ArticlePloS one2012
RETRACTED: Modeling and experimental analyses reveals signaling plasticity in a bi-modular assembly of CD40 receptor activated kinases.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Article
- NK Cells in the Lymph Nodes and Their Role in Anti-Tumour Immunity.Biomedicines · 2024Review
- Ras isoforms: signaling specificities in CD40 pathway.Cell communication and signaling : CCS · 2020Article
- Conceptual Evolution of Cell Signaling.International journal of molecular sciences · 2019Review
- Sharing of Phosphatases Promotes Response Plasticity in Phosphorylation Cascades.Biophysical journal · 2018Article
- TLR-CD40 Cross-Talk in Anti-Leishmanial Immune Response.Frontiers in immunology · 2014Review
- RETRACTED: Comprehensive logic based analyses of Toll-like receptor 4 signal transduction pathway.PloS one · 2014Article
Corrections and comments
- Retraction · 2026-04-21Concerns/Issues about Image · Concerns/Issues about Results and/or Conclusions · Duplication of/in Image · Euphemisms for Duplication · Original Data and/or Images not Provided and/or not Available · · See also: https://pubpeer.com/publications/9FC5C2E3FF8C1E8DA5627D86BFF173
- Retracted
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depending on the strength of signal dose, CD40 receptor (CD40) controls ERK-1/2 and p38MAPK activation. At low signal dose, ERK-1/2 is maximally phosphorylated but p38MAPK is minimally phosphorylated; as the signal dose increases, ERK-1/2 phosphorylation is reduced whereas p38MAPK phosphorylation is reciprocally enhanced. The mechanism of reciprocal activation of these two MAPKs remains un-elucidated. Here, our computational model, coupled to experimental perturbations, shows that the observed reciprocity is a system-level behavior of an assembly of kinases arranged in two modules. Experimental perturbations with kinase inhibitors suggest that a minimum of two trans-modular negative feedback loops are required to reproduce the experimentally observed reciprocity. The bi-modular architecture of the signaling pathways endows the system with an inherent plasticity which is further expressed in the skewing of the CD40-induced productions of IL-10 and IL-12, the respective anti-inflammatory and pro-inflammatory cytokines. Targeting the plasticity of CD40 signaling significantly reduces Leishmania major infection in a susceptible mouse strain. Thus, for the first time, using CD40 signaling as a model, we show how a bi-modular assembly of kinases imposes reciprocity to a receptor signaling. The findings unravel that the signalling plasticity is inherent to a reciprocal system and that the principle can be used for designing a therapy.
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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.