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171.
172.
P. La Colla O. Zuffardi C. de Giuli A. M. Cioglia B. Loddo 《Cellular and molecular life sciences : CMLS》1971,27(4):479-481
Riassunto La scarsa incorporazione di precursori dello ARN in cellule infette da poliovirus ed incubate a 41,5°C è dovuta ad una inibizione della sintesi dello ARN virale più che non ad una sua digestione ad opera di nucleasi.
Work supported by a Grant of Consiglio Nazionale delle Ricerche, Rome. 相似文献
Work supported by a Grant of Consiglio Nazionale delle Ricerche, Rome. 相似文献
173.
Axonal transport of neurofilaments in normal and disease states 总被引:5,自引:0,他引:5
Miller CC Ackerley S Brownlees J Grierson AJ Jacobsen NJ Thornhill P 《Cellular and molecular life sciences : CMLS》2002,59(2):323-330
Neurofilaments are among the most abundant organelles in neurones. They are synthesised in cell bodies and then transported
into and through axons by a process termed 'slow axonal transport' at a rate that is distinct from that driven by conventional
fast motors. Several recent studies have now demonstrated that this slow rate of transport is actually the consequence of
conventional fast rates of movement that are interrupted by extended pausing. At any one time, most neurofilaments are thus
stationary. Accumulations of neurofilaments are a pathological feature of several human neurodegenerative diseases suggesting
that neurofilament transport is disrupted in disease states. Here, we review recent advances in our understanding of neurofilament
transport in both normal and disease states. Increasing evidence suggests that phosphorylation of neurofilaments is a mechanism
for regulating their transport properties, possibly by promoting their detachment from the motor(s). In some neurodegenerative
diseases, signal transduction mechanisms involving neurofilament kinases and phosphatases may be perturbed leading to disruption
of transport.
Received 11 July 2001; received after revision 30 August 2001; accepted 31 August 2001 相似文献
174.
Theopold U Li D Fabbri M Scherfer C Schmidt O 《Cellular and molecular life sciences : CMLS》2002,59(2):363-372
In contrast to both vertebrates and non-insect arthropods, little is known about the coagulation of hemolymph (hemostasis) in insects. We discuss the integration of the hemostatic response with other branches of the insect immune system. We also describe the present stage in the characterization of both soluble and cellular factors that contribute to hemostasis in insects. The factors of the well-characterized clotting cascades of vertebrates, primitive chelicerates and crustaceans are used to assess the implications of sequencing the whole Drosophila genome for searching candidate genes involved in hemostasis. Some striking similarities between blood clotting in vertebrates and the reaction of insect cells involved in hemolymph coagulation have implications for a phylogenetic comparison of hemostasis between divergent animal classes. 相似文献
175.
Transmitter-evoked local calcium release stabilizes developing dendrites 总被引:10,自引:0,他引:10
In the central nervous system, dendritic arborizations of neurons undergo dynamic structural remodelling during development. Processes are elaborated, maintained or eliminated to attain the adult pattern of synaptic connections. Although neuronal activity influences this remodelling, it is not known how activity exerts its effects. Here we show that neurotransmission-evoked calcium (Ca(2+)) release from intracellular stores stabilizes dendrites during the period of synapse formation. Using a ballistic labelling method to load cells with Ca(2+) indicator dyes, we simultaneously monitored dendritic activity and structure in the intact retina. Two distinct patterns of spontaneous Ca(2+) increases occurred in developing retinal ganglion cells--global increases throughout the arborization, and local 'flashes' of activity restricted to small dendritic segments. Blockade of local, but not global, activity caused rapid retraction of dendrites. This retraction was prevented locally by focal uncaging of caged Ca(2+) that triggered Ca(2+) release from internal stores. Thus, local Ca(2+) release is a mechanism by which afferent activity can selectively and differentially regulate dendritic structure across the developing arborization. 相似文献
176.
177.
Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms 总被引:39,自引:0,他引:39
Barouch LA Harrison RW Skaf MW Rosas GO Cappola TP Kobeissi ZA Hobai IA Lemmon CA Burnett AL O'Rourke B Rodriguez ER Huang PL Lima JA Berkowitz DE Hare JM 《Nature》2002,416(6878):337-339
Subcellular localization of nitric oxide (NO) synthases with effector molecules is an important regulatory mechanism for NO signalling. In the heart, NO inhibits L-type Ca2+ channels but stimulates sarcoplasmic reticulum (SR) Ca2+ release, leading to variable effects on myocardial contractility. Here we show that spatial confinement of specific NO synthase isoforms regulates this process. Endothelial NO synthase (NOS3) localizes to caveolae, where compartmentalization with beta-adrenergic receptors and L-type Ca2+ channels allows NO to inhibit beta-adrenergic-induced inotropy. Neuronal NO synthase (NOS1), however, is targeted to cardiac SR. NO stimulation of SR Ca2+ release via the ryanodine receptor (RyR) in vitro, suggests that NOS1 has an opposite, facilitative effect on contractility. We demonstrate that NOS1-deficient mice have suppressed inotropic response, whereas NOS3-deficient mice have enhanced contractility, owing to corresponding changes in SR Ca2+ release. Both NOS1-/- and NOS3-/- mice develop age-related hypertrophy, although only NOS3-/- mice are hypertensive. NOS1/3-/- double knockout mice have suppressed beta-adrenergic responses and an additive phenotype of marked ventricular remodelling. Thus, NOS1 and NOS3 mediate independent, and in some cases opposite, effects on cardiac structure and function. 相似文献
178.
