The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ

Abstract The human retinoid X receptor γ (hRXRγ) is one of three characterized RXR subtypes, transcription factors belonging to the nuclear receptor superfamily. All RXR subtypes share nearly identical structural elements, including a conserved DNA-binding domain, a D region, a ligand-binding domain...

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Main Authors: Katarzyna Sołtys, Krzysztof Skowronek, Dominika Bystranowska, Krzysztof Wycisk, Andrzej Ożyhar
Format: Article
Language:English
Published: BMC 2025-05-01
Series:Cell Communication and Signaling
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Online Access:https://doi.org/10.1186/s12964-025-02247-3
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author Katarzyna Sołtys
Krzysztof Skowronek
Dominika Bystranowska
Krzysztof Wycisk
Andrzej Ożyhar
author_facet Katarzyna Sołtys
Krzysztof Skowronek
Dominika Bystranowska
Krzysztof Wycisk
Andrzej Ożyhar
author_sort Katarzyna Sołtys
collection DOAJ
description Abstract The human retinoid X receptor γ (hRXRγ) is one of three characterized RXR subtypes, transcription factors belonging to the nuclear receptor superfamily. All RXR subtypes share nearly identical structural elements, including a conserved DNA-binding domain, a D region, a ligand-binding domain, and an F region. However, each subtype possesses a unique N-terminal AB region, which modulates the transcriptional activation of target genes in a cell- and promoter-dependent manner through its ligand-independent activation function involved in protein–protein interactions. Despite the functional significance of the AB region, its structural contributions, particularly in the context of the full-length receptor, remain largely unexplored. Here, we uncover the role of the AB region of hRXRγ in modulating the molecular properties of the receptor. A comparative analysis of the full-length receptor (hRXRγ) and a deletion mutant lacking the AB region (ΔABhRXRγ) highlights the critical role of the intrinsically disordered AB region in modulating the structural and functional properties of hRXRγ, including its ability to oligomerize, its overall stability, and conformation heterogeneity. The AB region does not act as an independent unit but amalgamates with the rest of the receptor, which fine-tunes the structural variability of hRXRγ, making it responsive to environmental conditions. These findings highlight the AB region as a critical determinant of hRXRγ's structural features and, potentially, its transcriptional potential.
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spelling doaj-art-7101e46a1bb94fe8bbc34144b332b2c42025-08-20T03:22:12ZengBMCCell Communication and Signaling1478-811X2025-05-0123112310.1186/s12964-025-02247-3The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγKatarzyna Sołtys0Krzysztof Skowronek1Dominika Bystranowska2Krzysztof Wycisk3Andrzej Ożyhar4Department of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wrocław University of Science and TechnologyInternational Institute of Molecular and Cell BiologyDepartment of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wrocław University of Science and TechnologyInternational Institute of Molecular and Cell BiologyDepartment of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wrocław University of Science and TechnologyAbstract The human retinoid X receptor γ (hRXRγ) is one of three characterized RXR subtypes, transcription factors belonging to the nuclear receptor superfamily. All RXR subtypes share nearly identical structural elements, including a conserved DNA-binding domain, a D region, a ligand-binding domain, and an F region. However, each subtype possesses a unique N-terminal AB region, which modulates the transcriptional activation of target genes in a cell- and promoter-dependent manner through its ligand-independent activation function involved in protein–protein interactions. Despite the functional significance of the AB region, its structural contributions, particularly in the context of the full-length receptor, remain largely unexplored. Here, we uncover the role of the AB region of hRXRγ in modulating the molecular properties of the receptor. A comparative analysis of the full-length receptor (hRXRγ) and a deletion mutant lacking the AB region (ΔABhRXRγ) highlights the critical role of the intrinsically disordered AB region in modulating the structural and functional properties of hRXRγ, including its ability to oligomerize, its overall stability, and conformation heterogeneity. The AB region does not act as an independent unit but amalgamates with the rest of the receptor, which fine-tunes the structural variability of hRXRγ, making it responsive to environmental conditions. These findings highlight the AB region as a critical determinant of hRXRγ's structural features and, potentially, its transcriptional potential.https://doi.org/10.1186/s12964-025-02247-3Nuclear receptorsRetinoid X receptorOligomerization9cRAStabilityIntrinsically disordered regions
spellingShingle Katarzyna Sołtys
Krzysztof Skowronek
Dominika Bystranowska
Krzysztof Wycisk
Andrzej Ożyhar
The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ
Cell Communication and Signaling
Nuclear receptors
Retinoid X receptor
Oligomerization
9cRA
Stability
Intrinsically disordered regions
title The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ
title_full The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ
title_fullStr The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ
title_full_unstemmed The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ
title_short The intrinsically disordered AB region: a key modulator of the molecular properties of human RXRγ
title_sort intrinsically disordered ab region a key modulator of the molecular properties of human rxrγ
topic Nuclear receptors
Retinoid X receptor
Oligomerization
9cRA
Stability
Intrinsically disordered regions
url https://doi.org/10.1186/s12964-025-02247-3
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