Moreover, the unique genome carries a nonbleaching protein A (NblA) gene (open reading frame [ORF] 022L), which is present in all phycobilisome-containing organisms and mediates phycobilisome
degradation. Western blot detection confirmed that 022L was expressed after PaV-LD infection in the host filamentous cyanobacterium. In addition, its appearance was companied by Buparlisib concentration a significant decline of phycocyanobilin content and a color change of the cyanobacterial cells from blue-green to yellow-green. The biological function of PaV-LD nblA was further confirmed by expression in a model cyanobacterium via an integration platform, by spectroscopic analysis and electron microscopy observation. The data indicate that PaV-LD is an exceptional cyanophage of filamentous cyanobacteria, and this novel cyanophage will also provide us with a new vision of the cyanophage-host interactions.”
“The mitochondrial inhibitor 1-methyl-4-phenylpyridinium (MPP+) is the toxicologically relevant metabolite of 1-methyl-4-phenyltetrahydropyridine (MPTP), which causes relatively selective degeneration of dopaminergic neurons in the substantia nigra. Dopaminergic LUHMES PS-341 mw cells were used
to investigate whether ATP-depletion can be uncoupled from cell death as a downstream event in these fully post-mitotic human neurons. Biochemical assays indicated that in the homogeneously differentiated cell cultures, MPP+ was taken up by the dopamine transporter (DAT). MPP+ then triggered oxidative stress and caspase activation, as well as ATP-depletion followed by cell death. Enhanced survival of the neurons in the presence of agents interfering with mitochondrial pathology, such as the fission inhibitor Mdivi-1 or a Bax channel click here blocker suggested a pivotal role of mitochondria in this model. However, these compounds did not prevent cellular ATP-depletion. To further investigate whether cells could be rescued despite respiratory chain inhibition by MPP+, we have chosen a diverse set of
pharmacological inhibitors well-known to interfere with MPP+ toxicity. The antioxidant ascorbate, the iron chelator desferoxamine, the stress kinase inhibitor CEP1347, and different caspase inhibitors reduced cell death, but allowed ATP-depletion in protected cells. None of these compounds interfered with MPP+ accumulation in the cells. These findings suggest that ATP-depletion, as the initial mitochondrial effect of MPP+, requires further downstream processes to result in neuronal death. These processes may form self-enhancing signaling loops, that aggravate an initial energetic impairment and eventually determine cell fate. (C) 2011 Elsevier Inc. All rights reserved.”
“Increased conversion of glucose to lactate is a key feature of many cancer cells that promotes rapid growth. Pyruvate kinase M2 (PKM2) expression is increased and facilitates lactate production in cancer cells.