Vitamin derivatives as potential drugs for Influenza Hemagglutinin.

The objective of the study was to identify potential inhibitors of Influenza surface Hemagglutinin (HA), which plays key role in the entry and replication of Influenza virus into the host cell. As ligands, seven vitamins and their derivatives were selected after initial screening based on their metabolizable capacity with no reported side effects, for studies. Docking, and Post docking analysis (X Score and Ligplot+) were performed against nine Influenza HA targets for the vitamins and its derivatives.

Functional characterization of GNE mutations prevalent in Asian subjects with GNE myopathy, an ultra-rare neuromuscular disorder.

UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is a bifunctional enzyme (N-terminal epimerase and C-terminal Kinase domain) that catalyses the rate limiting step in sialic acid biosynthesis. More than 200 homozygous missense or compound heterozygous mutations in GNE have been reported worldwide to cause a rare neuromuscular disorder, GNE myopathy. It is characterized by a slowly progressive defect in proximal and distal skeletal muscles with patients becoming wheel-chair-bound.

Fighting the Cause of Alzheimer's and GNE Myopathy.

Age is the common risk factor for both neurodegenerative and neuromuscular diseases. Alzheimer disease (AD), a neurodegenerative disorder, causes dementia with age progression while GNE myopathy (GNEM), a neuromuscular disorder, causes muscle degeneration and loss of muscle motor movement with age. Individuals with mutations in presenilin or amyloid precursor protein (APP) gene develop AD while mutations in GNE (UDP -acetylglucosamine 2 epimerase/-acetyl Mannosamine kinase), key sialic acid biosynthesis enzyme, cause GNEM.

Mutation in GNE Downregulates Peroxiredoxin IV Altering ER Redox Homeostasis.

GNE myopathy is a rare neuromuscular genetic disorder characterized by early adult onset and muscle weakness due to mutation in sialic acid biosynthetic enzyme, UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE). More than 180 different GNE mutations are known all over the world with unclear pathomechanism. Although hyposialylation of glycoproteins is speculated to be the major cause, but cellular mechanism leading to loss of muscle mass has not yet been deciphered.