2,974 research outputs found
Characterization and physiological-function of class-I low-molecular-mass, heat-shock protein complex in soybean.
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Azetidine-induced accumulation of class I small heat shock proteins in the soluble fraction provides thermotolerance in soybean seedlings.
No full textTissue-type-specific heat-shock response and immunolocalization of class I low-molecular-weight heat-shock proteins in soybean.
No full textCloning and characterization of a cDNA-encoding an 18.0-kda class-1 low-molecular-weight heat-shock protein from rice.
No full textA copper chaperone for superoxide dismutase that confers three types of copper/zinc superoxide dismutase activity in Arabidopsis.
No full textCharacterization of the genomic structures and selective expression profiles of nine class I small heat shock protein genes clustered on two chromosomes in rice. (Oryza sativa L.)
No full textInduction of a cDNA clone from rice encoding a class II small heat shock protein by heat stress, mechanical injury, and salicylic acid
No full textTangle-bearing neurons survive despite disruption of membrane integrity in a mouse model of tauopathy
Full text linkNeurofibrillary tangles (NFTs) are associated with neuronal loss and correlate with cognitive impairment in Alzheimer disease, but how NFTs relate to neuronal death is not clear. We studied cell death in Tg4510 mice that reversibly express P301L mutant human tau and accumulate NFTs using in vivo multiphoton imaging of neurofibrillary pathology, propidium iodide (PI) incorporation into cells, caspase activation, and DNA labeling. We first observed that in live mice, a minority of neurons were labeled with the caspase probe or with PI fluorescence. These markers of cell stress were localized in the same cells and appeared specifically within NFT-bearing neurons. Contrary to expectations, the PI-stained neurons did not die during a day of observation; the presence of Hoechst-positive nuclei in them on the subsequent day indicated that the NFT-associated membrane disruption, as suggested by PI staining, and caspase activation do not lead to immediate death of neurons in this tauopathy model. This unique combination of in vivo multiphoton imaging with markers of cell death and pathological alteration is a powerful tool for investigating neuronal damage associated with neurofibrillary pathology
The charge transfer and ion formation in liquid Li-Tl alloys
Full text linkThe 7Li NMR Knight shift, K, and the spin-lattice relaxation time, T1, were measured for liquid Li–Tl alloys. The K decreases rapidly with the addition of Tl up to 20 at.% Tl. In the concentration from 20 to 50 at.% Tl, the K decreases only slightly and the K of 50 at.% Tl is 60% of K for the pure liquid Li. Such a decrease of K is considered as an indication for the strong charge transfer from Li to Tl. These tendencies are similar to those from previous studies for liquid Li–Ga and Li–In alloys. However, beyond 50 at.% Tl, the K increases and reaches to an almost constant value (70% of K for the pure liquid Li). Such a back donation of charge is absent for liquid Li–Ga and Li–In alloys. It is considered that the tendency of the formation of ionic structural unit for liquid Li–Tl alloys is slightly weaker compared with the cases of liquid Li–Ga and Li–In alloys. The T1 is also discussed with the relation to the Knight shift and the electronic properties
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