Evidence map›Paper›PMID 38830107›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Asymmetric allostery in estrogen receptor-α homodimers drives responses to the ensemble of estrogens in the hormonal milieu.

Charles K Min, Jerome C Nwachukwu, Yingwei Hou, Robin J Russo, Alexandra Papa, Jian Min, Rouming Peng, Sung Hoon Kim, Yvonne Ziegler, Erumbi S Rangarajan and 4 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Charles K MinDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.
Jerome C NwachukwuDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.ORCID 0000-0003-4313-9187
Yingwei HouDepartment of Chemistry and Cancer Center, University of Illinois at Urbana-Champaign, Urbana, IL 61801.
Robin J RussoDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.
Alexandra PapaDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.
Jian MinState Key Laboratory of Biocatalysis and Enzyme Engineering, National & Local Joint Engineering Research Center of High-throughput Drug Screening Technology, School of Life Sciences, Hubei University, Wuhan 430062, China.ORCID 0000-0002-6341-2462
Rouming PengState Key Laboratory of Biocatalysis and Enzyme Engineering, National & Local Joint Engineering Research Center of High-throughput Drug Screening Technology, School of Life Sciences, Hubei University, Wuhan 430062, China.
Sung Hoon KimDepartment of Chemistry and Cancer Center, University of Illinois at Urbana-Champaign, Urbana, IL 61801.ORCID 0000-0001-9167-5617
Yvonne ZieglerDepartment of Molecular and Integrative Physiology, Cancer Center at University of Illinois at Urbana-Champaign, Urbana, IL 61801.ORCID 0000-0001-6811-7457
Erumbi S RangarajanDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.
Tina IzardDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.ORCID 0000-0002-2895-483X
Benita S KatzenellenbogenDepartment of Molecular and Integrative Physiology, Cancer Center at University of Illinois at Urbana-Champaign, Urbana, IL 61801.ORCID 0000-0002-8847-2752
John A KatzenellenbogenDepartment of Chemistry and Cancer Center, University of Illinois at Urbana-Champaign, Urbana, IL 61801.ORCID 0000-0003-0914-0010
Kendall W NettlesDepartment of Immunology and Microbiology, The Herbert Wertheim University of Florida Scripps Institute for Biomedical Innovation and Technology, Jupiter, FL 33458.ORCID 0000-0003-2917-7574

Funding

Molecular Mechanisms of Cell AdhesionR35GM139604 · NIGMS · UNIVERSITY OF FLORIDA · PI TINA IZARD · 2021 to 2026
$2.8M
Chemical, structural and molecular rules for fully antagonizing the estrogen receptorR01CA220284 · NCI · UNIVERSITY OF FLORIDA · PI KATZENELLENBOGEN, BENITA S, KATZENELLENBOGEN, JOHN A. · 2018 to 2022
$2.8M
Mechanisms of estrogen receptor ligand signalingR01CA275142 · NCI · UNIVERSITY OF FLORIDA · PI Kendall W Nettles · 2023 to 2026
$1.9M
Breast Cancer Research Foundation (BCRF) BCRF-083 BCRF-084HHS | NIH | National Cancer Institute (NCI) R01CA220284HHS | NIH | National Cancer Institute (NCI) R01CA275142NCI NIH HHS R01 CA220284NCI NIH HHS R01 CA275142NIGMS NIH HHS R35 GM139604
6 · The paper itself

Abstract

The estrogen receptor-α (ER) is thought to function only as a homodimer but responds to a variety of environmental, metazoan, and therapeutic estrogens at subsaturating doses, supporting binding mixtures of ligands as well as dimers that are only partially occupied. Here, we present a series of flexible ER ligands that bind to receptor dimers with individual ligand poses favoring distinct receptor conformations-receptor conformational heterodimers-mimicking the binding of two different ligands. Molecular dynamics simulations showed that the pairs of different ligand poses changed the correlated motion across the dimer interface to generate asymmetric communication between the dimer interface, the ligands, and the surface binding sites for epigenetic regulatory proteins. By examining the binding of the same ligand in crystal structures of ER in the agonist vs. antagonist conformers, we also showed that these allosteric signals are bidirectional. The receptor conformer can drive different ligand binding modes to support agonist vs. antagonist activity profiles, a revision of ligand binding theory that has focused on unidirectional signaling from the ligand to the coregulator binding site. We also observed differences in the allosteric signals between ligand and coregulator binding sites in the monomeric vs. dimeric receptor, and when bound by two different ligands, states that are physiologically relevant. Thus, ER conformational heterodimers integrate two different ligand-regulated activity profiles, representing different modes for ligand-dependent regulation of ER activity.

Indexed as

Estrogen Receptor alphaEstrogensMolecular Dynamics SimulationProtein MultimerizationAllosteric RegulationBinding SitesHumansLigandsProtein BindingProtein ConformationESR1 protein, humanEstrogen Receptor alphaEstrogensLigandsestrogen receptormolecular dynamics simulationsX-ray crystallography

Identifiers

PMID38830107
PMCPMC11181081

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.