ArticleScientific reports2016
Inhibition of CDK9 as a therapeutic strategy for inflammatory arthritis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 37 citations in OpenAlex.
- CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models.Cell communication and signaling : CCS · 2026Article
- Circulating exhausted CD8+ effector memory cells differentiate immune checkpoint inhibitor-induced liver injury from other acute immune-mediated liver injuries.Journal for immunotherapy of cancer · 2026Article
- Machine Learning-Based Virtual Screening for the Identification of Novel CDK-9 Inhibitors.Biomolecules · 2025Article
- RNA kinetics influence the response to transcriptional perturbation in leukaemia cell lines.NAR cancer · 2024Article
- Dying to Defend: Neutrophil Death Pathways and their Implications in Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- A preclinical platform for assessing antitumor effects and systemic toxicities of cancer drug targets.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Targeting CDK9 for the Treatment of Glioblastoma.Cancers · 2021Review
- Article
- Targeting CDK9 for Anti-Cancer Therapeutics.Cancers · 2021Review
- CDK13 upregulation-induced formation of the positive feedback loop among circCDK13, miR-212-5p/miR-449a and E2F5 contributes to prostate carcinogenesis.Journal of experimental & clinical cancer research : CR · 2021Article
- Transcriptome-Wide High-Throughput m6A Sequencing of Differential m6A Methylation Patterns in the Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes Cell Line MH7A.Journal of inflammation research · 2021Article
- Targeting the rheumatoid arthritis synovial fibroblast via cyclin dependent kinase inhibition: An early phase trial.Medicine · 2020Article
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- The CUL5 ubiquitin ligase complex mediates resistance to CDK9 and MCL1 inhibitors in lung cancer cells.eLife · 2019Article
- Review: Enhancers in Autoimmune Arthritis: Implications and Therapeutic Potential.Arthritis & rheumatology (Hoboken, N.J.) · 2017Review
- Defining a therapeutic window for kinase inhibitors in leukemia to avoid neutropenia.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
Rheumatoid arthritis is characterised by synovial inflammation and proliferation of fibroblast-like synoviocytes. The induction of apoptosis has long been proposed as a target for proliferative autoimmune diseases, and has further been shown to act as a successful treatment of experimental models of arthritis, such as collagen-induced arthritis. Here we examined the effects of specific oral small-molecule inhibitors of the transcription regulating cyclin-dependent kinase 9 on the development and progression of collagen-induced arthritis. DBA/1 mice were immunised with bovine collagen type II and treated orally with specific CDK9 inhibitors. The effects of CDK9 inhibition on RNA levels and protein expression, apoptosis induction, caspase activation and lymphocyte phenotype were further analysed. Mice showed a significant delay in disease onset and a reduction in disease severity following treatment with CDK9 inhibitors. Inhibiting CDK9 activity in peripheral blood mononuclear cells resulted in the loss of Mcl-1 expression at both the protein and RNA levels, along with a subsequent increase in apoptosis. CDK9 specific inhibitors may be a potential alternative treatment not only of cancer, but also for autoimmune- and inflammatory diseases. Taken together, these results show that transient inhibition of CDK9 induces apoptosis in leukocyte subsets and modulates the immune response.
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Registered trials
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.