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71.
本文对国内流行的猪肠毒素源性大肠杆菌K88ac抗原的结构基因的核苷酸序列进行了测定。该基因由849对核苷酸组成,编码了283个氨基酸的蛋白亚单位及21个氨基酸的信号肽。与国外报道的K88ac序列的不同是我们发现一个碱基的点突变,导致在抗原决定簇内一个氨基酸的改变。从核苷酸序列推导出的氨基酸序列与另两种亚型进行了比较。 相似文献
72.
T.-H. Hwang D.-J. Suh H.-R. Bae S.-H. Lee J.-S. Jung 《The Journal of membrane biology》1996,154(3):251-257
To study K+ channels in the basolateral membrane of chloride-secreting epithelia, rat tracheal epithelial monolayers were cultured on
permeable filters and mounted into an Ussing chamber system. The mucosal membrane was permeabilized with nystatin (180 μg/ml)
in the symmetrical high K+ (145 mm) Ringer solution. During measurement of the macroscopic K+ conductance properties of the basolateral membrane under a transepithelial voltage clamp, we detected at least two types
of K+ currents: one is an inwardly rectifying K+ current and the other is a slowly activating outwardly rectifying K+ current. The inwardly rectifying K+ current is inhibited by Ba2+. The slowly activating K+ current was potentiated by cAMP and inhibited by clofilium, phorbol 12-myristae 13-acetate (PMA) and lowering temperature.
This is consistent with the biophysical characteristics of I
SK channel. RT-PCR analysis revealed the presence of I
SK cDNA in the rat trachea epithelia. Although 0.1 mm Ba2+ only had minimal affect on short-circuit current (I
sc) induced by cAMP in intact epithelia, 0.1 mm clofilium strongly inhibited it. These results indicate that I
SK might be important for maintaining cAMP-induced chloride secretion in the rat trachea epithelia.
Received: 1 March 1996/Revised: 5 August 1996 相似文献
73.
The Ca2+-activated maxi K+ channel is predominant in the basolateral membrane of the surface cells in the distal colon. It may play a role in the regulation
of the aldosterone-stimulated Na+ reabsorption from the intestinal lumen. Previous measurements of these basolateral K+ channels in planar lipid bilayers and in plasma membrane vesicles have shown a very high sensitivity to Ca2+ with a K
0.5 ranging from 20 nm to 300 nm, whereas other studies have a much lower sensitivity to Ca2+. To investigate whether this difference could be due to modulation by second messenger systems, the effect of phosphorylation
and dephosphorylation was examined. After addition of phosphatase, the K+ channels lost their high sensitivity to Ca2+, yet they could still be activated by high concentrations of Ca2+ (10 μm). Furthermore, the high sensitivity to Ca2+ could be restored after phosphorylation catalyzed by a cAMP dependent protein kinase. There was no effect of addition of
protein kinase C. In agreement with the involvement of enzymatic processes, lag periods of 30–120 sec for dephosphorylation
and of 10–280 sec for phosphorylation were observed. The phosphorylation state of the channel did not influence the single
channel conductance. The results demonstrate that the high sensitivity to Ca2+ of the maxi K+ channel from rabbit distal colon is a property of the phosphorylated form of the channel protein, and that the difference
in Ca2+ sensitivity between the dephosphorylated and phosphorylated forms of the channel protein is more than one order of magnitude.
The variety in Ca2+ sensitivities for maxi K+ channels from tissue to tissue and from different studies on the same tissue could be due to modification by second messenger
systems.
Received: 28 February 1995/Revised: 22 December 1995 相似文献
74.
