ReviewImmunologic research2001
Mechanisms of signal transduction activated by sublytic assembly of terminal complement complexes on nucleated cells.
Review in Immunologic research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 68 citations in OpenAlex.
- Transcriptomic Characterization of Terminal Complement Complex-bound Cells in Human Choroid Using Single-Cell RNA Sequencing.bioRxiv : the preprint server for biology · 2026Article
- Complement system in tumor growth and metastases.British journal of cancer · 2026Review
- Complement-mediated and direct activation of human neutrophils induced byFrontiers in immunology · 2025Article
- The relationship between complement C1q and coronary plaque vulnerability based on optical coherence tomography analysis.Scientific reports · 2024Observational
- Article
- High Expression of Complement Component C7 Indicates Poor Prognosis of Breast Cancer and Is Insensitive to Taxane-Anthracycline Chemotherapy.Frontiers in oncology · 2021Article
- Role of C5b-9 and RGC-32 in Cancer.Frontiers in immunology · 2019Review
- Human anti-thrombospondin type 1 domain-containing 7A antibodies induce membranous nephropathy through activation of lectin complement pathway.Bioscience reports · 2018Article
- The mystery behind membrane insertion: a review of the complement membrane attack complex.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Target deletion of complement component 9 attenuates antibody-mediated hemolysis and lipopolysaccharide (LPS)-induced acute shock in mice.Scientific reports · 2016Article
- Role of complement and complement regulatory proteins in the complications of diabetes.Endocrine reviews · 2015Review
- Complement factors C1q, C3 and C5b-9 in the posterior sclera of guinea pigs with negative lens-defocused myopia.International journal of ophthalmology · 2015Article
- Complement regulation in renal disease models.Seminars in nephrology · 2013Review
- Role of C5b-9 complement complex and response gene to complement-32 (RGC-32) in cancer.Immunologic research · 2013Review
- STEC-HUS, atypical HUS and TTP are all diseases of complement activation.Nature reviews. Nephrology · 2012Review
- T cell activation by terminal complex of complement and immune complexes.The Journal of biological chemistry · 2011Article
- Membrane attack by complement: the assembly and biology of terminal complement complexes.Immunologic research · 2011Review
- Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration.Eye (London, England) · 2011Article
- Redox signaling and the innate immune system in alcoholic liver disease.Antioxidants & redox signaling · 2011Review
- Complement and periodontitis.Biochemical pharmacology · 2010Review
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
The sublytic assembly of C5b-7, C5b-8, and C5b-9, activates membrane phospholipases through heterotrimeric G proteins and stimulates a variety of cellular activities including prostanoids, leukotrienes, and cytokines synthesis. Activation of mitotic signaling through Ras, Raf-1, ERK1, and phosphatidylinositol-3 kinase (PI3-K) was induced in B lymphocytes, endothelial, and smooth muscle cells. PI3-K activation by C5b-9 induced STAT3 phosphorylation and translocation from cytoplasm to nucleus. This complex signaling mechanism is directly involved in many biological functions such as endo- and exocytosis, cell cycle progression, activation of transcription, and protein synthesis. The key role of this signaling pathway is reflected on cell survival and proliferation in acute and chronic inflammation where complement activation is an ubiquitous event.
Indexed as
Identifiers
What OpenQuestion holds
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.