scholarly journals Anoctamin 1—role in proton secretion and protein resorption

2014 ◽  
Vol 10 (4) ◽  
pp. 182-182
Keyword(s):  
Anoctamin 1 ◽  
Proton Secretion

scholarly journals Secreted Human CLCA1 Activates Calcium-Dependent Chloride Currents via Interaction with TMEM16A (Anoctamin 1)

2015 ◽  
Vol 108 (2) ◽  
pp. 435a
Author(s):  
Monica Sala-Rabanal ◽  
Zeynep Yurtsever ◽  
Colin G. Nichols ◽  
Tom J. Brett
Keyword(s):  
Anoctamin 1 ◽  
Chloride Currents ◽  
Calcium Dependent

scholarly journals Presynaptic Localization and Possible Function of Calcium-Activated Chloride Channel Anoctamin 1 in the Mammalian Retina

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e67989 ◽  
Author(s):  
Ji Hyun Jeon ◽  
Sun Sook Paik ◽  
Myung-Hoon Chun ◽  
Uhtaek Oh ◽  
In-Beom Kim
Keyword(s):  
Chloride Channel ◽  
Anoctamin 1 ◽  
Mammalian Retina

Disorders of Proton Secretion by the Kidney

1986 ◽  
pp. 957-983 ◽  
Author(s):  
Philip R. Steinmetz ◽  
Joseph Palmisano
Keyword(s):  
Proton Secretion

Role of membrane fusion in CO2 stimulation of proton secretion by turtle bladder

1983 ◽  
Vol 245 (1) ◽  
pp. C113-C120 ◽  
Author(s):  
D. L. Stetson ◽  
P. R. Steinmetz
Keyword(s):  
Deuterium Oxide ◽  
Cell Structure ◽  
Proton Secretion ◽  
Luminal Membrane ◽  
Turtle Bladder ◽  
Cytoplasmic Vesicles ◽  
Resultant Increase ◽  
Electron Lucent ◽  
Stimulation Of

The changes in cell structure produced during stimulation of proton secretion by CO2 in turtle bladder were examined using ultrastructural morphometric methods. One hour after CO2 addition, the area of the luminal membrane of the carbonic anhydrase-containing (CA) cell population was increased 2.5-fold and the volume percent of electron-lucent cytoplasmic vesicles in these CA cells was decreased by 61%. No changes were observed in the epithelial granular cells. These results suggest that during CO2 stimulation the vesicles fuse with the luminal membrane. CO2 stimulation of proton secretion is inhibited by the cytoskeleton-disrupting drugs colchicine and cytochalasin B and by 99% deuterium oxide as the Ringer solvent. Deuterium oxide also inhibits the decrease in cytoplasmic vesicles. Thus stimulation of proton secretion by turtle bladder CA cells depends to a large extent on vesicle fusion and the resultant increase in luminal surface area.

scholarly journals Anoctamin-1 affects the migration and invasion of anaplastic thyroid carcinoma cells

2019 ◽  
Vol 23 (4) ◽  
pp. 294-301 ◽  
Author(s):  
Jae-Young Kim ◽  
Hwa Young Youn ◽  
June Choi ◽  
Seung Kuk Baek ◽  
Soon Young Kwon ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Anoctamin 1

Mechanisms of acid release in isolated gas gland cells of the European eel Anguilla anguilla

1995 ◽  
Vol 269 (4) ◽  
pp. R793-R799 ◽  
Author(s):  
B. Pelster
Keyword(s):  
Carbonic Anhydrase ◽  
Disulfonic Acid ◽  
European Eel ◽  
Proton Release ◽  
Isolated Cells ◽  
Extracellular Medium ◽  
Proton Secretion ◽  
Gland Cells ◽  
Acid Release ◽  
Gas Gland

Mechanisms of acid production and of acid release have been analyzed in isolated gas gland cells of the eel swimbladder using a cytosensor microphysiometer. Incubation of isolated cells with oxamic acid caused a dose-dependent decrease in the rate of proton release. At the highest oxamic acid concentration used (20 mmol/l), proton release was reduced by approximately 40%; incubation with sodium fluoride (10 mmol/l) or removal of glucose from the extracellular medium caused 60 and 80% reduction, respectively. NaCN had little effect on proton secretion. Proton release of isolated gas gland cells was largely dependent on the extracellular sodium concentration, and this sodium effect was in part inhibitable by amiloride. A 15-20% reduction in the rate of proton secretion was observed in the presence of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, an inhibitor of anion exchange. Inhibition of mammalian H(+)-K(+)-adenosinetriphosphatase with omeprazole had no effect, whereas bafilomycin, an inhibitor of vesicular H(+)-adenosinetriphosphatase, induced a 25% reduction in proton secretion. Ethoxzolamide, a membrane-permeable inhibitor of carbonic anhydrase, caused a 60% reduction in proton secretion (inhibition constant = 54.4 nmol/l). Prontosil-dextran, a membrane-impermeable sulfonamide, also reduced the proton release, thus indicating the presence of a membrane-bound carbonic anhydrase facing the extracellular space.

Glucocorticoids regulate NHE-3 transcription in OKP cells

1996 ◽  
Vol 270 (1) ◽  
pp. F164-F169 ◽  
Author(s):  
M. Baum ◽  
M. Amemiya ◽  
V. Dwarakanath ◽  
R. J. Alpern ◽  
O. W. Moe
Keyword(s):  
Gene Transcription ◽  
Half Life ◽  
Time Course ◽  
In Vitro Transcription ◽  
Mrna Abundance ◽  
Proton Secretion ◽  
Threefold Increase ◽  
Mrna Half Life ◽  
Synthetic Glucocorticoid

OKP cells express NHE-3, an amiloride-resistant Na+/H+ antiporter, which is likely an isoform responsible for apical proton secretion by the proximal tubule. We have previously shown that an amiloride-resistant Na+/H+ antiporter in OKP cells is regulated by dexamethasone, a synthetic glucocorticoid. The purpose of the present study was to examine the mechanism for the glucocorticoid-mediated increase in Na+/H+ antiporter activity. Incubation of OKP cells with 10(-6) M dexamethasone resulted in a two- to threefold increase in NHE-3 mRNA abundance. This increase was seen after 4 h of incubation with dexamethasone, a time course similar to that found for Na+/H+ antiporter activity. To examine the mechanism for the increase in NHE-3 mRNA abundance, mRNA half-life and in vitro transcription experiments were performed. NHE-3 mRNA had a half-life of 8 h in control and dexamethasone-treated cells. The rate of in vitro transcription was 1.8-fold greater when OKP cells were treated with dexamethasone. These data suggest that the glucocorticoid-mediated increase in Na+/H+ antiporter activity is due to an increase in NHE-3 gene transcription.

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