ArticleClinical and experimental immunology2001
Involvement of the ERK mitogen-activated protein kinase in cell resistance to complement-mediated lysis.
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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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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
24 citing papers in PubMed, 57 citations in OpenAlex.
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- Innate Immune Defense Mechanisms by Myeloid Cells That Hamper Cancer Immunotherapy.Frontiers in immunology · 2020Review
- TNF-α promotes human antibody-mediated complement-dependent cytotoxicity of porcine endothelial cells through downregulating P38-mediated Occludin expression.Cell communication and signaling : CCS · 2019Article
- C3a Receptor Inhibition Protects Brain Endothelial Cells Against Oxygen-glucose Deprivation/Reperfusion.Experimental neurobiology · 2019Article
- Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention.Frontiers in immunology · 2019Review
- Receptor-Interacting Protein Kinases 1 and 3, and Mixed Lineage Kinase Domain-Like Protein Are Activated by Sublytic Complement and Participate in Complement-Dependent Cytotoxicity.Frontiers in immunology · 2018Article
- The role of the complement system in cancer.The Journal of clinical investigation · 2017Review
- Complement and macrophage crosstalk during process of angiogenesis in tumor progression.Journal of biomedical science · 2015Review
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- Longitudinally extensive NMO spinal cord pathology produced by passive transfer of NMO-IgG in mice lacking complement inhibitor CD59.Journal of autoimmunity · 2014Article
- Retinal pigment epithelial cell death by the alternative complement cascade: role of membrane regulatory proteins, calcium, PKC, and oxidative stress.Investigative ophthalmology & visual science · 2014Article
- The role of complement in tumor growth.Advances in experimental medicine and biology · 2014Review
- Complement inhibition in cancer therapy.Seminars in immunology · 2013Review
- Complement in animal development: unexpected roles of a highly conserved pathway.Seminars in immunology · 2013Review
- Sublytic complement protects prostate cancer cells from tumour necrosis factor-α-induced cell death.Clinical and experimental immunology · 2012Article
- Identification of a central role for complement in osteoarthritis.Nature medicine · 2011Article
- Membrane attack by complement: the assembly and biology of terminal complement complexes.Immunologic research · 2011Review
- Emission of membrane vesicles: roles in complement resistance, immunity and cancer.Springer seminars in immunopathology · 2005Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sublytic doses of complement desensitize cells and make them resistant to lytic complement doses. This process, named complement-induced protection, requires calcium ion influx, protein kinase C activation and protein synthesis. The involvement of the extracellular signal-regulated kinase, ERK, in cell desensitization by sublytic complement was examined in erythroleukaemia K562 cells and in COS-7 cells. As shown here, ERK is activated in K562 and COS-7 cells within 10 min of sublytic immune attack and then shows a decline and a second peak of activation at 20 min. C7- and C8-deficient human sera have a small effect on ERK activity. However, a significant increase in ERK activation is observed when C7 or C8, respectively, is added back to these sera. Complement-induced ERK activation was blocked in cells treated with GF109203X or Go6976, two selective PKC inhibitors, as well as by treatment with PD098059, an inhibitor of MEK1, the ERK kinase. PD098059 treatment also sensitized K562 cells to complement-mediated lysis and prevented complement-induced protection. COS-7 cells transfected with a dominant-negative MEK plasmid were incapable of undergoing the process of complement-induced protection. In conclusion, cell desensitization by sublytic doses of the complement membrane attack complex involves a signalling cascade that includes PKC-mediated ERK activation.
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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.