- 関
- microtubule、MT
WordNet
- a microscopically small tubule
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- Montana
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English Journal
- Combretastatin A-4 induces p53 mitochondrial-relocalisation independent-apoptosis in non-small lung cancer cells.
- Méndez-Callejas GM1, Leone S, Tanzarella C, Antoccia A.Author information 1Departament of Science University 'Roma Tre', V.le G. Marconi 446, 00146, Rome, Italy; Universidad de Ciencias Aplicadas y Ambientales, Calle 222, 55-37, Bogotá, Colombia.AbstractCombretastatin A-4 (CA-4) is one of the most effective agents used in chemotherapy. Nevertheless, the contribution of p53 and Bim proteins in the CA-4-induced apoptosis in non-small lung cancer cells (NSCLC) remains unresolved, specifically on involving of p53 in the mitochondrial pathway activation by a transcription-independent mechanism. In this context, the p53-null H1299 and wt-p53 H460 NSCLC cells, in the absence and presence of pifithrin-µ (PFTµ), an inhibitor of p53 mitochondrial-translocation, were treated with CA-4 and different cellular endpoints were analysed. In contrast to previous observations in H460 cells, CA-4 failed in the activation of an apoptotic response in H1299 cells, thus indicating an involvement of p53 in the cell death induced by the drug. We found that CA-4 led to p53 cellular re-localisation in H460 cells; in particular, p53 was released from the microtubular network and accumulated at mitochondria where it interacts with Bim protein and other proteins of the Bcl-2 (B-cell leukaemia-2) family, leading to cytochrome c release, alteration in the mitochondrial membrane polarisation, cell cycle arrest at the G2/M-phase, and cell death. Interestingly, the cytosolic and the mitochondrial accumulation of protein Bim was strictly dependent on p53 status. The extent of cell death was not reduced in H460 after combined treatment of PFTµ with CA-4. Overall, the data support a model of CA-4-induced apoptosis in NSCLC, for which the expression of p53 protein is essential, but its mitochondrial function, linked to p53-transcription independent apoptosis pathway, is negligible.
- Cell biology international.Cell Biol Int.2014 Mar;38(3):296-308. doi: 10.1002/cbin.10199. Epub 2013 Nov 14.
- Combretastatin A-4 (CA-4) is one of the most effective agents used in chemotherapy. Nevertheless, the contribution of p53 and Bim proteins in the CA-4-induced apoptosis in non-small lung cancer cells (NSCLC) remains unresolved, specifically on involving of p53 in the mitochondrial pathway activation
- PMID 24155061
- Phosphatidic acid integrates calcium signaling and microtubule dynamics into regulating ABA-induced stomatal closure in Arabidopsis.
- Jiang Y1, Wu K, Lin F, Qu Y, Liu X, Zhang Q.Author information 1State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Life Sciences, Nanjing Agricultural University, Nanjing, 210095, People's Republic of China.AbstractSpecific cellular components have been identified to function in abscisic acid (ABA) regulation of stomatal apertures, including calcium, the cytoskeleton, and phosphatidic acid. In this study, the regulation and dynamic organization of microtubules during ABA-induced stomatal closure by phospholipase D (PLD) and its product PA were investigated. ABA induced microtubule depolymerization and stomatal closure in wide-type (WT) Arabidopsis, whereas these processes were impaired in PLD mutant (pldα1). The microtubule-disrupting drugs oryzalin or propyzamide induced microtubule depolymerization, but did not affect the stomatal aperture, whereas their co-treatment with ABA resulted in stomatal closure in both WT and pldα1. In contrast, the microtubule-stabilizing drug paclitaxel arrested ABA-induced microtubule depolymerization and inhibited ABA-induced stomatal closure in both WT and pldα1. In pldα1, ABA-induced cytoplasmic Ca(2+) ([Ca(2+)]cyt) elevation was partially blocked, and exogenous Ca(2+)-induced microtubule depolymerization and stomatal closure were impaired. These results suggested that PLDα1 and PA regulate microtubular organization and Ca(2+) increases during ABA-induced stomatal closing and that crosstalk among signaling lipid, Ca(2+), and microtubules are essential for ABA signaling.
