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91.
爪蟾卵母细胞经注射鲫鱼视网总RNA后,可表达大量电压依赖性钾离子通道。在此基础上,我们进一步发现,一个特定序列的寡核苷酸能专一地抑制该通道的表达。由于我们设计与合成的该片段与果蝇、小鼠中已克隆的钾通道中编码N端的一个多肽的mRNA完全互补,因此推测:鲫鱼视网膜中的K这个区域与其它物种的K通道有高度同源性,这为克隆该基因和研究它的功能提供了重要资料。 相似文献
92.
Synopsis We collected schools of young, guarded by parents, of six common cichlid species to investigate the frequency and origin of interspecific brood-mixing. The main host species were a piscivore Lepidiolamprologus elongatus and a scale-eater Perissodus microlepis; more than half of their schools included heterospecific young, accounting for 20–40% of the total young. Most of the foreign young belonged to four biparental mouth-brooders whose parents have a habit of carrying their young in their mouths. Many of these young were smaller than the largest young brooded by their own parents. We concluded that adoption of young before independence results from farming-out, a behavior by which parents actively transfer their young to foster parents. 相似文献
93.
细胞外Ca^2+内流入胞质的机制 总被引:11,自引:0,他引:11
细胞外Ca^2+主要是通过塌压依赖性Ca^2+通道和钙池耗竭依赖性Ca^2+通道而内流的。前者主要见于电兴奋细胞,这一过程比较清楚;后者主要见非兴奋细胞,情况远较复杂:外来信号激活内贮钙池,钙池在释放Ca^2+同时通过目前尚不清楚的途径将直接或间接传至质膜Ca^2+通道,而诱发Ca^2+内流。 相似文献
94.
Henning Ursula Wallukat Gerd Holtzhauer Martin 《Molecular and cellular biochemistry》1996,160(1):47-52
In primary cultures of neonatal rat heart cells we found a linear correlation between the number of L-type calcium channel-specific dihydropyridine (DHP) binding sites and spontaneous beating frequency (v).Formation of glycoproteins in tissue culture was suppressed by different inhibitors of N-glycosylation. This inhibition alters to a different extent the binding of the DHP ligand (+)-[methyl-3H]PN 200-110 and v. The most severe but reversible effect occurs at 6 g/ml tunicamycin (Bmax 45% and v 6%, resp., of control), a slight increase in Bmax at 0.1–0.5 mM castanospermine and 0.05–2.5 mM deoxymannojirimycin. The other inhibitors gave no significant alterations of Bmax. 相似文献
95.
High-conductance calcium-activated potassium channels; Structure,pharmacology, and function 总被引:19,自引:0,他引:19
Gregory J. Kaczorowski Hans -Günther Knaus Reid J. Leonard Owen B. McManus Maria L. Garcia 《Journal of bioenergetics and biomembranes》1996,28(3):255-267
High-conductance calcium-activated potassium (maxi-K) channels comprise a specialized family of K+ channels. They are unique in their dual requirement for depolarization and Ca2+ binding for transition to the open, or conducting, state. Ion conduction through maxi-K channels is blocked by a family of venom-derived peptides, such as charybdotoxin and iberiotoxin. These peptides have been used to study function and structure of maxi-K channels, to identify novel channel modulators, and to follow the purification of functional maxi-K channels from smooth muscle. The channel consists of two dissimilar subunits, and . The subunit is a member of theslo Ca2+-activated K+ channel gene family and forms the ion conduction pore. The subunit is a structurally unique, membrane-spanning protein that contributes to channel gating and pharmacology. Potent, selective maxi-K channel effectors (both agonists and blockers) of low molecular weight have been identified from natural product sources. These agents, together with peptidyl inhibitors and site-directed antibodies raised against and subunit sequences, can be used to anatomically map maxi-K channel expression, and to study the physiologic role of maxi-K channels in various tissues. One goal of such investigations is to determine whether maxi-K channels represent novel therapeutic targets. 相似文献
96.
The mitochondrial inner membrane anion channel (IMAC) is a channel, identified by flux studies in intact mitochondria, which has a broad anion selectivity and is maintained closed or inactive by matrix Mg2+ and H+. We now present evidence that this channel, like many other chloride/anion channels, is reversibly blocked/inhibited by stilbene-2,2-disulfonates. Inhibition of malonate transport approaches 100% with IC50 values of 26, 44, and 88 M for DIDS, H2-DIDS, and SITS respectively and Hill coefficients 1. In contrast, inhibition of Cl– transport is incomplete, reaching a maximum of about 30% at pH 7.4 and 65% at pH 8.4 with an IC50 which is severalfold higher than that for malonate. The IC50 for malonate transport is decreased about 50% by pretreatment of the mitochondria withN-ethylmaleimide. Raising the assay pH from 7.4 to 8.4 increases the IC50 by about 50%, but under conditions where only the matrix pH is made alkaline the IC50 is decreased slightly. These properties and competition studies suggest that DIDS inhibits by binding to the same site as Cibacron blue 3GA. In contrast, DIDS does not appear to compete with the fluorescein derivative Erythrosin B for inhibition. These findings not only provide further evidence that IMAC may be more closely related to other Cl– channels than previously thought, but also suggest that other Cl– channels may be sensitive to some of the many regulators of IMAC which have been identified. 相似文献
97.
