Evidence map›Paper›PMID 41507360›Full record

ArticleCell death and differentiation2026

GPS2 regulates embryonic angiogenesis by enhancing endothelial cell survival through stabilizing HOIP.

Ying Lu, Huan-Huan Tian, Wen-Bing Ma, Jin-Jin Lu, Jun Wang, Jun-Jie Bi, Guang-Ming Ren, Xian Liu, Ya-Ting Li, Ting Wang and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2026. 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. 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

20 authors.

Ying LuFaculty of Chemistry and Life Sciences, Beijing University of Technology, Beijing, China.
Huan-Huan TianState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Wen-Bing MaInstitute of Health Service and Transfusion Medicine, Beijing, China.
Jin-Jin LuBeijing Institute of Lifeomics, Beijing, China.
Jun WangBeijing Institute of Lifeomics, Beijing, China.
Jun-Jie BiState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Guang-Ming RenState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Xian LiuInstitute of Health Service and Transfusion Medicine, Beijing, China.ORCID http://orcid.org/0000-0002-4448-1841
Ya-Ting LiFaculty of Chemistry and Life Sciences, Beijing University of Technology, Beijing, China.
Ting WangFaculty of Chemistry and Life Sciences, Beijing University of Technology, Beijing, China.
Shen-Si XiangState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Chang-Yan LiState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Miao YuState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Ke ZhaoState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Jing-Jing LiState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Hui-Ying GaoState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Hui ChenState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Yi-Qun ZhanState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China.
Rong-Hua YinState Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, China. yrh1980110@126.com.ORCID http://orcid.org/0000-0001-8119-3657
Xiao-Ming YangFaculty of Chemistry and Life Sciences, Beijing University of Technology, Beijing, China. xiaomingyang@sina.com.ORCID http://orcid.org/0000-0003-3629-0946

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of endothelial cell (EC) death is essential for normal angiogenesis. The E3 ubiquitin ligase HOIP, the catalytic subunit of the linear ubiquitin chain assembly complex (LUBAC), is particularly important for EC survival during embryogenesis. The stability of HOIP is critical for LUBAC function. However, the mechanisms underlying the regulation of HOIP stability are largely unknown. Here, we uncovered a novel role of G protein pathway suppressor 2 (GPS2) in regulating EC survival and embryonic vascularization via control of HOIP stability. EC-specific GPS2 deletion mice (Gps2

Indexed as

AngiogenesisEndothelial CellsIntracellular Signaling Peptides and ProteinsNeovascularization, PhysiologicUbiquitin-Protein LigasesAnimalsCell SurvivalDeubiquitinating EnzymesEmbryo, MammalianHumansMiceMice, KnockoutProtein StabilityReceptors, Tumor Necrosis Factor, Type IUbiquitinationDeubiquitinating EnzymesIntracellular Signaling Peptides and ProteinsOtulin protein MouseReceptors, Tumor Necrosis Factor, Type IRnf31 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID41507360
PMCPMC13342588

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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.