- Planta.Planta.2014 Mar;239(3):565-75. doi: 10.1007/s00425-013-1999-5. Epub 2013 Nov 23.
- Specific cellular components have been identified to function in abscisic acid (ABA) regulation of stomatal apertures, including calcium, the cytoskeleton, and phosphatidic acid. In this study, the regulation and dynamic organization of microtubules during ABA-induced stomatal closure by phospholipa
- PMID 24271006
- Myosin IIA is critical for organelle distribution and F-actin organization in megakaryocytes and platelets.
- Pertuy F1, Eckly A, Weber J, Proamer F, Rinckel JY, Lanza F, Gachet C, Léon C.Author information 1Unité Mixte de Recherche S949, Institut National de la Santé et de la Recherche Médicale-Université de Strasbourg, Etablissement Français du Sang-Alsace, Strasbourg, France.AbstractDuring proplatelet formation, a relatively homogeneous content of organelles is transported from the megakaryocyte (MK) to the nascent platelets along microtubule tracks. We found that platelets from Myh9(-/-) mice and a MYH9-RD patient were heterogeneous in their organelle content (granules and mitochondria). In addition, Myh9(-/-) MKs have an abnormal cytoplasmic clustering of organelles, suggesting that the platelet defect originates in the MKs. Myosin is not involved in the latest stage of organelle traffic along microtubular tracks in the proplatelet shafts as shown by confocal observations of proplatelet buds. By contrast, it is required for the earlier distribution of organelles within the large MK preplatelet fragments shed into the sinusoid circulation before terminal proplatelet remodeling. We show here that F-actin is abnormally clustered in the cytoplasm of Myh9(-/-) MKs and actin polymerization is impaired in platelets. Myosin IIA is required for normal granule motility and positioning within MKs, mechanisms that may be dependent on organelle traveling and tethering onto F-actin cytoskeleton tracks. Altogether, our results indicate that the distribution of organelles within platelets critically depends on a homogeneous organelle distribution within MKs and preplatelet fragments, which requires myosin IIA.
- Blood.Blood.2014 Feb 20;123(8):1261-9. doi: 10.1182/blood-2013-06-508168. Epub 2013 Nov 15.
- During proplatelet formation, a relatively homogeneous content of organelles is transported from the megakaryocyte (MK) to the nascent platelets along microtubule tracks. We found that platelets from Myh9(-/-) mice and a MYH9-RD patient were heterogeneous in their organelle content (granules and mit
- PMID 24243973
Japanese Journal
- Adjustment of GDC layer microstructure and its influence on the electrochemical properties of microtubular SOFCs
- , , , ,
- Journal of the Ceramic Society of Japan 123(1436), 171-177, 2015
- The development of a dense chemical reaction blocking layer (CRBL) for micro-tubular solid oxide fuel cells (SOFC) was the aim of this study. The electrochemical performance and stability of SOFCs wer …
- NAID 130005064024
- Direct hydrocarbon utilization in microtubular solid oxide fuel cells
- , , , , ,
- Journal of the Ceramic Society of Japan 123(1436), 213-216, 2015
- … However, microtubular SOFCs with nickel-gadolinia doped ceria (Ni-GDC) anode can generate power continuously at 650°C over a period of 100 h in propane and butane, because the Ni-GDC has high catalytic activities of hydrocarbon reforming and carbon oxidation. …
- NAID 130005064018
- Microtubular SOFC using doped LaGaO3 electrolyte film prepared with dip coating method
- , , , ,
- Journal of the Ceramic Society of Japan 123(1436), 182-186, 2015
- … Preparation of Microtubular cell using doped lanthanum gallate (LSGM) electrolyte with a dip coating and co-sintering process was studied. …
- NAID 130005064016
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- microtubule [mi″kro-tu´būl] any of the slender, tubular structures, composed chiefly of tubulin, found in the cytoplasmic ground substance of nearly all cells; they are involved in maintenance of cell shape and in the movements of ...
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