Evidence map›Paper›PMID 40977735›Full record

ArticleFrontiers in immunology2025

Impact of ERAP1 downregulation on the pathogenesis of DSS-induced colitis and therapeutic response to sulfasalazine.

Bushra Riaz, Hye-Myung Ryu, S M Shamsul Islam, Rahar Babita, Je Kyung Seong, Ho Lee, Eunjoo H Lee, Seonghyang Sohn

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. 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
–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

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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

8 authors.

Bushra Riaz *Department of Biomedical Sciences, Graduate School of Ajou University, Suwon, Republic of Korea.
Hye-Myung Ryu *Department of Microbiology, Ajou University School of Medicine, Suwon, Republic of Korea.
S M Shamsul Islam *Department of Biomedical Sciences, Graduate School of Ajou University, Suwon, Republic of Korea.
Rahar BabitaDepartment of Microbiology, Ajou University School of Medicine, Suwon, Republic of Korea.
Je Kyung SeongLaboratory of Developmental Biology and Genomics, Research Institute for Veterinary Science, Seoul National University, Seoul, Republic of Korea.
Ho LeeGraduate School of Cancer Science and Policy, National Cancer Center, Goyang, Republic of Korea.
Eunjoo H LeeDepartment of East-West Medical Science, Kyung Hee University, Yongin, Republic of Korea.
Seonghyang SohnDepartment of Biomedical Sciences, Graduate School of Ajou University, Suwon, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Ulcerative colitis (UC) is a life-threatening heterogeneous condition characterized by inflammation of the colon. Endoplasmic reticulum aminopeptidase 1 (ERAP1) is essential for antigen processing and immune regulation, however, its specific role in UC pathogenesis and therapeutic response remains unclear. This study aimed to investigate the role of ERAP1 in the response to sulfasalazine, a standard treatment for UC, using an ERAP1-heterozygous (ERAP1 Methods: Wild-type (WT) and ERAP1 Results: ERAP1 Conclusion: Collectively, our findings show that partial ERAP1 deficiency promotes immune dysregulation, alters the expression of inflammation-associated genes, and impairs sulfasalazine efficacy. Therefore, ERAP1 may serve as a key regulator in the pathogenesis of UC and a potential target for therapy.

Indexed as

AminopeptidasesColitisColitis, UlcerativeMinor Histocompatibility AntigensSulfasalazineAnimalsColonDextran SulfateDisease Models, AnimalDown-RegulationMiceMice, Inbred C57BLMice, KnockoutAminopeptidasesDextran SulfateERAP1 protein, mouseMinor Histocompatibility AntigensSulfasalazineDSS-induced colitisendoplasmic reticulum aminopeptidase-1immune responsemouse modelsulfasalazine

Identifiers

PMID40977735
PMCPMC12446291

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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.