Evidence map›Paper›PMID 8568853›Full record

ArticleThe Journal of membrane biology1995

Volume-activated chloride currents in pancreatic duct cells.

B Verdon, J P Winpenny, K J Whitfield, B E Argent, M A Gray

Abstract read
PubMed Publisher
In one paragraph

Article in The Journal of membrane biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Involvement of stretch-activated Cl- channels in ramification of murine microglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  13. Mitogen-activated protein and tyrosine kinases in the activation of astrocyte volume-activated chloride current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  14. Autocrine signaling through ATP release represents a novel mechanism for cell volume regulation.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Article
  15. Review
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

B VerdonDepartment of Physiological Sciences, University Medical School, Newcastle upon Tyne, UK.
J P Winpenny
K J Whitfield
B E Argent
M A Gray

Funding

ANION CONDUCTANCES IN DUCTAL EPITHELIAL CELLS AND CFR01DK043956 · NIDDK · UNIVERSITY OF NEWCASTLE · PI GRAY, MICHAEL · 1991 to 1993
–
NIDDK NIH HHS DK 43956
6 · The paper itself

Abstract

We have used the patch clamp technique to study volume-activated Cl- currents in the bicarbonate-secreting pancreatic duct cell. These currents could be elicited by a hypertonic pipette solution (osmotic gradient 20 mOsm/l), developed over about 8 min to a peak value of 91 +/- 5.8 pA/pF at 60 mV (n = 123), and were inhibited by a hypertonic bath solution. The proportion of cells which developed currents increased from 15% in freshly isolated ducts to 93% if the ducts were cultured for 2 days. The currents were ATP-dependent, had an outwardly rectifying current/voltage (I-V) plot, and displayed time-dependent inactivation at depolarizing potentials. The anion selectivity sequence was: ClO4 = I = SCN > Br = NO3 > Cl > F > HCO3 > gluconate, and the currents were inhibited to a variable extent by DIDS, NPPB, dideoxyforskolin, tamoxifen, verapamil and quinine. Increasing the intracellular Ca2+ buffering capacity, or lowering the extracellular Ca2+ concentration, reduced the proportion of duct cells which developed currents. However, removal of extracellular Ca2+ once the currents had developed was without effect. Inhibiting protein kinase C (PKC) with either the pseudosubstrate PKC (19-36), calphostin C or staurosporine completely blocked development of the currents. We speculate that cell swelling causes Ca2+ influx which activates PKC which in turn either phosphorylates the Cl- channel or a regulatory protein leading to channel activation.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAdenosine TriphosphateAnimalsAnionsCalciumCell SizeChloride ChannelsChloridesIn Vitro TechniquesIon TransportMembrane PotentialsPancreatic DuctsPhosphorylationProtein Kinase CRatsRats, Wistar4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAdenosine TriphosphateAnionsCalciumChloride ChannelsChloridesProtein Kinase C

Identifiers

PMID8568853
OpenAlexW2047184821

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.