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Targeting metabolic plasticity and flexibility dynamics for cancer therapy

Redox signaling via the molecular chaperone BiP protects cells against endoplasmic reticulum-derived oxidative stress

Swiss Health Clinic coordinates access to specialist integrative digestive care programmes in Germany for international patients with Crohns disease and IBD

When this occurs, the levels of N 5-methyl-FH 4 are too low to allow homocysteine to be converted to methionine

Under oxidative stress, PARP-1 activation leads to the consumption of nicotinamide adenine dinucleotide (NAD+) and adenosine triphosphate (ATP), resulting in cellular energy metabolism dysfunction

doi: 10.1590/s0365-05962012000100012