We previously reported that AAK1 and GAK, kinase regulators of the host adaptor proteins AP1 and AP2, are essential for hepatitis C virus (HCV) infection, but the underlying mechanism and relevance to other viruses or in vivo infections remained unknown.
AAK1 or GAK depletion impaired epidermal growth factor (EGF)-mediated enhanced HCV entry and endocytosis of EGF receptor (EGFR), an HCV entry cofactor and erlotinib's cancer target.
Furthermore, AAK1 and GAK, serine/threonine kinases known to stimulate binding of AP2M1 to host cargo proteins, regulate core-AP2M1 binding and are essential for HCV assembly.
Hence, AAK1 inhibitors are a novel therapeutic approach to neuropathic pain with activity in animal models that is mechanistically linked (behaviorally and electrophysiologically) to α2 adrenergic signaling, a pathway known to be antinociceptive in humans.
One of the lines from this screen, which contained a null allele of the adapter protein-2 associated kinase 1 (AAK1) gene, had a normal response in acute pain assays (hot plate, phase I formalin), but a markedly reduced response to persistent pain in phase II formalin.
We present here the first genome sequence of A. aquariorum strain AAk1, which was isolated as the sole pathogen from the blood of a patient with septicemia and necrotizing fasciitis.
We present here the first genome sequence of A. aquariorum strain AAk1, which was isolated as the sole pathogen from the blood of a patient with septicemia and necrotizing fasciitis.
We present here the first genome sequence of A. aquariorum strain AAk1, which was isolated as the sole pathogen from the blood of a patient with septicemia and necrotizing fasciitis.