Evidence map›Paper›PMID 40918324›Full record

ArticleACS omega2025

Identification and Validation of Inverse Agonists for Nuclear Receptor Subfamily 4 Group A Member 2.

Lulu Tian, Yushan Lin, Cheng Cheng, Huijia Yang, Xinhui Qiu, Song Li, Congcong Jia, Weidong Le

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Lulu TianKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Yushan LinKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Cheng ChengKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Huijia YangKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Xinhui QiuKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Song LiKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Congcong JiaKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.
Weidong LeKey Laboratory of Liaoning Province for Research on the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, 116021 Dalian, China.ORCID https://orcid.org/0000-0001-7459-2705

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Former studies indicate that nuclear receptor subfamily 4 group A member 2 (Nurr1, NR4A2), a transcription factor, is regarded as a potential therapeutic target for central nervous system diseases, and many studies have focused on the development and optimization of agonists of Nurr1. Recent studies have shown that Nurr1 is upregulated in many other diseases. However, there is still a lack of effective inverse Nurr1 agonists as a therapeutic strategy or as pharmacological tools to counteract the receptor's inherent activity. In this study, we screened Nurr1 ligands through a high-throughput screening system and identified a novel Nurr1 inverse agonist (K-strophanthoside). We further validated the binding site of K-strophanthoside on Nurr1 and investigated its effect on regulating Nurr1 function. K-strophanthoside directly binds to the ligand-binding domain of Nurr1 (Glu445, Glu514, Arg515, and His516) and mimics the function of Nurr1 knockdown by suppressing the intrinsic Nurr1 transcriptional activity. Our study contributes a valuable chemical tool for Nurr1 modulators and provides a potential treatment target for Nurr1-related disorders.

Identifiers

PMID40918324
PMCPMC12409540

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.