ArticleFrontiers in cell and developmental biology2019
Combined Knockout of RIPK3 and MLKL Reveals Unexpected Outcome in Tissue Injury and Inflammation.
Article in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Necroptosis and the RIPK1-RIPK3-MLKL pathway in chronic kidney disease: mechanisms, crosstalk, and therapeutic opportunities.Renal failure · 2026Review
- CRISPR-Cas9 Therapeutics in Early Clinical Development: Delivery and Molecular Diagnostics.Cells · 2026Review
- Cyclodextrins as Modulators of Regulated Cell Death: Implications for Immunometabolism and Therapeutic Innovation.Pharmaceutics · 2026Review
- PANoptosis: a new perspective for targeting programmed cell death after spinal cord injury.Frontiers in immunology · 2026Review
- Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies.Journal of cardiovascular translational research · 2025Review
- NETosis-specific cell death: a novel mechanism in the pathogenesis of gouty arthritis.European journal of medical research · 2025Review
- Necroptotic and Apoptotic Pathways in Sepsis: A Comparative Analysis of Pediatric and Adult ICU Patients.Biomedicines · 2025Article
- MLKL is involved in the regulation of skin wound healing and interplay between macrophages and myofibroblasts in mice.Scientific reports · 2025Article
- Targeting TNFR1-driven necroptosis in breast cancer.EXCLI journal · 2025Review
- Involvement of necroptosıs and apoptosıs ın protectıve effects of cyclosporın a on ischemıa-reperfusıon injury in rat kıdney.Journal of molecular histology · 2024Article
- Osteogenesis imperfecta type 10 and the cellular scaffolds underlying common immunological diseases.Genes and immunity · 2024Review
- The emerging role of regulated cell death in ischemia and reperfusion-induced acute kidney injury: current evidence and future perspectives.Cell death discovery · 2024Review
- The host-directed therapeutic imatinib mesylate accelerates immune responses to Mycobacterium marinum infection and limits pathology associated with granulomas.PLoS pathogens · 2023Article
- Role of necroptosis in kidney health and disease.Nature reviews. Nephrology · 2023Review
- Regulated cell death pathways in kidney disease.Nature reviews. Nephrology · 2023Review
- MLKL signaling regulates macrophage polarization in acute pancreatitis through CXCL10.Cell death & disease · 2023Article
- Approaches to Evaluating Necroptosis in Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Systematic Review of Potential Anticancerous Activities ofPlants (Basel, Switzerland) · 2021Review
- Cell-specific activation of RIPK1 and MLKL after intracerebral hemorrhage in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- The Role of the Key Effector of Necroptotic Cell Death, MLKL, in Mouse Models of Disease.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis, initially identified as a backup cell death program when apoptosis is hindered, is a prominent feature in the etiology and progression of many human diseases, such as ischemic injury and sepsis. Receptor-interacting protein kinase 3 (RIPK3) is the cardinal regulator of this cell death modality, recruiting and phosphorylating the executioner mixed lineage kinase domain-like protein (MLKL) to signal necroptosis, which is terminated by a cellular plasma membrane rupture and the leakage of intracellular contents from dying cells. Experimental data to date indicate that RIPK3 and MLKL is the core machinery essential for all necroptotic cell death responses. By using CRISPR/Cas9 (clustered regularly interspaced short palindromic repeat/CRISPR-associated protein 9) technology, we showed that
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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.