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Complete genome sequence of Methanobacterium thermoautotrophicum deltaH: functional analysis and comparative genomics
The complete 1,751,377-bp sequence of the genome of the thermophilic archaeon Methanobacterium thermoautotrophicum deltaH has been determined by a whole-genome shotgun sequencing approach. A total of
The Small Molecule GMX1778 Is a Potent Inhibitor of NAD+ Biosynthesis: Strategy for Enhanced Therapy in Nicotinic Acid Phosphoribosyltransferase 1-Deficient Tumors
Findings indicating that GMX1778 is a potent and specific inhibitor of the NAD+ biosynthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT) indicate that cancer cells have a very high rate of NAD+ turnover, which makes NAD+ modulation an attractive target for anticancer therapy.
Preclinical development of the nicotinamide phosphoribosyl transferase inhibitor prodrug GMX1777
Results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose and support the design of an open-label, dose-escalation trial, in which patients with refractory solid tumors and lymphomas receive 24 h infusions of GMX 1777 as a single agent in 3-week cycles.
Mutational analysis of the mouse mitochondrial cytochrome b gene.
Inhibition of 7,12-dimethylbenz(a)anthracene-induced mammary tumors and DNA adducts by dietary selenite.
It is demonstrated that selenite can inhibit the initiation stage of mammary carcinogenesis and reduce the tumor incidence, likely due to a reduction in carcinogen metabolism and ultimately adduct formation.
Modulation of bacteriolysis by cooperative effects of penicillin-binding proteins 1a and 3 in Escherichia coli
It is concluded that cooperative effects between PBPs in E. coli can lead to a dissociation of bacterial killing and lysis, which is highly bactericidal without causing cell wall degradation or lysis.
Sequence Analysis of Mammalian Cytochrome b Mutants
Biochemical and somatic cell genetic analyses indicated that resistance phenotypes to inhibitors of electron transport through the protonmotive cytochrome h of Complex III were determined by mutations within the mitochondrial gene encoding the apocytochrome b.