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Arterial Inflammation in Mice Lacking the Interleukin 1 Receptor Antagonist Gene
- M. Nicklin, D. Hughes, J. Barton, J. Ure, G. Duff
- Biology, MedicineThe Journal of experimental medicine
- 17 January 2000
It is shown that mice that are homozygous for a null mutation in the gene encoding an endogenous antiinflammatory cytokine, interleukin 1 receptor antagonist (IL-1ra), develop lethal arterial inflammation involving branch points and flexures of the aorta and its primary and secondary branches, suggesting that expression of IL-1 is likely to have a significant role in signaling artery wall damage.
The new IL-1 family member IL-1F8 stimulates production of inflammatory mediators by synovial fibroblasts and articular chondrocytes
IL-1F8 exerts proinflammatory effects in primary human joint cells, and it remains to be determined whether circulating IL-1f8 can contribute to joint inflammation in rheumatoid arthritis.
A new nomenclature for IL-1-family genes.
A tissue specific IL‐1 receptor antagonist homolog from the IL‐1 cluster lacks IL‐1, IL‐1ra, IL‐18 and IL‐18 antagonist activities
- J. Barton, R. Herbst, D. Bosisio, L. Higgins, M. Nicklin
- Biology, MedicineEuropean journal of immunology
- 1 November 2000
IL‐1L1 had no detectable agonistic or antagonistic effect on IFN‐γ production in response to IL‐18 in KG‐1 cells and was concluded, contrary to a recent suggestion made by others, that IL‐ 1L1 is not a functional IL‐1ra.
A sequence-based map of the nine genes of the human interleukin-1 cluster.
Six novel genes encoding proteins with the interleukin (IL)-1 fold have been identified recently, allowing determination of the gene structures, precise localization of exons, and determination of distances between conventional SNP and microsatellite markers.
Glucocorticoids increase C/EBPbeta activity in the lung epithelium via phosphorylation.
Airway epithelial cell differentiation during lung organogenesis requires C/EBPα and C/EBPβ
- A. Roos, T. Berg, J. Barton, L. Didon, M. Nord
- Biology, MedicineDevelopmental dynamics : an official publication…
- 1 May 2012
It is demonstrated that C/EBPα and C/ EBPβ play pivotal, and partly overlapping roles in determining airway epithelial differentiation, with possible implications for tissue regeneration in lung homeostasis and disease.
Lung epithelial CCAAT/enhancer-binding protein-β is necessary for the integrity of inflammatory responses to cigarette smoke.
- L. Didon, J. Barton, M. Nord
- Medicine, BiologyAmerican journal of respiratory and critical care…
- 15 July 2011
The data suggest a previously unknown role for C/EBPβ and the airway epithelium in mediating inflammatory and innate immune responses to cigarette smoke.
The pattern recognition receptor Nod1 activates CCAAT/enhancer binding protein β signalling in lung epithelial cells
The results demonstrate a novel pathway downstream of the nucleotide-binding oligomerisation domain protein 1 receptor in these cells and suggest that C/EBPβ may play a role in immune responses to meso-diaminopimelic acid-containing bacteria in the lung.
Characterization of RNA aptamers that disrupt the RUNX1–CBFβ/DNA complex
High-affinity RNA aptamers represent new reagents that target a novel surface on the RHD required to stabilize the recombinant RHD–CBFβ complex and thus will further aid exploring the functions of this key transcription factor.