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De Franceschi L Scardoni G Tomelleri C Danek A Walker RH Jung HH Bader B Mazzucco S Dotti MT Siciliano A Pantaleo A Laudanna C 《PloS one》2012,7(2):e31015
Acanthocytes, abnormal thorny red blood cells (RBC), are one of the biological hallmarks of neuroacanthocytosis syndromes (NA), a group of rare hereditary neurodegenerative disorders. Since RBCs are easily accessible, the study of acanthocytes in NA may provide insights into potential mechanisms of neurodegeneration. Previous studies have shown that changes in RBC membrane protein phosphorylation state affect RBC membrane mechanical stability and morphology. Here, we coupled tyrosine-phosphoproteomic analysis to topological network analysis. We aimed to predict signaling sub-networks possibly involved in the generation of acanthocytes in patients affected by the two core NA disorders, namely McLeod syndrome (MLS, XK-related, Xk protein) and chorea-acanthocytosis (ChAc, VPS13A-related, chorein protein). The experimentally determined phosphoproteomic data-sets allowed us to relate the subsequent network analysis to the pathogenetic background. To reduce the network complexity, we combined several algorithms of topological network analysis including cluster determination by shortest path analysis, protein categorization based on centrality indexes, along with annotation-based node filtering. We first identified XK- and VPS13A-related protein-protein interaction networks by identifying all the interactomic shortest paths linking Xk and chorein to the corresponding set of proteins whose tyrosine phosphorylation was altered in patients. These networks include the most likely paths of functional influence of Xk and chorein on phosphorylated proteins. We further refined the analysis by extracting restricted sets of highly interacting signaling proteins representing a common molecular background bridging the generation of acanthocytes in MLS and ChAc. The final analysis pointed to a novel, very restricted, signaling module of 14 highly interconnected kinases, whose alteration is possibly involved in generation of acanthocytes in MLS and ChAc. 相似文献
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Gary W. Arendash William J. Millard Ralph Dawson Jr. Adrian J. Dunn Edwin M. Meyer 《Neurochemical research》1989,14(11):1113-1118
Young adult rats received either unilateral or bilateral ibotenic acid infusions in their nucleus basalis, destroying most of the cholinesterase-staining neurons in that region. Cerebral cortex levels of choline acetyltransferase, somatostatin, neuropeptide Y, and monoamines were then assayed 2.5 and 10 months after bilateral lesions, or, 2.5, 10, and 14 months after unilateral lesions. Entorhinal and cerebral cortex levels of several amino acid transmitters were also measured. As expected, choline acetyltransferase activity was decreased in the frontal cortex ipsilateral to the ibotenic acid infusion in unilaterally or bilaterally lesioned animals. Parietal cortex concentrations of somatostatin and neuropeptide Y were altered by lesioning in a complicated, time-dependent manner. Thus, while unilateral lesions transiently decreased or had no effect on these neuropeptide levels, bilateral lesions elevated the level of each neuropeptide by over 100% at 10 months. Other cortical transmitter systems investigated appeared to be less affected by nucleus basalis-lesions. Unilateral lesions had no effect on prefrontal cortex norepinephrine, serotonin, or dopamine content at 14 months post-lesioning. These different neurochemical effects of unilateral and bilateral nucleus basalis lesions may be important for developing a model for the trans-synaptic effects of cortical cholinergic deafferentation. 相似文献
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Recent progress in understanding the interaction between avermectins and ligand-gated ion channels: putting the pests to sleep 总被引:1,自引:0,他引:1
Wolstenholme AJ 《Invertebrate neuroscience : IN》2010,10(1):5-10
Avermectins and milbemycins are an important family of anthelmintics, insecticides and acaricides. Their mode of action is
as positive allosteric modulators of ligand-gated chloride channels, and at higher concentrations, they gate some channels
directly. Though it has long been known that the avermectins do not compete for the ligand binding site, the actual site at