Reeves JN Watson D Osborne JP Pounds KA O'Brien PT Short AD Turner MJ Watson MG Mason KO Ehle M Schartel N 《Nature》2002,416(6880):512-515
Now that gamma-ray bursts (GRBs) have been determined to lie at cosmological distances, their isotropic burst energies are estimated to be as high as 1054 erg (ref. 2), making them the most energetic phenomena in the Universe. The nature of the progenitors responsible for the bursts remains, however, elusive. The favoured models range from the merger of two neutron stars in a binary system to the collapse of a massive star. Spectroscopic studies of the afterglow emission could reveal details of the environment of the burst, by indicating the elements present, the speed of the outflow and an estimate of the temperature. Here we report an X-ray spectrum of the afterglow of GRB011211, which shows emission lines of magnesium, silicon, sulphur, argon, calcium and possibly nickel, arising in metal-enriched material with an outflow velocity of the order of one-tenth the speed of light. These observations strongly favour models where a supernova explosion from a massive stellar progenitor precedes the burst event and is responsible for the outflowing matter. 相似文献
179.
The pathophysiologic pathways and clinical expression of mitochondrial DNA (mtDNA) mutations are not well understood. This is mainly the result of the heteroplasmic nature of most pathogenic mtDNA mutations and of the absence of clinically relevant animal models with mtDNA mutations. mtDNA mutations predisposing to hearing impairment in humans are generally homoplasmic, yet some individuals with these mutations have severe hearing loss, whereas their maternal relatives with the identical mtDNA mutation have normal hearing. Epidemiologic, biochemical and genetic data indicate that nuclear genes are often the main determinants of these differences in phenotype. To identify a mouse model for maternally inherited hearing loss, we screened reciprocal backcrosses of three inbred mouse strains, A/J, NOD/LtJ and SKH2/J, with age-related hearing loss (AHL). In the (A/J x CAST/Ei) x A/J backcross, mtDNA derived from the A/J strain exerted a significant detrimental effect on hearing when compared with mtDNA from the CAST/Ei strain. This effect was not seen in the (NOD/LtJ x CAST/Ei) x NOD/LtJ and (SKH2/J x CAST/Ei) x SKH2/J backcrosses. Genotyping revealed that this effect was seen only in mice homozygous for the A/J allele at the Ahl locus on mouse chromosome 10. Sequencing of the mitochondrial genome in the three inbred strains revealed a single nucleotide insertion in the tRNA-Arg gene (mt-Tr) as the probable mediator of the mitochondrial effect. This is the first mouse model with a naturally occurring mtDNA mutation affecting a clinical phenotype, and it provides an experimental model to dissect the pathophysiologic processes connecting mtDNA mutations to hearing loss. 相似文献
180.
Mutations in GFAP, encoding glial fibrillary acidic protein, are associated with Alexander disease 总被引:15,自引:0,他引:15
Brenner M Johnson AB Boespflug-Tanguy O Rodriguez D Goldman JE Messing A 《Nature genetics》2001,27(1):117-120
Alexander disease is a rare disorder of the central nervous system of unknown etiology. Infants with Alexander disease develop a leukoencephalopathy with macrocephaly, seizures and psychomotor retardation, leading to death usually within the first decade; patients with juvenile or adult forms typically experience ataxia, bulbar signs and spasticity, and a more slowly progressive course. The pathological hallmark of all forms of Alexander disease is the presence of Rosenthal fibers, cytoplasmic inclusions in astrocytes that contain the intermediate filament protein GFAP in association with small heat-shock proteins. We previously found that overexpression of human GFAP in astrocytes of transgenic mice is fatal and accompanied by the presence of inclusion bodies indistinguishable from human Rosenthal fibers. These results suggested that a primary alteration in GFAP may be responsible for Alexander disease. Sequence analysis of DNA samples from patients representing different Alexander disease phenotypes revealed that most cases are associated with non-conservative mutations in the coding region of GFAP. Alexander disease therefore represents the first example of a primary genetic disorder of astrocytes, one of the major cell types in the vertebrate CNS. 相似文献