![]() This modification allows for the peptide to embed into the membrane of cells and enter the cell through a ‘flip-flop’ mechanism. The team modified the endocytic motif by adding an N-terminal myristoyl group to increase its lipophilicity. “This novel peptide molecule is a lipidated endocytic dileucine sequence found in the human CD4 protein known to bind to the AP2 complex at the sigma/alpha-subunit interface,” explained Powell. The researchers developed a novel peptide molecule that could prevent endocytosis to reduce the hyperactivity of these pain neurons and thereby minimise pain perception. ![]() “So, we began with an in vivo genetic knockdown technique to knockdown a nociceptor sub-type specific isoform of the alpha-AP2 subunit.”įurthermore, the team did not just make use of animal experimentation, but utilised electrophysiology, biochemical approaches and various immunofluorescent approaches to validate their claim that endocytosis is a key contributor to the initiation and maintenance of inflammatory pain. “We wanted to make use complementary techniques to validate the voracity of our observations,” Powell elaborated. The team used an extensive range of techniques and approaches to verify their results. ![]() ![]() Using genetic and pharmacological approaches, the researchers found that endocytosis in these neurons was essential for both the development and maintenance of inflammatory pain. If we can understand this at the molecular and cellular level, we can then identify novel pain-killing targets” At the molecular level, our research is helping unravel how tissue injury signals to pain-sensing neurons. ![]()
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