Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0002-8844-8402
Xinyuan LinDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Zhengkang HuaDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Di ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Xinlin HuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Xuyang DingDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Jiameng LiDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Ping YangDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China.
Hongjun YuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases and Hubei Key Laboratory of Natural Active Polysaccharides, Huazhong University of Science and Technology, Wuhan, China. hongjun_yu@hust.edu.cn.ORCID http://orcid.org/0000-0002-1483-2962

Funding

National Natural Science Foundation of China (National Science Foundation of China) 92478121
6 · The paper itself

Abstract

Fungal inositol phosphorylceramide (IPC) synthase is an essential enzyme complex that catalyzes a critical step in sphingolipid biosynthesis. It is the molecular target of potent antifungal aureobasidin A (AbA). Despite its therapeutic relevance, the lack of structural and mechanistic insights into IPC synthase function and inhibition has impeded rational antifungal drug development. Here, we present cryo-EM structures of Saccharomyces cerevisiae IPC synthase in two distinct functional states: a ceramide-bound form and an AbA-inhibited complex. Our study reveals a conserved heterodimeric architecture formed by Aur1 and Kei1, stabilized through extensive protein-protein and lipid-mediated interactions. Within catalytic Aur1, we identify a membrane-embedded reaction chamber harboring a conserved H-H-D catalytic triad (H255, H294, and D298) essential for IPC synthesis. Structural comparisons illuminate the mechanism of ceramide recognition and reveal how AbA acts as a competitive inhibitor by occupying the substrate-binding pocket. Further analyses identify key residues involved in AbA binding and explain the molecular basis of drug resistance. Together, these findings advance the mechanistic understanding of fungal IPC biosynthesis and inhibition, and establish a foundation for developing new antifungal drugs targeting IPC synthase.

Indexed as

DepsipeptidesGlycosphingolipidsHexosyltransferasesAntifungal AgentsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsAntifungal Agentsaureobasidin ADepsipeptidesGlycosphingolipidsHexosyltransferasesinositolphosphorylceramidephosphatidylinositol-ceramide phosphoinositol transferaseSaccharomyces cerevisiae Proteins

Identifiers

PMID41708645
PMCPMC13133130

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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.