which they interact with their receptors has been unclear. Recent data demonstrate the importance to drug binding of amino
acid residues predicted to line a water-filled pocket in the channel domain. This pocket acts as the binding site for anaesthetics
and other modulators of mammalian GABAA and glycine receptors, suggesting similarities in the mode of action between these drugs and the avermectins/milbemycins. 相似文献
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Penn Lloyd Adrian J.F.K. Craig Pat E. Hulley M. Faadiel Essop Paulette Bloomer Timothy M. Crowe 《Ostrich》2013,84(2-4):90-96
Lloyd, P., Craig, A.J.F.K., Hulley, P.E., Essop, M.F., Bloomer, P. & Crowe, T.M. 1997. Ecology and genetics of hybrid zones in the southern African Pycnonotus bulbul species complex. Ostrich 68 (2–4): 90–96. The closely related Blackeyed Bulbul Pycnonotus barbatus, Cape Bulbul P. capensis and Redeyed Bulbul P. nigricans have parapatric to locally sympatric distributions within southern Africa. Extensive hybridization along narrow transition zones between each of the three species pairs is described in a region of the Eastern Cape province, South Africa. The transition zones coincide with ecotones between different vegetation types, which in turn follow escarpments or mountain ranges. The lack of population density depressions within the hybrid zones, together with the variability of the hybrids, suggests the hybrids are viable. Sharp step clines in various phenotypic characters are described across the P. barbatus/P. nigricans hybrid zone. A mtDNA analysis found evidence of possible introgression between P. barbatus and P. capensis. All eight P. barbatus x P. nigricans hybrids analysed possessed P. barbatus mtDNA, suggesting the existence of either positive assortative mating or strong directional selection, but our data are unable to distinguish which. Our results do not support the dynamic-equilibrium model, but are compatible with the bounded-hybrid-superiority model. We conclude that the maintenance of the parapatric distributions of the different taxa is due mainly to differences in environmentally-associated fitness between parental phenotypes or among parental and hybrid phenotypes along an ecotone, with the narrowness of the hybrid zones maintained by the steepness of the environmental gradients crossing them. 相似文献
957.
Frequency modulation of Ca2+ sparks is involved in regulation of arterial diameter by cyclic nucleotides 总被引:1,自引:0,他引:1
Porter Valerie A.; Bonev Adrian D.; Knot Harm J.; Heppner Thomas J.; Stevenson Andra S.; Kleppisch Thomas; Lederer W. J.; Nelson Mark T. 《American journal of physiology. Cell physiology》1998,274(5):C1346
Forskolin, which elevates cAMP levels, and sodium nitroprusside(SNP) and nicorandil, which elevate cGMP levels, increased, by two- tothreefold, the frequency of subcellularCa2+ release("Ca2+ sparks") throughryanodine-sensitive Ca2+ release(RyR) channels in the sarcoplasmic reticulum (SR) of myocytes isolatedfrom cerebral and coronary arteries of rats. Forskolin, SNP,nicorandil, dibutyryl-cAMP, and adenosine increased the frequency ofCa2+-sensitiveK+(KCa) currents["spontaneous transient outward currents" (STOCs)] bytwo- to threefold, consistent withCa2+ sparks activating STOCs.These agents also increased the mean amplitude of STOCs by 1.3-fold, aneffect that could be explained by activation ofKCa channels, independent ofeffects on Ca2+ sparks. To testthe hypothesis that cAMP could act to dilate arteries throughactivation of the Ca2+sparkKCa channel pathway,the effects of blockers of KCachannels (iberiotoxin) and of Ca2+sparks (ryanodine) on forskolin-induced dilations of pressurized cerebral arteries were examined. Forskolin-induced dilations were partially inhibited by iberiotoxin and ryanodine (with no additive effects) and were entirely prevented by elevating externalK+. Forskolin lowered averageCa2+ in pressurized arteries whileincreasing ryanodine-sensitive, caffeine-inducedCa2+ transients. These experimentssuggest a new mechanism for cyclic nucleotide-mediated dilationsthrough an increase in Ca2+ sparkfrequency, caused by effects on SRCa2+ load and possibly on the RyRchannel, which leads to increased STOC frequency, membrane potentialhyperpolarization, closure of voltage-dependentCa2+ channels, decrease inarterial wall Ca2+, and,ultimately, vasodilation. 相似文献
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