In our previous studies on sheep parotid secretory cells, we showed that the K+ current evoked by acetylcholine (ACh) was not carried by the high-conductance voltage- and Ca2+-activated K+ (BK) channel which is so conspicuous in unstimulated cells, notwithstanding that the BK channel is activated by ACh. Since
several studies from other laboratories had suggested that the BK channel did carry the ACh-evoked K+ current in the secretory cells of the mouse mandibular gland, and that the current could be blocked with tetraethylammonium
(TEA), a known blocker of BK channels, we decided to investigate the ACh-evoked K+ current in mouse cells more closely. We studied whether the ACh-evoked K+ current in the mouse is inhibited by TEA and quinine. Using the whole-cell patch-clamp technique and microspectrofluorimetric
measurement of intracellular Ca2+, we found that TEA and quinine do inhibit the ACh-evoked K+ current but that the effect is due to inhibition of the increase in intracellular Ca2+ evoked by ACh, not to blockade of a K+ conductance. Furthermore, we found that the K+ conductance activated when ionomycin is used to increase intracellular free Ca2+ was inhibited only by quinine and not by TEA. We conclude that the ACh-evoked K+ current in mouse mandibular cells does not have the blocker sensitivity pattern that would be expected if it were being carried
by the high-conductance, voltage- and Ca2+-activated K+ (BK) channel. The properties of this current are, however, consistent with those of a 40 pS K+ channel that we have reported to be activated by ACh in these cells [16].
Received: 9 January 1996/Revised: 17 April 1996 相似文献
75.
ABA stimulation of outward K+ current (I
K,out) in Vicia faba guard cells has been correlated with a rise in cytosolic pH (pH
i
). However, the underlying mechanism by which I
K,out is affected by pH
i
has remained unknown. Here, we demonstrate that pH
i
regulates outward K+ current in isolated membrane patches from Vicia faba guard cells. The stimulatory effect of alkalinizing pH
i
was voltage insensitive and independent of the two free calcium levels tested, 50 nm and 1 μm. The single-channel conductance was only slightly affected by pH
i
. Based on single-channel measurements, the kinetics of time-activated whole-cell current, and the analysis of current noise
in whole-cell recordings, we conclude that alkaline pH
i
enhances the magnitude of I
K,out by increasing the number of channels available for activation. The fact that the pH
i
effect is seen in excised patches indicates that signal transduction pathways involved in the regulation of I
K,out by pH
i
, and by implication, components of hormonal signal transduction pathways that are downstream of pH
i
, are membrane-delimited.
Received: 5 June 1996/Revised: 1 August 1996 相似文献
76.
Inward-rectifying potassium channels in plant cells provide important mechanisms for low-affinity K+ uptake and membrane potential control in specific cell types, including guard cells, pulvinus cells, aleurone cells and root
hair cells. K+ channel blockers are potent tools for studying the physiological functions and structural properties of K+ channels. In the present study the structural and biophysical mechanisms of Cs+ and TEA+ block of a cloned Arabidopsis inward-rectifying K+ channel (KAT1) were analyzed. Effects of the channel blockers Cs+ and TEA+ were characterized both extracellularly and intracellularly. Both external Cs+ and TEA+ block KAT1 currents. A mutant of KAT1 (``m2KAT1'; H267T, E269V) was produced by site-directed mutagenesis of two amino acid
residues in the C-terminal portion of the putative pore (P) domain. This mutant channel was blocked less by external Cs+ and TEA+ than the wild-type K+ channel. Internal TEA+ and Cs+ did not significantly block either m2KAT1 or KAT1 channels. Other properties, such as cation selectivity, voltage-dependence
and proton activation did not show large changes between m2KAT1 and KAT1, demonstrating the specificity of the introduced
mutations. These data suggest that the amino acid positions mutated in the inward-rectifying K+ channel, KAT1, are accessible to external blockers and may be located on the external side of the membrane, as has been suggested
for outward-rectifying K+ channels.
Received: 31 July 1995/Revised: 5 January 1996 相似文献
77.
