“
“Sonic hedgehog (Shh) plays critical roles during nervous system development, yet little is known about its function in the sympathetic nervous system. Using a mouse Shh null line, we examined the roles of Shh during SNS development. Loss of Shh did not prevent formation of the sympathetic trunk, but the ganglia are hypoplastic and misspatterned. Neuronal differentiation was delayed in Shh mutant embryos showing that Shh is required for correct developmental timing in addition to

its role in sympathetic nervous system Anlotinib research buy patterning. Immunohistochemical analyses of the ganglia for expression of the pan-neuronal marker beta(3)-tubulin, the noradrenergic biosynthetic enzyme tyrosine hydroxylase and the glial marker B-FABP showed that Shh is not required for differentiation of sympathetic neurons or glia. NeuroReport 20:684-688 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Most paramyxovirus fusion proteins require

coexpression of and activation by a homotypic attachment protein, hemagglutinin-neuraminidase (HN), to promote membrane fusion. However, the molecular mechanism of the activation remains unknown. We previously showed that the incorporation of a monohistidylated lipid into F-virosome (Sendai viral envelope containing only fusion protein) enhanced its fusion GW3965 research buy to hepatocytes, suggesting that the histidine residue in the lipid accelerated membrane fusion. Therefore, we explored whether a histidine moiety in HN could similarly direct activation of the fusion protein. In membrane fusion assays, the histidine substitution mutants of HN (H247A of Sendai virus and H245A of human parainfluenza virus 3) had impaired membrane fusion promotion activity without significant changes in other biological activities. Synthetic

30-mer peptides corresponding to regions of the two HN proteins containing A-1210477 these histidine residues rescued the fusion promoting activity of the mutants, whereas peptides with histidine residues substituted by alanine did not. These histidine-containing peptides also activated F-virosome fusion with hepatocytes both in the presence and in the absence of mutant HN in the virosome. We provide evidence that the HN-mimicking peptides promote membrane fusion, revealing a specific histidine “”switch”" in HN that triggers fusion.”
“Reactive oxygen species (ROS) play a role in the degeneration of auditory hair cells because of aging, noise trauma, or ototoxic drugs. Hydrogenation is a fundamental reduction/deoxidation reaction in living organisms. This study thus examined the potential of hydrogen to protect auditory hair cells from ROS-induced damage.