ArticleCell regulation1990
Simultaneous analysis of cell Ca2+ and Ca2(+)-stimulated chloride conductance in colonic epithelial cells (HT-29).
Article in Cell regulation, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 54 citations in OpenAlex.
- Control of TMEM16A by INO-4995 and other inositolphosphates.British journal of pharmacology · 2013Article
- Expression of rotavirus NSP4 alters the actin network organization through the actin remodeling protein cofilin.Journal of virology · 2007Article
- Redesigning channel-forming peptides: amino acid substitutions that enhance rates of supramolecular self-assembly and raise ion transport activity.Biophysical journal · 2006Article
- Mutations in rotavirus nonstructural glycoprotein NSP4 are associated with altered virus virulence.Journal of virology · 1998Article
- The rotavirus enterotoxin NSP4 mobilizes intracellular calcium in human intestinal cells by stimulating phospholipase C-mediated inositol 1,4,5-trisphosphate production.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Calcium- and CaMKII-dependent chloride secretion induced by the microsomal Ca(2+)-ATPase inhibitor 2,5-di-(tert-butyl)-1,4-hydroquinone in cystic fibrosis pancreatic epithelial cells.The Journal of clinical investigation · 1995Article
- A non-selective cation current activated via the multifunctional Ca(2+)-calmodulin-dependent protein kinase in human epithelial cells.The Journal of physiology · 1995Article
- Ion-transporting activity in the murine colonic epithelium of normal animals and animals with cystic fibrosis.Pflugers Archiv : European journal of physiology · 1994Article
- Role of calcium in carbachol- and neurotensin-induced mucin exocytosis in a human colonic goblet cell line and cross-talk with the cyclic AMP pathway.The Biochemical journal · 1994Article
- Voltage-dependent Ca2+ influx in the epithelial cell line HT29: simultaneous use of intracellular Ca2+ measurements and nystatin perforated patch-clamp technique.Pflugers Archiv : European journal of physiology · 1994Article
- Taurodeoxycholate activates potassium and chloride conductances via an IP3-mediated release of calcium from intracellular stores in a colonic cell line (T84)The Journal of clinical investigation · 1993Article
- Activation of ion transport by combined effects of ionomycin, forskolin and phorbol ester on cultured HT-29cl.19A human colonocytes.Pflugers Archiv : European journal of physiology · 1993Article
- Cyclic AMP and Ca2+ interactions affecting epithelial chloride secretion in human cultured colonic epithelia.British journal of pharmacology · 1993Article
- Antagonism of kinin effects on epithelial by Hoe 140: apparently competitive and non-competitive interactions.British journal of pharmacology · 1992Article
- Activation of basolateral Cl- channels in the rat colonic epithelium during regulatory volume decrease.Pflugers Archiv : European journal of physiology · 1992Article
- Effect of calcitonin on the regulation of intracellular pH in primary cultures of rabbit early distal tubule.Pflugers Archiv : European journal of physiology · 1992Article
- Calcium- and cyclic-AMP-mediated secretory responses in isolated colonic crypts.Pflugers Archiv : European journal of physiology · 1991Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We used perforated patch, whole-cell current recordings and video-based fluorescence ratio imaging to monitor the relation of plasma membrane ionic conductances to intracellular free Ca2+ within individual colonic epithelial cells (HT-29). The Ca2(+)-mediated agonist, neurotensin, activated K+ and Cl- conductances that showed different sensitivities to [Ca2+]i. The Cl- conductance was sensitive to increases or decreases in [Ca2+]i around the resting value of 76 +/- 32 (mean +/- SD) nM (n = 46), whereas activation of the K+ conductance required at least a 10-fold rise in [Ca2+]i. Neurotensin increased [Ca2+]i by stimulating a transient intracellular Ca2+ release, which was followed by a sustained rise in [Ca2+]i due to Ca2+ influx from the bath. The onset of the initial [Ca2+]i transient, monitored at a measurement window over the cell interior, lagged behind the rise in Cl- current during agonist stimulation. This lag was not present when the [Ca2+]i rise was due to Ca2+ entry from the bath, induced either by the agonist or by the Ca2+ ionophore ionomycin. The temporal differences in [Ca2+]i and Cl- current during the agonist-induced [Ca2+]i transient can be explained by a localized Ca2+ release from intracellular stores in the vicinity of the plasma membrane Cl- channel. Chloride currents recover toward basal values more rapidly than [Ca2+]i after the agonist-induced [Ca2+]i transient, and, during a sustained neurotensin-induced [Ca2+]i rise, Cl- currents inactivate. These findings suggest that an inhibitory pathway limits the increase in Cl- conductance that can be evoked by agonist. Because this Cl- current inhibition is not observed during a sustained [Ca2+]i rise induced by ionomycin, the inhibitory pathway may be mediated by another agonist-induced messenger, such as diacylglycerol.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.