P-bodies are cytoplasmic granules that are linked to mRNA decay, mRNA storage, and RNA interference (RNAi). They are known to interact with stress granules in stressed cells, and with late endosomes. Here, we report that P-bodies also interact with mitochondria, as previously described for P-body-related granules in germ cells. The interaction is dynamic, as a large majority of P-bodies contacts mitochondria at least once within a 3-min interval, and for about 18 s. This association requires an intact microtubule network. The depletion of P-bodies does not seem to affect mitochondria, nor the mitochondrial activity to be required for their contacts with P-bodies. However, inactivation of mitochondria leads to a strong decrease of miRNAmediated RNAi efficiency, and to a lesser extent of siRNA-mediated RNAi. The defect occurs during the assembly of active RISC and is associated with a specific delocalization of endogeneous Ago2 from P-bodies. Our study reveals the possible involvement of RNAi defect in pathologies involving mitochondrial deficiencies. P-bodies are ribonucleoprotein granules present in the cytoplasm of eukaryotic cells. They contain all proteins involved in the 5Ј to 3Ј mRNA degradation pathway, such as the decapping enzyme Dcp2, its enhancers Dcp1, Lsm1-7, Edc3, Hedls/Ge1, and the exonuclease Xrn1. This list extends to factors involved in specific degradation pathways, such as RNAi, NMD, and NGD (1, 2). They also contain proteins involved in translational repression, such as eIF4ET, Rck/p54/Dhh1, CPEB1, and the RISC complex. Some of the latter proteins also play a role in mRNA degradation, in particular Rck/p54/Dhh1, which is known as an enhancer of decapping, and the RISC complex when it is guided by a siRNA. Such catalogue of components indicates that P-bodies participate in these two aspects of mRNA metabolism. In addition, P-bodies increase in number and size when free untranslated mRNA accumulates. In mammals, this is observed when degradation is compromised by XrnI silencing (3) or when polysomes are disrupted with puromycin or arsenite (4). Taken together, these data support a role of P-bodies in mRNA degradation, mRNA storage, and RNA interference. Yet, their exact participation is unclear, as none of these functions is markedly affected in cells where P-bodies have been depleted (5-9).Live cell observations show that the number of P-bodies is quite stable over hours, although occasional formation of new P-bodies or fusions of pre-existing ones are observed (10).
Novel ADCC effector cells expressing the V-variant or F-variant of FcγRIIIa (CD16a) and firefly luciferase under the control of a chimeric promoter incorporating recognition sequences for the principal transcription factors involved in FcγRIIIa signal transduction, together with novel target cells overexpressing a constant high level of the specific antigen recognized by rituximab, trastuzumab, cetuximab, infliximab, adalimumab, or etanercept, confer improved sensitivity, specificity, and dynamic range in an ADCC assay relative to effector cells expressing a NFAT-regulated reporter gene and wild-type target cells. The effector cells also contain a normalization gene rendering ADCC assays independent of cell number or serum matrix effects. The novel effector and target cells in a frozen thaw-and-use format exhibit low vial-to-vial and lot-to-lot variation in their performance characteristics reflected by CVs of 10% or less. Homologous control target cells in which the specific target gene has been invalidated by genome editing providing an ideal control and a means of correcting for nonspecific effects were observed with certain samples of human serum. The novel effector cells and target cells expressing noncleavable membranebound TNFα have been used to quantify ADCC activity in serum from patients with Crohn's disease treated with infliximab and to relate ADCC activity to drug levels.
MnO x -cobalt tetramethoxyphenylporphyrin ͑CoTMPP͒/black pearls 2000 carbon black ͑BP͒ composite catalysts were synthesized by depositing CoTMPP onto carbon-supported MnO x ͑MnO x /BP͒, followed by heat-treatment from 500 to 900°C in N 2 atmosphere. The electrochemical characteristics of the catalysts for oxygen reduction reaction ͑ORR͒ were evaluated by the rotating disk electrode technique in half cells using 1 M KOH solution. BP2000 was used as a carbon support, which was pretreated with 30% H 2 O 2 to enhance the catalytic activities. Koutecky-Levich plots reveal a two-electron process, giving evidence that the ORR is mainly controlled by the formation of H 2 O 2 . Doping MnO x into the carbon support improves the activity of catalysts for ORR. There are two oxygen reduction peaks produced from these catalysts during the negative cyclic voltammetry scan. We obtained the best results using 800°C for the heat-treatment. At these conditions the X-ray diffraction results revealed that is mainly cubic MnO. The battery performance of a zinc-air single cell using MnO x -CoTMPP/BP as cathode catalyst was investigated, and the results show that the battery has good performance; the maximum output current density reached 216.3 mA/cm 2 at a potential of 1.0 V.
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