Evidence map›Paper›PMID 42595111›Full record

ArticleThe Journal of biological chemistry2026

OTUD5 maintains STAT1/2 stability and promotes IFNγ-driven intestinal inflammation.

Huiyuan Guan, Changzhou Cai, Jiewei Wang, Zhaoxue Liu, Jin Peng, Xupeng Bai, Lingzhi Wu, Kun Jiang, Xinghua Zhen, Chaohui Yu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 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
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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

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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

12 authors.

Huiyuan GuanZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Institute of Translational Medicine, Zhejiang University Medical School, Hangzhou, Zhejiang, China.
Changzhou CaiDepartment of Gastroenterology, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jiewei WangDepartment of Gastroenterology, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Zhaoxue LiuDepartment of Gastroenterology, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Jin PengZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xupeng BaiZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Lingzhi WuZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Kun JiangChaser Therapeutics Inc., Hangzhou, Zhejiang, China.
Xinghua ZhenZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Chaohui YuDepartment of Gastroenterology, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Pumin ZhangZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Institute of Translational Medicine, Zhejiang University Medical School, Hangzhou, Zhejiang, China; Cancer Center, Zhejiang University, Hangzhou, Zhejiang, China. Electronic address: pzhangbcm@zju.edu.cn.
Zhe ShenDepartment of Gastroenterology, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. Electronic address: shenzdr@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease is characterized by unresolved mucosal inflammation driven mainly by TNFα and/or interferon gamma (IFNγ). While anti-TNFα biologics are a clinical mainstay, therapeutic resistance remains a significant hurdle. The molecular mechanisms that sustain inflammation in anti-TNFα nonresponders are not fully understood. In human colon biopsies, we identified significant upregulation of the deubiquitinase OTUD5 in nonresponders compared to responders, suggesting its involvement in therapy resistance. Using an intestinal epithelial cell -specific Otud5 KO mouse model, we show that Otud5 deficiency significantly alleviated the IFNγ-dependent colitis induced by dextran sulfate sodium, as evidenced by reduced weight loss and diminished infiltration of Ly6C

Indexed as

anti-TNFα resistanceIBDIFNγ-ISGF3 signalingOTUD5STAT1/2

Identifiers

PMID42595111
PMCPMC13559827

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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.