98.
C. L. Devlin P. J. S. Smith 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1996,166(4):270-277
To determine possible sources of Ca2+ during excitation-contraction coupling in smooth muscle, a vibrating Ca2+-selective electrode was used to measure Ca2+ flux during the process of contraction. The smooth muscle model was the longitudinal muscle of the body wall of a sea cucumberSclerodactyla briareus. Because acetylcholine caused slow contractions of the muscle that were inhibited by Ca2+ channel blockers diltiazem and verapamil in earlier mechanical studies, we chose a vibrating Ca2+-selective electrode as our method to test the hypothesis that acetylcholine may be stimulating Ca2+ influx across the sarcolemma, providing a Ca2+ source during excitation-contraction coupling. Acetylcholine treatment stimulated a net Ca2+ efflux that was both dose and time dependent. We then tested two L-type Ca2+ channel blockers, diltiazem and verapamil, and two non-specific Ca2+ blockers, cobalt (Co2+) and lanthanum (La3+) on acetylcholine-induced Ca2+ flux. All four Ca2+ blockers tested potently inhibited Ca2+ efflux induced by physiological doses of acetylcholine. We propose that the acetylcholine-induced Ca2+ efflux was the result of, first, Ca2+ influx through voltage-sensitive L-type Ca2+ channels, then the rapid extrusion of Ca2+ by an outwardly directed carrier such as the Na–Ca exchanger as suggested by Li+ substitution experiments. The vibrating Ca2+ electrode has provided new insights on the active and complex role the sarcolemma plays in Ca2+ homeostasis and regulating Ca2+ redistribution during excitation-contraction coupling.Abbreviations
ACh
acetylcholine
-
E-C coupling
excitation-contraction coupling
-
LMBW
longitudinal muscle of the body wall 相似文献
99.
Summary 1. We examined the actions of mercury (Hg2+) and zinc (Zn2+) on voltage-activated calcium channel currents of cultured rat dorsal root ganglion (DRG) neurons, using the whole-cell patch clamp technique.2. Micromolar concentrations of both cations reduced voltage-activated calcium channel currents. Calcium channel currents elicited by voltage jumps from a holding potential of –80 to 0 mV (mainly L- and N-currents) were reduced by Hg2+ and Zn2+. The threshold concentration for Hg2+ effects was 0.1 µM and that for Zn2+ was 10µM. Voltage-activated calcium channel currents were abolished (>80%) with 5µM Hg2+ or 200µM Zn2+. The peak calcium current was reduced to 50% (IC50) by 1.1µM Hg2+ or 69µM Zn2+. While Zn2+ was much more effective in reducing the T-type calcium channel current—activated by jumping from –80 to –35 mV—Hg2+ showed some increased effectiveness in reducing this current.3. The effects of both cations occurred rapidly and a steady state was reached within 1–3 min. While the action of Zn2+ was not dependent on an open channel state, Hg2+ effects depended partially on channel activation.4. While both metal cations reduced the calcium channel currents over the whole voltage range, some charge screening effects were detected with Hg2+ and with higher concentrations (>100µM) of Zn2+.5. As Zn2+ in the concentration range used had no influence on resting membrane currents, Hg2+ caused a clear inward current at concentrations µM.6. In the present study we discuss whether the actions of both metals on voltage-activated calcium channel currents are mediated through the same binding site and how they may be related to their neurotoxic effects. 相似文献
100.
《FEBS letters》1994,350(2-3):155-158
While many ion channels are modulated by phosphorylation, there is growing evidence that they can also be regulated by Ca2+-calmodulin, apparently through direct binding. In some cases, this binding activates channels; in others, it modulates channel activities. These phenomena have been documented in Paramecium, in Drosophila, in vertebrate photoreceptors and olfactory receptors, as well as in ryanodine receptor Ca2+-release channels. Furthermore, studies on calmodulin mutants in Paramecium have shown a clear bipartite distribution of two groups of mutations in the calmodulin gene that lead to opposite behavioral and electrophysiological phenotypes. These results indicate that the N-lobe of calmodulin specifically interacts with one class of ion-channel proteins and the C-lobe with another. 相似文献