ReviewMolecules (Basel, Switzerland)2016
Recent Progress in the Molecular Recognition and Therapeutic Importance of Interleukin-1 Receptor-Associated Kinase 4.
Review in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- Pharmacokinetics and Pharmacodynamics of KT-474, a Novel Selective Interleukin-1 Receptor-Associated Kinase 4 (IRAK4) Degrader, in Healthy Adults.Clinical and translational science · 2025Trial
- Bridging neuroinflammation, oxidative stress, and neurogenesis: aromatic turmerone as a multifunctional modulator via NF-κB and Nrf2 pathways.Inflammopharmacology · 2026Review
- Role of TLRs as signaling cascades to combat infectious diseases: a review.Cellular and molecular life sciences : CMLS · 2025Review
- Emerging interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitors or degraders as therapeutic agents for autoimmune diseases and cancer.Acta pharmaceutica Sinica. B · 2024Review
- Discovery of KT-474─a Potent, Selective, and Orally Bioavailable IRAK4 Degrader for the Treatment of Autoimmune Diseases.Journal of medicinal chemistry · 2024Article
- GRB7 plays a promoting role in the progression of gastric cancer.BMC cancer · 2023Article
- Discovery of 5-Aryl-2,4-diaminopyrimidine Compounds as Potent and Selective IRAK4 Inhibitors.ACS medicinal chemistry letters · 2022Article
- Discovery of Potent Benzolactam IRAK4 Inhibitors with Robust in Vivo Activity.ACS medicinal chemistry letters · 2020Article
- Differential Effects of MitoVitE, α-Tocopherol and Trolox on Oxidative Stress, Mitochondrial Function and Inflammatory Signalling Pathways in Endothelial Cells Cultured under Conditions Mimicking Sepsis.Antioxidants (Basel, Switzerland) · 2020Article
- The Roles of Alternative Splicing in Tumor-immune Cell Interactions.Current cancer drug targets · 2020Review
- PROTAC Degradation of IRAK4 for the Treatment of Cancer.ACS medicinal chemistry letters · 2019Article
- PROTAC Degradation of IRAK4 for the Treatment of Neurodegenerative and Cardiovascular Diseases.ACS medicinal chemistry letters · 2019Article
- Overcoming adaptive therapy resistance in AML by targeting immune response pathways.Science translational medicine · 2019Article
- TLR Signaling Is Activated in Lymph Node-Resident CLL Cells and Is Only Partially Inhibited by Ibrutinib.Cancer research · 2019Article
- Fatigue, Sleep, and Autoimmune and Related Disorders.Frontiers in immunology · 2019Review
- Genetic variant of IRAK2 in the toll-like receptor signaling pathway and survival of non-small cell lung cancer.International journal of cancer · 2018Article
- Upregulated IRAK1 and IRAK4 promoting the production of IFN-γ and IL-17 in Behcet's disease.International ophthalmology · 2018Article
- TLR4 Signaling Pathway Modulators as Potential Therapeutics in Inflammation and Sepsis.Vaccines · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are the most upstream pattern recognition receptors in the cell, which detect pathogen associated molecular patterns and initiate signal transduction, culminating in the transcription of pro-inflammatory cytokines and antiviral interferon. Interleukin-1 receptor-associated kinase 4 (IRAK4) is a key mediator in TLR (except for TLR3) and interleukin-1 receptor signaling pathways. The loss of kinase function of IRAK4 is associated with increased susceptibility to various pathogens, while its over-activation causes autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, and cancer. The therapeutic importance of this master kinase has been advocated by a number of recent preclinical studies, where potent inhibitors have been administered to improve various TLR-mediated pathologies. Increasing studies of X-ray crystallographic structures with bound inhibitors have improved our knowledge on the molecular recognition of ligands by IRAK4, which will be crucial for the development of new inhibitors with improved potencies. In this review, we briefly discuss the structural aspect of ligand recognition by IRAK4 and highlight its therapeutic importance in the context of TLR-associated unmet medical needs.
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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.