Evidence map›Paper›PMID 7603835›Full record

ArticlePflugers Archiv : European journal of physiology1995

Physiological and molecular characterization of an IRK-type inward rectifier K+ channel in a tumour mast cell line.

E Wischmeyer, K U Lentes, A Karschin

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 69 citations in OpenAlex.

  1. Triclosan disrupts immune cell function by depressing CaToxicology and applied pharmacology · 2020
    Article
  2. Channels (Austin, Tex.) · 2019
    Article
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  9. Differential distribution and function of hyperpolarization-activated channels in sensory neurons and mechanosensitive fibers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  10. Article
  11. Distinct properties of CRAC and MIC channels in RBL cells.The Journal of general physiology · 2002
    Article
  12. Article
  13. Neuronal inwardly rectifying K(+) channels differentially couple to PDZ proteins of the PSD-95/SAP90 family.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  14. Article
  15. The epithelial inward rectifier channel Kir7.1 displays unusual K+ permeation properties.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  16. Inwardly rectifying potassium (IRK) currents are correlated with IRK subunit expression in rat nucleus accumbens medium spiny neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  17. Kir2.4: a novel K+ inward rectifier channel associated with motoneurons of cranial nerve nuclei.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
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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

3 authors at 2 institutions in 1 country.

E WischmeyerMax-Planck-Institute for Biophysical Chemistry, Göttingen, Germany.
K U Lentes
A Karschin
Max Planck Institute for Biophysical Chemistry · DEMax Planck Society · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The basophilic leucaemia cell line RBL-2H3 exhibits a robust inwardly rectifying potassium current, IKIR, which is likely to be modulated by G proteins. We examined the physiological and molecular properties of this KIR conductance to define the nature of the underlying channel species. The macroscopic conductance revealed characteristics typical of classical K+ inward rectifiers of the IRK type. Channel gating was rapid, first order (tau approximately 1 ms at -100 mV) and steeply voltage dependent. Both activation potential and slope conductance were dependent on extracellular K+ concentration ([K+]o) and inward rectification persisted in the absence of internal Mg2+. The current was susceptible to a concentration- and voltage-dependent block by extracellular Na+, Cs+ and Ba2+. Initial IKIR whole-cell amplitudes as well as current rundown were dependent on the presence of 1 mM internal ATP. Perfusion of intracellular guanosine 5'-Q-(3-thiotriphosphate) (GTP[gamma S]) suppressed IKIR with an average half-time of decline of approximately 400 s. It was demonstrated that the dominant IRK-type 25 pS conductance channel was indeed suppressed by 100 microM preloaded GTP[gamma S]. Reverse transcriptase-polymerase chain reactions (RT-PCR) with RBL cell poly(A)+ RNA identified a full length K+ inward rectifier with 94% base pair homology to the recently cloned mouse IRK1 channel. It is concluded that RBL cells express a classical voltage-dependent IRK-type K+ inward rectifier RBL-IRK1 which is negatively controlled by G proteins.

Indexed as

Adenosine TriphosphateAmino Acid SequenceAnimalsBariumBase SequenceCesiumEdetic AcidElectric ConductivityGuanosine 5'-O-(3-Thiotriphosphate)Ion Channel GatingKineticsLeukemia, Basophilic, AcuteMagnesiumMast CellsMolecular Sequence DataPolymerase Chain ReactionAdenosine TriphosphateBariumCesiumEdetic AcidGuanosine 5'-O-(3-Thiotriphosphate)MagnesiumPotassiumPotassium ChannelsSodium

Identifiers

PMID7603835
OpenAlexW2046768627

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.