Evidence map›Paper›PMID 40593796›Full record

ArticleNature communications2025

Molecular architecture and catalytic mechanism of human glycogen debranching enzyme.

Huiyi Guan, Huan Chen, He Geng, Ruifang Ma, Zhongmin Liu, Yong Wang, Yifang Chen, Kaige Yan

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Off-Target Binding of Miglustat to Glycogen Debranching Enzyme.International journal of molecular sciences · 2026
    Article
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

8 authors.

Huiyi Guan *Shenzhen Key Laboratory of Biomolecular Assembling and Regulation, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Huan Chen *Shenzhen Key Laboratory of Biomolecular Assembling and Regulation, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
He Geng *Shenzhen Key Laboratory of Biomolecular Assembling and Regulation, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.ORCID http://orcid.org/0009-0000-6465-6269
Ruifang MaShenzhen Key Laboratory of Biomolecular Assembling and Regulation, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.ORCID http://orcid.org/0000-0002-3663-2240
Zhongmin LiuSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.ORCID http://orcid.org/0000-0002-3280-3890
Yong WangCollege of Life Sciences, Zhejiang University, Hangzhou, 310058, China.ORCID http://orcid.org/0000-0001-9156-0377
Yifang ChenCollege of Life Sciences, Zhejiang University, Hangzhou, 310058, China. yifang_chen7@outlook.com.ORCID http://orcid.org/0009-0009-6922-5332
Kaige YanShenzhen Key Laboratory of Biomolecular Assembling and Regulation, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China. yankg@sustech.edu.cn.ORCID http://orcid.org/0000-0003-4176-5109

Funding

Guangdong Innovative and Entrepreneurial Research Team Program 2021QN02Y429National Natural Science Foundation of China (National Science Foundation of China) 32271251Shenzhen Science and Technology Innovation Commission 20231120160100001Shenzhen Science and Technology Innovation Commission JCYJ20220530115214033Shenzhen Science and Technology Innovation Commission KQTD20210811090115021
6 · The paper itself

Abstract

Glycogen, a key branched glucose polymer, acts as a vital energy reservoir in mammalian cells, particularly during intense activity or fasting. The glycogen debranching enzyme (GDE) plays a key role in glycogen degradation by removing branches, ensuring efficient glucose release. Dysfunction of GDE leads to the accumulation of limit dextrin and is implicated in the pathogenesis of Glycogen Storage Disease Type III (GSD III). We present the cryo-EM structure of human GDE (hsGDE) at 3.23 Å resolution, providing molecular insights into its substrate selectivity and catalytic mechanism. Our study further investigates the molecular consequences of disease-associated mutations by correlating structural data with enzymatic activities of representative GSD III-causing variants. We discover that these mutations induce GSD III through diverse mechanisms, including significant reductions in enzymatic activity, and disruptions to the glycogen-bound region and overall structural integrity. The elucidation of these pathways not only advances our understanding of hsGDE's role in substrate recognition and catalysis but also illuminates the molecular pathology of GSD III. Our findings pave the way for the development of targeted therapeutic strategies for this disease.

Indexed as

Glycogen Debranching Enzyme SystemGlycogen Storage Disease Type IIICatalysisCryoelectron MicroscopyGlycogenHumansModels, MolecularMutationProtein ConformationSubstrate SpecificityGlycogenGlycogen Debranching Enzyme System

Identifiers

PMID40593796
PMCPMC12219210

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.