Suppression of Allergic Lung Inflammation and Hyperactivity
Non toxic Water soluble Effectiveness at nanomole level Enhanced therapeutic potential
Therapeutic potential to suppress allergic airway asthma
Myrisolyated alanine-rich C kinase substrate (MARCKS), a substrate of protein kinase C, is a key regulatory molecule controlling mucus granule secretion by airway epithelial cells as well as directed migration of leukocytes, stem cells, and fibroblasts. Previous research has shown that the non-canonical function of MARCKS relies on its ability to stay in membrane to trap PIP2 in allergic asthma. This activity is lost if MARCKS is phosphorylated and dissociated from the membrane. UC Davis researchers have shown elevated phosphorylated MARCKS associated with human and animal asthma tissues. Thus, inhibiting MARCKS signaling activity can potentially be therapeutic points of intervention for treating asthma. Researchers at the University of California, Davis have developed a novel non-toxic and water soluble peptide which targets MARCKS’ phosphorylation site domain and inhibits MARCKS phosphorylation and its activity. UC Davis researchers have shown that this novel peptide is able to suppress allergic lung asthma symptoms including airway Inflammation, hyper-reactivity and mucous cell metaplasia in mice models in vivo. The peptide is effective at a nanomole level with no cytotoxicity to normal as well as asthmatic airway epithelia. Mechanistically, this peptide can reduce PIP3 pools and phospho-MARCKS levels through trapping membrane PIP2, leading to blocking PIP3-mediated signaling networks such as PI3k/AKT, PDK1, GRP1 and ARNO signaling.
20170028019
Additional Technologies by these Inventors Tech ID/UC Case 24415/2014-228-0 Related Cases 2014-228-0
USA
