Evidence map›Paper›PMID 38890295›Full record

ArticleNature communications2024

Chemogenomics for NR1 nuclear hormone receptors.

Laura Isigkeit, Espen Schallmayer, Romy Busch, Lorene Brunello, Amelie Menge, Lewis Elson, Susanne Müller, Stefan Knapp, Alexandra Stolz, Julian A Marschner and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

11 authors.

Laura Isigkeit *Goethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.ORCID http://orcid.org/0000-0002-0168-1093
Espen Schallmayer *Goethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.
Romy BuschLudwig-Maximilians-Universität (LMU) München, Department of Pharmacy, Munich, Germany.
Lorene BrunelloGoethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.ORCID http://orcid.org/0000-0001-7222-3033
Amelie MengeGoethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.ORCID http://orcid.org/0000-0002-0423-6593
Lewis ElsonGoethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.
Susanne MüllerGoethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.ORCID http://orcid.org/0000-0003-2402-4157
Stefan KnappGoethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany.ORCID http://orcid.org/0000-0001-5995-6494
Alexandra StolzBuchmann Institute for Molecular Life Sciences and Institute of Biochemistry 2, Goethe University Frankfurt, Frankfurt, Germany.ORCID http://orcid.org/0000-0002-3340-439X
Julian A MarschnerLudwig-Maximilians-Universität (LMU) München, Department of Pharmacy, Munich, Germany.
Daniel MerkGoethe University Frankfurt, Institute of Pharmaceutical Chemistry, Frankfurt, Germany. daniel.merk@cup.lmu.de.ORCID http://orcid.org/0000-0002-5359-8128

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 512574446Deutsche Forschungsgemeinschaft (German Research Foundation) 515275293EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 101040355Innovative Medicines Initiative (IMI) 875510
6 · The paper itself

Abstract

Nuclear receptors (NRs) regulate transcription in response to ligand binding and NR modulation allows pharmacological control of gene expression. Although some NRs are relevant as drug targets, the NR1 family, which comprises 19 NRs binding to hormones, vitamins, and lipid metabolites, has only been partially explored from a translational perspective. To enable systematic target identification and validation for this protein family in phenotypic settings, we present an NR1 chemogenomic (CG) compound set optimized for complementary activity/selectivity profiles and chemical diversity. Based on broad profiling of candidates for specificity, toxicity, and off-target liabilities, sixty-nine comprehensively annotated NR1 agonists, antagonists and inverse agonists covering all members of the NR1 family and meeting potency and selectivity standards are included in the final NR1 CG set. Proof-of-concept application of this set reveals effects of NR1 members in autophagy, neuroinflammation and cancer cell death, and confirms the suitability of the set for target identification and validation.

Indexed as

AutophagyAnimalsCell Line, TumorGenomicsHEK293 CellsHumansLigandsMiceReceptors, Cytoplasmic and NuclearLigandsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID38890295
PMCPMC11189487

What OpenQuestion holds

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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 OpenQuestion graph.