Lujian Liao

A cascade of NO in Alzheimer's disease One of the ill effects of the amyloid-β peptide that accumulates in Alzheimer's disease (AD) is the promotion of the production of nitric oxide (NO) and consequent nitrosylation of thiols in proteins such as dynamin-related protein 1 (Drp1), which can lead to loss of neuronal synapses. Nakamura et al. found that this S-nitrosylation occurs in an unusual way.

Abstract We describe mechanistically-distinct enzymes, i.e., a kinase, a guanosine triphosphatase and a ubiquitin protein hydrolase, which function in disparate biochemical pathways, that can also act in concert to mediate a series of redox reactions. Each enzyme manifests a second, noncanonical function – transnitrosylation – triggering a pathological biochemical cascade in Alzheimer’s disease (AD).

A glycosylation strategy based on click chemistry was employed to develop naphthalimide-based Fe fluorescent probe with low cytotoxicity and good water-solubility. The selectivity and sensitivity to Fe of three synthesized naphthalimide-based fluorescent probes follows a Nap-PZ<Nap-OHNap-OH(2.73?10 M)>Nap-Glc(4.27?10 M) trend. Moreover, Nap-Glc could be used to detect Fe in living cells.