ArticleThe Journal of biological chemistry2013
Increased cAMP in monocytes augments Notch signaling mechanisms by elevating RBP-J and transducin-like enhancer of Split (TLE).
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 24 citations in OpenAlex.
- PGE2 inhibits neutrophil phagocytosis through the EP2R-cAMP-PTEN pathway.Immunity, inflammation and disease · 2022Article
- Association between host genetics of sheep and the rumen microbial composition.Tropical animal health and production · 2022Article
- Roles of transducin-like enhancer of split (TLE) family proteins in tumorigenesis and immune regulation.Frontiers in cell and developmental biology · 2022Review
- Probiotics and Trained Immunity.Biomolecules · 2021Review
- Ehrlichia TRP effectors: moonlighting, mimicry and infection.Pathogens and disease · 2021Review
- Unique, Intersecting, and Overlapping Roles of C/EBP β and CREB in Cells of the Innate Immune System.Scientific reports · 2018Article
- Functional heterogeneity of human tissue-resident memory T cells based on dye efflux capacities.JCI insight · 2018Article
- Epigenetic modification of TLE1 induce abnormal differentiation in diabetic mice intestinal epithelium.Molecular and cellular biochemistry · 2018Article
- Global analysis of glycoproteins identifies markers of endotoxin tolerant monocytes and GPR84 as a modulator of TNFα expression.Scientific reports · 2017Article
- cAMP-dependent protein kinase A (PKA) regulates angiogenesis by modulating tip cell behavior in a Notch-independent manner.Development (Cambridge, England) · 2016Article
- Article
- The heterogeneity of human CD127(+) innate lymphoid cells revealed by single-cell RNA sequencing.Nature immunology · 2016Article
- Tle1 tumor suppressor negatively regulates inflammation in vivo and modulates NF-κB inflammatory pathway.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- Potential mechanisms underlying the Runx2 induced osteogenesis of bone marrow mesenchymal stem cells.American journal of translational research · 2015Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In cells of the innate immune system, pathological increases in intracellular cAMP attenuate immune responses and contribute to infections by bacteria such as Bacillus anthracis. In this work, cAMP from B. anthracis edema toxin (ET) is found to activate the Notch signaling pathway in both mouse macrophages and human monocytes. ET as well as a cell-permeable activator of PKA induce Notch target genes (HES1, HEY1, IL2RA, and IL7R) and are able to significantly enhance the induction of these Notch target genes by a Toll-like receptor ligand. Elevated cAMP also resulted in increased levels of Groucho/transducin-like enhancer of Split (TLE) and led to increased amounts of a transcriptional repressor complex consisting of TLE and the Notch target Hes1. To address the mechanism used by ET to activate Notch signaling, components of Notch signaling were examined, and results revealed that ET increased levels of recombinant recognition sequence binding protein at the Jκ site (RBP-J), a DNA binding protein and principal transcriptional regulator of Notch signaling. Overexpression studies indicated that RBP-J was sufficient to activate Notch signaling and potentiate LPS-induced Notch signaling. Further examination of the mechanism used by ET to activate Notch signaling revealed that C/EBP β, a transcription factor activated by cAMP, helped activate Notch signaling and up-regulated RBP-J. These studies demonstrate that cAMP activates Notch signaling and increases the expression of TLE, which could be an important mechanism utilized by cAMP to suppress immune responses.
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.