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Protective effects of glycoprotein-specific monoclonal antibodies on the course of experimental mumps virus meningoencephalitis. 总被引:5,自引:3,他引:2 下载免费PDF全文
Newborn Syrian hamsters were challanged with an intracerebral inoculum containing 128 50% lethal doses of the Kilham strain of mumps virus and treated 24 h later with a single intraperitoneal injection of mouse monoclonal antibody. Monoclonal antibodies reactive with epitopes on the fusion glycoprotein of mumps virus could not inhibit hemagglutination or neutralize infectivity in vitro and failed to provide biologically important protection against the in vivo infection. In contrast, monoclonal antibodies reactive with epitopes on the hemagglutinin-neuraminidase glycoprotein of mumps virus inhibited hemagglutination and neutralized infectivity in vitro and protected infected animals from the otherwise lethal central nervous system virus infection. Similar protection was provided by both purified immunoglobulin and F(ab')2 fragments. Immuno-cytochemical and virological studies showed diminished virus antigen and virus titers in the brains of successfully treated animals. It appears that a topographically restricted region of the hemagglutinin-neuraminidase molecule of the Kilham strain of mumps virus is of critical importance for immune recognition by the infected host. 相似文献
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Putkey JA Kleerekoper Q Gaertner TR Waxham MN 《The Journal of biological chemistry》2003,278(50):49667-49670
IQ motifs are found in diverse families of calmodulin (CaM)-binding proteins. Some of these, like PEP-19 and RC3, are highly abundant in neuronal tissues, but being devoid of catalytic activity, their biological roles are not understood. We hypothesized that these IQ motif proteins might have unique effects on the Ca2+ binding properties of CaM, since they bind to CaM in the presence or absence of Ca2+. Here we show that PEP-19 accelerates by 40 to 50-fold both the slow association and dissociation of Ca2+ from the C-domain of free CaM, and we identify the sites of interaction between CaM and PEP-19 using NMR. Importantly, we demonstrate that PEP-19 can also increase the rate of dissociation of Ca2+ from CaM when bound to intact CaM-dependent protein kinase II. Thus, PEP-19, and presumably similar members of the IQ family of proteins, has the potential to alter the Ca2+-binding dynamics of free CaM and CaM that is bound to other target proteins. Since Ca2+ binding to the C-domain of CaM is the rate-limiting step for activation of CaM-dependent enzymes, the data reveal a new concept of importance in understanding the temporal dynamics of Ca2+-dependent cell signaling. 相似文献
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We used a particle-based Monte Carlo simulation to dissect the regulatory mechanism of molecular translocation of CaMKII,
a key regulator of neuronal synaptic function. Geometry was based upon measurements from EM reconstructions of dendrites in
CA1 hippocampal pyramidal neurons. Three types of simulations were performed to investigate the effects of geometry and other
mechanisms that control CaMKII translocation in and out of dendritic spines. First, the diffusional escape rate of CaMKII
from model spines of varied morphologies was examined. Second, a postsynaptic density (PSD) was added to study the impact
of binding sites on this escape rate. Third, translocation of CaMKII from dendrites and trapping in spines was investigated
using a simulated dendrite. Based on diffusion alone, a spine of average dimensions had the ability to retain CaMKII for duration
of ~4 s. However, binding sites mimicking those in the PSD controlled the residence time of CaMKII in a highly nonlinear manner.
In addition, we observed that F-actin at the spine head/neck junction had a significant impact on CaMKII trapping in dendritic
spines. We discuss these results in the context of possible mechanisms that may explain the experimental results that have
shown extended accumulation of CaMKII in dendritic spines during synaptic plasticity and LTP induction. 相似文献
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The tropane alkaloid (TA) scopolamine is suggested to protect Brugmansia suaveolens (Solanaceae) against herbivorous insects. To test this prediction in a natural environment, scopolamine was induced by methyl jasmonate (MJ) in potted plants which were left 10?days in the field. MJ-treated plants increased their scopolamine concentration in leaves and herbivory decreased. These findings suggest a cause?Ceffect relationship. However, experiments in laboratory showed that scopolamine affect differently the performance of the specialist larvae of the ithomiine butterfly Placidina euryanassa (C. Felder & R. Felder) and the generalist fall armyworm Spodoptera frugiperda (J. E. Smith): the specialist that sequester this TA from B. suaveolens leaves was not negatively affected, but the generalist was. Therefore, scopolamine probably acts only against insects that are not adapted to TAs. Other compounds that are MJ elicited may also play a role in plant resistance against herbivory by generalist and specialist insects, and deserve future investigations. 相似文献
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Calmodulin (CaM) is the major pathway that transduces intracellular Ca2+ increases to the activation of a wide variety of downstream signaling enzymes. CaM and its target proteins form an integrated signaling network believed to be tuned spatially and temporally to control CaM's ability to appropriately pass signaling events downstream. Here, we report the spatial diffusivity and availability of CaM labeled with enhanced green fluorescent protein (eGFP)-CaM, at basal and elevated Ca2+, quantified by the novel fluorescent techniques of raster image scanning spectroscopy and number and brightness analysis. Our results show that in basal Ca2+ conditions cytoplasmic eGFP-CaM diffuses at a rate of 10 μm2/s, twofold slower than the noninteracting tracer, eGFP, indicating that a significant fraction of CaM is diffusing bound to other partners. The diffusion rate of eGFP-CaM is reduced to 7 μm2/s when a large (646 kDa) target protein Ca2+/CaM-dependent protein kinase II is coexpressed in the cells. In addition, the presence of Ca2+/calmodulin-dependent protein kinase II, which can bind up to 12 CaM molecules per holoenzyme, increases the stoichiometry of binding to an average of 3 CaMs per diffusive molecule. Elevating intracellular Ca2+ did not have a major impact on the diffusion of CaM complexes. These results present us with a model whereby CaM is spatially modulated by target proteins and support the hypothesis that CaM availability is a limiting factor in the network of CaM-signaling enzymes. 相似文献
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F. E. Waxham 《BMJ (Clinical research ed.)》1888,2(1448):716-719
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The activities of Ca2+/calmodulin (CaM)-dependent, Ca2+/phospholipid-dependent, and cyclic AMP-dependent protein kinases (CaM-KII, PKC, and PKA, respectively) were determined in rat brains after global ischemia. Both CaM-KII and PKC activities were significantly depressed in both hippocampal and cerebral cortical regions of ischemic animals, whereas no change was detected in PKA activity. The loss of CaM-KII activity was more dramatic and more sustained than the loss of PKC activity and correlated with the duration of ischemia. These decreases in enzyme activity were found in both supernatant and pellet fractions from crude homogenates. When the supernatant and pellet were analyzed for the amount of CaM-KII 50-kDa protein, a significant decrease was detected in supernatant fractions that paralleled a gain in the amount of CaM-KII in the pellet. Thus, the loss of CaM-KII activity in the supernatant can be explained by translocation of the enzyme to the pellet. Whether inactivation of CaM-KII occurs during or after the enzyme translocates from the supernatant to the pellet is unknown. Our results indicate that loss in CaM-KII activity parallels neuronal damage associated with ischemia; down-regulation of CaM-KII activity coincided with translocation of the enzyme to the particulate fraction, and it is proposed that this may be, in fact, a mechanism for controlling excessive CaM-KII phosphorylation. 相似文献
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