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 6 papers.
0numbers the graph read from it
0cells of the map it votes in
6citing 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.
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
18 authors.
Yongkang Zou *Institute of Cancer Research, Shenzhen Bay Laboratory, Shenzhen, 518132, China.ORCID 0000-0002-0707-7380
Zhaoxiang Wang *Department of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0009-0009-3741-768X
Qiang Jiang *Department of Animal Genetics, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.ORCID 0000-0002-9880-9435
Xia KongDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0009-0007-5555-2557
Xiaohe MaDepartment of Cell Biology, School of Basic Medicine, Hangzhou Normal University, Hangzhou 311121, China.ORCID 0009-0002-4821-414X
Zhengyan LiangDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0000-0001-7465-0119
Zhiguo WangDepartment of Cell Biology, School of Basic Medicine, Hangzhou Normal University, Hangzhou 311121, China.ORCID 0000-0001-8732-4451
Beiying ChenDepartment of Cell Biology, School of Basic Medicine, Hangzhou Normal University, Hangzhou 311121, China.ORCID 0009-0002-7233-2760
Jiao YuanGuangzhou Medical University-Guangzhou Institutes of Biomedicine and Health Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Laboratory, Guangzhou Medical University, Guangzhou 510005, China.
Jiayue WenGuangzhou Medical University-Guangzhou Institutes of Biomedicine and Health Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Laboratory, Guangzhou Medical University, Guangzhou 510005, China.ORCID 0009-0000-6602-0766
Sheng YeInstitute of Cancer Research, Shenzhen Bay Laboratory, Shenzhen, 518132, China.ORCID 0009-0004-2780-4049
Yubin YanDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0009-0002-4162-949X
Binbin LiDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0000-0003-4185-4208
Xing-Dong XiongDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0000-0003-4956-0917
Xin-Guang LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.
Zhiwei HeDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.
Yafei CaiDepartment of Animal Genetics, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.ORCID 0000-0002-4123-0836
Junzhi ZhouDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory for Epigenetics of Dongguan City, Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Guangdong Medical University, Dongguan 523808, China.ORCID 0000-0002-0579-0916
Funding
MOST | National Natural Science Foundation of China (NSFC) 32270516MOST | National Natural Science Foundation of China (NSFC) 32400547MOST | National Natural Science Foundation of China (NSFC) 82372916
6 · The paper itself
Abstract
Activation of hypoxia signaling has been identified as an innate resistance signature against anti-PD-1 therapy, suggesting its potential as a target for combination treatments. Here, we demonstrate that UFMylation modification of HIF1α stabilizes the protein by antagonizing its ubiquitination and proteasomal degradation under hypoxic conditions. Mechanistically, depletion of
Indexed as
Breast NeoplasmsHypoxia-Inducible Factor 1, alpha SubunitProgrammed Cell Death 1 ReceptorAnimalsCell Line, TumorFemaleHumansMiceProteinsSignal TransductionTumor Suppressor Protein p53Ubiquitin-Activating EnzymesUbiquitinationXenograft Model Antitumor AssaysHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitProgrammed Cell Death 1 ReceptorProteinsTumor Suppressor Protein p53Ubiquitin-Activating EnzymesUFM1 protein, humanhypoxiaposttranslational modificationtumor microenvironmentUFMylation
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.
UFMylation: A supervisor of the HIF1α pathway and a potential therapeutic target for anti-PD-1 combination therapy in hypoxic tumors. · full record | OpenQuestion