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Cells
Special Issues
Protein and RNA Regulation in Cells
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Protein and RNA Regulation in Cells

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 June 2026 | Viewed by 3015

Special Issue Editors

Dr. Delai Huang

E-Mail Website
Guest Editor
Department of Biology, University of Virginia, Charlottesville, VA 22904, USA
Interests: nucleolar protein functions; protein degradation; phosphorylation; RNA processing; core regulatory network; single-cell RNA sequencing; signaling pathway; danio fishes
Dr. Denis Mottet

E-Mail Website
Guest Editor
Molecular Analysis and Gene Expression (MAGE) Laboratory, GIGA Research Institute, University of Liège, 4000 Liège, Belgium
Interests: transcription; epigenetic regulators (HDAC); post-transcription; spliceosome; splicing; cancer

Special Issue Information

Dear Colleagues,

Proteins and RNAs form the core of cellular functions, orchestrating diverse and essential biological processes. Regulatory networks involving proteins and RNAs ensure precise gene expression, enabling cells to respond effectively to internal signals and external stimuli, thus maintaining cellular homeostasis. Recent advancements in cutting-edge technologies have significantly deepened our understanding of the complex regulation mechanisms. Innovations such as high-resolution imaging, multi-omics, and cryo-electron microscopy have uncovered intricate details about how proteins and RNAs coordinate and control cellular functions.

This Special Issue, “Protein and RNA Regulation in Cells”, provides an open access platform dedicated to exploring the critical roles of proteins and RNAs in cellular regulation. We invite submissions of original research papers as well as comprehensive review articles that highlight recent discoveries driven by technological advances. Topics of particular interest include transcriptional and post-transcriptional regulation, translational and post-translational control, RNA and protein interactions, and innovative methods that have expanded our knowledge in cell and molecular biology. We especially encourage articles employing novel experimental strategies and integrative analyses that elucidate protein and RNA regulatory roles in health, disease, and developmental processes.

Dr. Delai Huang
Dr. Denis Mottet
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • gene expression
  • post-transcriptional regulation
  • post-translational modifications
  • non-coding RNAs
  • regulatory networks
  • protein degradation
  • RNA decay

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Published Papers (2 papers)

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Research

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13 pages, 1291 KB  
Article
Regulation of CLK1 Isoform Expression by Alternative Splicing in Activated Human Monocytes Contributes to Activation-Associated TNF Production
by Maurice J. H. van Haaren, Alejandra Bodelón, Lyanne J. P. M. Sijbers, Rianne Scholman, Lucas W. Picavet, Jorg J. A. Calis, Sebastiaan J. Vastert and Jorg van Loosdregt
Cells 2025, 14(23), 1925; https://doi.org/10.3390/cells14231925 - 3 Dec 2025
Viewed by 1092
Abstract
Alternative splicing is a key regulator of immune regulation by enabling rapid and context-specific responses. However, the role of splicing regulators such as CDC-like kinase 1 (CLK1) in monocyte biology remains poorly defined. Here, we identify and characterize distinct CLK1-splice isoforms in human [...] Read more.
Alternative splicing is a key regulator of immune regulation by enabling rapid and context-specific responses. However, the role of splicing regulators such as CDC-like kinase 1 (CLK1) in monocyte biology remains poorly defined. Here, we identify and characterize distinct CLK1-splice isoforms in human CD14+ monocytes using long-read RNA sequencing. In resting monocytes, we observe predominant expression of a truncated isoform lacking exon 4 (CLK1Δ4), which undergoes nonsense-mediated decay resulting in minimal protein output. Lipopolysaccharide (LPS) stimulation induces a shift toward the full-length isoform (CLK1+4), associated with increased transcript stability and protein expression. This splicing switch was confirmed by RT-qPCR, short-read RNA sequencing, and Western blot analysis. Pharmacological inhibition of CLK1 selectively reduced TNFα production without affecting cell viability, implicating that the isoform shift enhances pro-inflammatory signaling. These findings uncover a stimulus-dependent splicing mechanism that modulates monocyte activation through differential CLK1 isoform expression and suggest a potential therapeutic avenue by targeting splicing regulators in immune-related disease with an established role of activated monocytes. Full article
(This article belongs to the Special Issue Protein and RNA Regulation in Cells)
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Review

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27 pages, 1530 KB  
Review
Regulation of Translation of ATF4 mRNA: A Focus on Translation Initiation Factors and RNA-Binding Proteins
by Pauline Adjibade and Rachid Mazroui
Cells 2026, 15(2), 188; https://doi.org/10.3390/cells15020188 - 20 Jan 2026
Cited by 1 | Viewed by 1456
Abstract
Cells are continuously exposed to physiological and environmental stressors that disrupt homeostasis, triggering adaptive mechanisms such as the integrated stress response (ISR). A central feature of ISR is the selective translation of activating transcription factor 4 (ATF4), which orchestrates gene programs essential for [...] Read more.
Cells are continuously exposed to physiological and environmental stressors that disrupt homeostasis, triggering adaptive mechanisms such as the integrated stress response (ISR). A central feature of ISR is the selective translation of activating transcription factor 4 (ATF4), which orchestrates gene programs essential for metabolic adaptation and survival. Stress-induced acute ATF4 expression occurs in diverse mammalian cell types and is typically protective; however, chronic activation contributes to pathologies including cancer and neurodegeneration. Canonical ISR (c-ISR) is initiated by phosphorylation of eIF2α in response to stressors such as endoplasmic reticulum or mitochondrial dysfunction, hypoxia, nutrient deprivation, and infections. This modification suppresses global protein synthesis while promoting ATF4 translation through upstream open reading frames (uORFs) in its 5′UTR. Recently, an alternative pathway, split ISR (s-ISR), enabling ATF4 translation independently of eIF2α phosphorylation, was identified in mice, suggesting ISR adaptability, though its relevance in humans remains unclear. Under normal conditions, cap-dependent translation predominates, mediated by the eIF4F complex and requiring the activity of eIF2B at its initial steps. During translational stress, eIF2α phosphorylation inhibits eIF2B activity, resulting in the formation of stalled initiation complexes, which can aggregate into stress granules (SGs). SGs sequester mRNAs and translation initiation factors, further repressing global translation, while ATF4 mRNA largely escapes sequestration, enabling selective translation. This partitioning highlights a finely tuned regulatory mechanism balancing ATF4 expression during stress. Recent advances reveal that, beyond cis-regulatory uORFs, trans-acting factors such as translation initiation factors and associated RNA-binding proteins critically influence ATF4 translation. Understanding these mechanisms provides insight into ISR plasticity and its implications for development, aging, and disease. Full article
(This article belongs to the Special Issue Protein and RNA Regulation in Cells)
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