The mechanosensitive properties of large-conductance Ca2+-activated K+ (BK) channels from embryonic rat neuroepithelium were investigated with the cell-attached and inside-out configurations of
the patch-clamp technique. The channels were activated in both recording configurations by negative pressures applied to the
patch electrode, but reversal of the effect was total and immediate in inside-out patches whereas it was incomplete and delayed
in on-cell patches. This mechanosensitivity was not mediated by Ca2+ ions or fatty acids, suggesting that it is an intrinsic property of these channels. Cytochalasin B did not affect mechanosensitivity
in on-cell patches but increased it in inside-out patches. Kinetic studies showed that stretch increased the mean open time
of the channels and decreased the slowest time constant of their closed-time distributions. The present as well as previous
results suggest complex interactions between embryonic BK channels and their membranous and submembranous environment.
Received: 1 February 1996/Revised: 25 March 1996 相似文献
78.
Reconstituted Na+,K+-ATPase from either pig kidney or shark rectal glands was phosphorylated by cAMP dependent protein kinase, PKA. The stoichiometry was 0.9 mole Pi/mole -subunit in the pig kidney enzyme and 0.2 mol Pi/mol -subunit in the shark enzyme. In shark Na+,K+-ATPase PKA phosphorylation increased the maximum hydrolytic activity for cytoplasmic Na+ activation and extracellular K+ activation without affecting the apparent Km values. In contrast, no significant functional effect after PKA phosphorylation was observed in pig kidney Na+,K+-ATPase. 相似文献
79.
Abstract: K252a, an inhibitor of trk phosphorylation and nerve growth factor signal transduction in PC12 cells, blocked nerve growth factor-induced responses in cultured adult rat dorsal root ganglion sensory neurones. The nerve growth factor-dependent appearance of capsaicin sensitivity and accumulation of the neuropeptide substance P were inhibited when dorsal root ganglion neurones were grown in the presence of low concentrations (100 n M ) of K252a. At higher concentrations (3 µ M ), however, K252a stimulated the development of capsaicin sensitivity and the accumulation of substance P even in the absence of nerve growth factor. By using a wide dose range, therefore, we showed that K252a could either inhibit or mimic nerve growth factor's actions on sensory neurones. These results may explain the apparent paradox in the literature that some groups show a blocking effect of K252a on nerve growth factor-dependent survival of dorsal root ganglion sensory neurones, whereas others report that K252a can substitute for nerve growth factor or other trophic factors and promote neuronal survival. 相似文献
80.
Effect of Hypoxia on Na+-K+-Cl− Cotransport in Cultured Brain Capillary Endothelial Cells of the Rat
Abstract: The effect of hypoxia on Na+,K+-ATPase and Na+-K+-Cl? cotransport activity in cultured rat brain capillary endothelial cells (RBECs) was investigated by measuring 86Rb+ uptake as a tracer for K+. RBECs expressed both Na+,K+-ATPase and Na+-K+-Cl? cotransport activity (4.6 and 5.5 nmol/mg of protein/min, respectively). Hypoxia (24 h) decreased cellular ATP content by 43.5% and reduced Na+,K+-ATPase activity by 38.9%, whereas it significantly increased Na+-K+-Cl? cotransport activity by 49.1% in RBECs. To clarify further the mechanism responsible for these observations, the effect of oligomycin-induced ATP depletion on these ion transport systems was examined. Exposure of RBECs to oligomycin led to a time-dependent decrease of cellular ATP content (by ~65%) along with a complete inhibition of Na+,K+-ATPase and a coordinated increase of Na+-K+-Cl? cotransport activity (up to 100% above control values). Oligomycin augmentation of Na+-K+-Cl? cotransport activity was not observed in the presence of 2-deoxy-d -glucose (a competitive inhibitor of glucose transport and glycolysis) or in the absence of glucose. These results strongly suggest that under hypoxic conditions when Na+,K+-ATPase activity is reduced, RBECs have the ability to increase K+ uptake through Na+-K+-Cl? cotransport. 相似文献