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Gene therapeutic approaches are needed that can simultaneously induce the well-controlled expression of therapeutic genes and suppress the expression of disease-causing genes for maximization of their efficacy. To address this challenge, we designed an allosteric ribozyme that comprises a Tetrahymena group I-based trans-splicing ribozyme as an active domain for RNA replacement, a small molecule-specific RNA aptamer as a sensor domain, and a communication module as an active transfer domain. The effectiveness of this approach was assessed by constructing various ribozymes in combination with a theophylline-binding aptamer to identify an allosteric ribozyme, which is controlled by theophylline both in vitro and in cells. Moreover, we constructed adenoviral vectors encoding the ribozymes and validated allosteric regulation of trans-gene expression via theophylline-dependent RNA replacement in target RNA-expressing cells. Results demonstrate that an allosteric trans-splicing ribozyme is an applicable RNA-based framework for engineering external ligand-controlled gene expression regulatory systems that exhibit adjustable regulation, design modularity, and target specificity.
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http://dx.doi.org/10.1021/cb500567v | DOI Listing |
JCI Insight
September 2025
Division of Nephrology, Boston University Chobanian & Avedisian School of Medicine, Boston, United States of America.
Background: Active vitamin D metabolites, including 25-hydroxyvitamin D (25D) and 1,25-dihydroxyvitamin D (1,25D), have potent immunomodulatory effects that attenuate acute kidney injury (AKI) in animal models.
Methods: We conducted a phase 2, randomized, double-blind, multiple-dose, 3-arm clinical trial comparing oral calcifediol (25D), calcitriol (1,25D), and placebo among 150 critically ill adult patients at high-risk of moderate-to-severe AKI. The primary endpoint was a hierarchical composite of death, kidney replacement therapy (KRT), and kidney injury (baseline-adjusted mean change in serum creatinine), each assessed within 7 days following enrollment using a rank-based procedure.
JTCVS Open
August 2025
Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif.
Objectives: Loeys-Dietz syndrome comprises genetically discrete subtypes of varying clinical severity. This study integrates longitudinal Loeys-Dietz syndrome clinical outcomes after aortic root replacement with transcriptomic analysis of aortic smooth muscle cell dysregulation to investigate mechanisms governing this subtype-specific aortic vulnerability.
Methods: Single institutional experience with aortic root replacement for nondissected aneurysm in patients with Loeys-Dietz syndrome was reviewed for midterm survival and distal aortic events (subsequent aortic intervention, aneurysm, or dissection).
Mol Ther Methods Clin Dev
September 2025
Versiti Blood Research Institute, Milwaukee, WI 53226, USA.
Plasminogen activator inhibitor-1 (PAI-1) deficiency is a rare disorder that causes moderate to severe bleeding and cardiac fibrosis, caused by mutation in the gene and no detectable circulating PAI-1 protein. There are currently no therapies that can effectively replace PAI-1 because the protein has a short half-life. An alternative approach to using recombinant protein is to endogenously increase circulating PAI-1 levels using mRNA therapy.
View Article and Find Full Text PDFJ Autoimmun
September 2025
Garvan Institute of Medical Research, Darlinghurst, NSW, Australia; Cellular Genomics Futures Institute & School of Biomedical Sciences, UNSW Sydney, Australia. Electronic address:
Background: In autoimmune disease it is not understood how self-reactive B cells escape immune tolerance checkpoints to produce pathogenic autoantibodies.
Objective: In patients with demyelinating polyneuropathy caused by IgM autoantibodies against myelin associated glycoprotein (MAG) and the sulphated trisaccharide CD57, we aimed to test the hypothesis that B cells making the autoantibody escaped tolerance by acquiring lymphoma driver somatic mutations.
Methods: Deep single-cell RNA, DNA, flow cytometric and antibody specificity analysis of blood from three patients with MAG neuropathy.
Cell Rep
September 2025
Department of Biochemistry, University of Colorado, Boulder, CO 80303, USA. Electronic address:
RNA polymerase II (RNAPII) is regulated by sequence-specific transcription factors (TFs) and the pre-initiation complex (PIC): TFIIA, TFIIB, TFIID, TFIIE, TFIIF, TFIIH, and Mediator. TFs, Mediator, and RNAPII contain intrinsically disordered regions (IDRs) and form phase-separated condensates, but how IDRs control RNAPII function remains poorly understood. Using purified PIC factors, we developed a real-time in vitro fluorescence transcription (RIFT) assay for second-by-second visualization of transcription at hundreds of promoters simultaneously.
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