Papers on
Annexin A1
Genetic overexpression of Serpina3n attenuates muscular dystrophy in mice.Molkentin et al., Cincinnati, United States. In Hum Mol Genet, Feb 2016
Mechanistically, we show that increased Serpina3n promotes increased sarcolemma membrane integrity and stability in dystrophic mouse models in association with greater membrane residence of the integrins, the dystrophin/utrophin-glycoprotein complex of proteins, and annexin A1.
Bone marrow and splenic histology in hairy cell leukaemia.Sena Teixeira Mendes et al., London, United Kingdom. In Best Pract Res Clin Haematol, Dec 2015
The cells stain for B-cell related antigens as well as with antibodies against tartrate-resistant acid phosphatase, DBA44 (CD72), CD11c, CD25, CD103, CD123, cyclin D1 and annexin A1.
Wound repair: role of immune-epithelial interactions.Nusrat et al., München, Germany. In Mucosal Immunol, Sep 2015
This process is highly regulated by proteins and lipids, proresolving mediators such as Annexin A1 protein and resolvins released into the epithelial milieu by the epithelium itself and infiltrating innate immune cells including neutrophils and macrophages.
The resolution of inflammation: Principles and challenges.Norling et al., London, United Kingdom. In Semin Immunol, May 2015
These mediators are diverse in nature, and include specialized lipid mediators (lipoxins, resolvins, protectins and maresins) proteins (annexin A1, galectins) and peptides, gaseous mediators including hydrogen sulphide, a purine (adenosine), as well as neuromodulator release under the control of the vagus nerve.
Targeting pro-resolution pathways to combat chronic inflammation in COPD.Vlahos et al., Melbourne, Australia. In J Thorac Dis, 2014
In this perspective, we discuss an alternative view on why inflammation persists with a focus on why pro-resolution mediators such as lipoxin A4 (LXA4), D-series resolving and Annexin A1 fail to effectively switch off inflammation in COPD.