Cholera toxin increases the rate of antigen-stimulated calcium influx in rat basophilic leukemia cells.
نویسندگان
چکیده
Cholera toxin pretreatment has been found to cause a 3-fold increase in the initial rate of antigen-stimulated secretion of serotonin from rat basophilic leukemia (RBL) cells. Under similar conditions, cholera toxin enhances the antigen-stimulated rise in cytoplasmic free ionized calcium levels and causes a 2-3-fold increase in the rate of antigen-stimulated influx of 45Ca. In intact RBL cells cholera toxin pretreatment potentiates the antigen-stimulated production of inositol phosphates, but in permeabilized cells, with strongly buffered free calcium levels, no effect of cholera toxin pretreatment on the antigen-stimulated activation of cellular phospholipase activities is observed. In addition, pretreatment of cells with tetradecanoylphorbol acetate inhibits antigen-stimulated production of inositol phosphates by greater than 95%, while the stimulated influx of 45Ca remains unaffected. These data indicate that the antigen-stimulated influx of calcium into RBL cells can be dissociated from the production of inositol phosphates in these cells. The observed effects of cholera toxin on exocytosis and Ca2+ influx in RBL cells are not due to the elevation of cellular cyclic AMP levels since a variety of agents capable of elevating cellular cyclic AMP levels do not mimic these effects. Together, these data suggest that a cholera toxin-sensitive guanine nucleotide-binding protein is involved in the pathway responsible for the antigen-stimulated influx of calcium into RBL cells.
منابع مشابه
Toxin: Possible Mediation by ADP Ribosylation Factor
Antigen-evoked influx of extracellular Ca 2 1 into mast cells may occur via store-operated Ca 2 1 channels called calcium release–activated calcium (CRAC) channels. In mast cells of the rat basophilic leukemia cell line (RBL-2H3), cholera toxin (CT) potentiates antigen-driven uptake of 45 Ca 2 1 through cAMP-independent means. Here, we have used perforated patch clamp recording at physiological...
متن کاملPotentiation of Fc∈ Receptor I–Activated Ca2+ Current (ICRAC) by Cholera Toxin
Antigen-evoked influx of extracellular Ca(2+) into mast cells may occur via store-operated Ca(2+) channels called calcium release-activated calcium (CRAC) channels. In mast cells of the rat basophilic leukemia cell line (RBL-2H3), cholera toxin (CT) potentiates antigen-driven uptake of (45)Ca(2+) through cAMP-independent means. Here, we have used perforated patch clamp recording at physiologica...
متن کاملDepolarization of rat basophilic leukemia cells inhibits calcium uptake and exocytosis
We have investigated the unusual observation that depolarization of rat basophilic leukemia cells in high potassium not only fails to induce secretion, but also inhibits the secretion induced when receptors for IgE are aggregated by antigen. Antigen-stimulated 45Ca uptake and the rise in cytoplasmic free ionized calcium measured with the fluorescent indicator quin2 were both inhibited in depola...
متن کاملRegulation of the antigen-induced F-actin response in rat basophilic leukemia cells by protein kinase C
Multivalent antigen that is capable of binding to and crosslinking the IgE receptors on rat basophilic leukemia (RBL) cells, induces a rapid and sustained rise in the content of filamentous actin. This reorganization of the actin may be responsible for changes in cellular morphology during the degranulation process. The antigen-stimulated polymerization of actin can be blocked in a dose-depende...
متن کاملOpiate Agonists Inhibit Ca2+ Influx in Rat Spinal Cord-Dorsal Root Ganglion Cocultures
The aim of the present study has been to characterize the regulation by opiates of “Ca2+ influx in rat spinal cord-dorsal root ganglion cocultures. We have demonstrated that K*-induced depolarization, in the presence of the Ca” channel agonist Bay K8644, stimulated Ca” influx (3-4-fold) via the dihydropyridine class of voltage-dependent Ca” channels. While p and 6 opiates had no effect, K opiat...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The Journal of biological chemistry
دوره 263 36 شماره
صفحات -
تاریخ انتشار 1988