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Protein–RNA Interactions: Function, Mechanism, and Identification

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 3871

Special Issue Editor


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Guest Editor
1. Department of Biology and Biotechnologies “Charles Darwin”, Sapienza University of Rome, 00185 Rome, Italy
2. Center for Life Nano- and Neuro-Science, RNA Systems Biology Lab, Fondazione Istituto Italiano di Tecnologia (IIT), 00161 Rome, Italy
Interests: bioinformatics; macromolecular interaction; next-generation sequencing; non-coding RNA; RNA-binding protein; gene regulatory network

Special Issue Information

Dear Colleagues,

Protein–RNA interactions (PRIs) are fundamental to all cellular processes, playing a critical role in gene expression, RNA processing, and protein synthesis. These interactions are mediated by RNA-binding proteins (RBPs) that recognize specific RNA targets through their sequences, structures, and modifications. Understanding these interactions is essential for deciphering the complex regulatory networks that govern cellular function.

We are pleased to invite you to submit your work to this Special Issue of IJMS focused on the intricate interplay between proteins and RNA molecules. This Special Issue aims to delve into the multifaceted functions and mechanisms underlying PRIs, while also showcasing innovative techniques for their identification.

In this Special Issue, original research articles and reviews are welcome. Topics of interest include, but are not limited to, the following:

  • Functional roles of RBP-RNA interactions in gene expression regulation;
  • Mechanisms governing protein–RNA recognition and RBP specificity;
  • Experimental and computational methodologies for identifying PRIs;
  • The impact of PRIs on RNA processing, stability, and translation;
  • The dysregulation of PRIs in human diseases and development;
  • Therapeutic strategies targeting aberrant PRIs.

Looking forward to receiving your contributions.

Dr. Alessio Colantoni
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • RNA-binding protein (RBP)
  • protein–RNA interaction
  • RNA structure
  • RNA processing
  • RNA stability
  • RNA modification
  • translation
  • gene regulatory network

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Published Papers (2 papers)

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Research

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23 pages, 3338 KiB  
Article
Understanding the Role of the SMN Complex Component GEMIN5 and Its Functional Relationship with Demethylase KDM6B in the Flunarizine-Mediated Neuroprotection of Motor Neuron Disease Spinal Muscular Atrophy
by Badih Salman, Emeline Bon, Perrine Delers, Steve Cottin, Elena Pasho, Sorana Ciura, Delphine Sapaly and Suzie Lefebvre
Int. J. Mol. Sci. 2024, 25(18), 10039; https://doi.org/10.3390/ijms251810039 - 18 Sep 2024
Cited by 2 | Viewed by 1356
Abstract
Dysregulated RNA metabolism caused by SMN deficiency leads to motor neuron disease spinal muscular atrophy (SMA). Current therapies improve patient outcomes but achieve no definite cure, prompting renewed efforts to better understand disease mechanisms. The calcium channel blocker flunarizine improves motor function in [...] Read more.
Dysregulated RNA metabolism caused by SMN deficiency leads to motor neuron disease spinal muscular atrophy (SMA). Current therapies improve patient outcomes but achieve no definite cure, prompting renewed efforts to better understand disease mechanisms. The calcium channel blocker flunarizine improves motor function in Smn-deficient mice and can help uncover neuroprotective pathways. Murine motor neuron-like NSC34 cells were used to study the molecular cell-autonomous mechanism. Following RNA and protein extraction, RT-qPCR and immunodetection experiments were performed. The relationship between flunarizine mRNA targets and RNA-binding protein GEMIN5 was explored by RNA-immunoprecipitation. Flunarizine increases demethylase Kdm6b transcripts across cell cultures and mouse models. It causes, in NSC34 cells, a temporal expression of GEMIN5 and KDM6B. GEMIN5 binds to flunarizine-modulated mRNAs, including Kdm6b transcripts. Gemin5 depletion reduces Kdm6b mRNA and protein levels and hampers responses to flunarizine, including neurite extension in NSC34 cells. Moreover, flunarizine increases the axonal extension of motor neurons derived from SMA patient-induced pluripotent stem cells. Finally, immunofluorescence studies of spinal cord motor neurons in Smn-deficient mice reveal that flunarizine modulates the expression of KDM6B and its target, the motor neuron-specific transcription factor HB9, driving motor neuron maturation. Our study reveals GEMIN5 regulates Kdm6b expression with implications for motor neuron diseases and therapy. Full article
(This article belongs to the Special Issue Protein–RNA Interactions: Function, Mechanism, and Identification)
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Review

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16 pages, 1453 KiB  
Review
Alternative Splicing in the Heart: The Therapeutic Potential of Regulating the Regulators
by Francesca Briganti and Zilu Wang
Int. J. Mol. Sci. 2024, 25(23), 13023; https://doi.org/10.3390/ijms252313023 - 4 Dec 2024
Cited by 1 | Viewed by 1487
Abstract
Alternative splicing allows a single gene to produce a variety of protein isoforms. Changes in splicing isoform usage characterize virtually every stage of the differentiation process and define the physiological differences between cardiomyocytes with different function, at different stages of development, and pathological [...] Read more.
Alternative splicing allows a single gene to produce a variety of protein isoforms. Changes in splicing isoform usage characterize virtually every stage of the differentiation process and define the physiological differences between cardiomyocytes with different function, at different stages of development, and pathological function. Recent identification of cardiac splicing factors provided insights into the mechanisms underlying alternative splicing and revealed how these splicing factors impact functional properties of the heart. Alterations of the splicing of sarcomeric genes, cell signaling proteins, and ion channels have been associated with the development of pathological conditions such as cardiomyopathy and arrhythmia. RBM20, RBM24, PTBP1, RBFOX, and QKI play key roles in cardiac development and pathology. A better understanding of their regulation will yield insights into healthy cardiac development and inform the development of molecular therapeutics. Full article
(This article belongs to the Special Issue Protein–RNA Interactions: Function, Mechanism, and Identification)
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