Evidence map›Paper›PMID 40208944›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

Neddylation modification stabilizes LC3B by antagonizing its ubiquitin-mediated degradation and promoting autophagy in skin.

Linlin Xu, Xinxing Lyu, Yibo Wang, Li Ni, Pin Li, Piao Zeng, Qixia Wang, Yunhao Chang, Chenglong Pan, Qingxia Hu and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Review
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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

12 authors.

Linlin XuDepartment of Dermatology, Shandong Provincial Hospital, Shandong University, Jinan 250021, Shandong, China.ORCID 0000-0002-5656-0248
Xinxing LyuHospital for Skin Diseases, Shandong First Medical University, Jinan 250022, Shandong, China.ORCID 0000-0002-6310-6772
Yibo WangDepartment of Dermatology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, Shandong, China.ORCID 0000-0003-3633-8276
Li NiDepartment of Dermatology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, Shandong, China.ORCID 0009-0009-0268-1640
Pin LiDepartment of Dermatology, Shandong Provincial Hospital, Shandong University, Jinan 250021, Shandong, China.ORCID 0009-0006-8828-6753
Piao ZengSchool of Clinical and Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, Shandong, China.ORCID 0009-0004-7258-4700
Qixia WangSchool of Clinical and Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, Shandong, China.ORCID 0009-0008-3913-2189
Yunhao ChangSchool of Clinical and Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, Shandong, China.
Chenglong PanSchool of Clinical and Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, Shandong, China.ORCID 0009-0008-0087-2980
Qingxia HuSchool of Clinical and Basic Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan 250117, Shandong, China.ORCID 0000-0002-2508-5552
Shuhong HuangDepartment of Dermatology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, Shandong, China.ORCID 0000-0001-6298-6192
Ningning DangDepartment of Dermatology, Shandong Provincial Hospital, Shandong University, Jinan 250021, Shandong, China.ORCID 0000-0002-2764-4995

Funding

MOST | National Natural Science Foundation of China (NSFC) 82273527Natural Science Foundation of Shandong Province ZR2022MH242Natural Science Foundation of Shandong Province ZR2024MH138
6 · The paper itself

Abstract

The Atg8-family proteins, including LC3B (microtubule-associated protein 1 light chain 3 beta), are pivotal for key steps in the autophagy process. Proper regulation of LC3B homeostasis is essential for its function. Although LC3B is modulated by various posttranslational modifications (PTMs), the impact of these modifications on LC3B protein homeostasis remains unclear. Neddylation, a recently identified ubiquitin-like modification, plays diverse biological roles. Here, we identify LC3B as a specific target for neddylation. This modification weakens LC3B's interaction with the ubiquitin E3 ligases VHL and BIRC6, thereby reducing LC3B ubiquitination. Depletion of ubiquitin-conjugating enzyme E2M (UBE2M), the primary E2 enzyme in the neddylation pathway, destabilizes LC3B and suppresses autophagy activity. Heterozygous

Indexed as

AgingAutophagyAutophagy-Related ProteinsMicrotubule-Associated ProteinsNEDD8 ProteinProtein Processing, Post-TranslationalProteolysisSkinUbiquitinUbiquitin-Conjugating EnzymesAnimalsCarrier ProteinsCullin ProteinsFemaleMaleMiceAutophagy-Related ProteinsCarrier ProteinsCul2 protein, mouseCullin ProteinsMap1lc3b protein, mouseMicrotubule-Associated ProteinsNEDD8 ProteinNedd8 protein, mouseRBX1 protein, mouseUbe2m protein, mouseUbiquitinUbiquitin-Conjugating EnzymesautophagyLC3Bneddylationskin agingUBE2M

Identifiers

PMID40208944
PMCPMC12012473

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.