Evidence map›Paper›PMID 21363929›Full record

ArticleMolecular pharmacology2011

Negative gating modulation by (R)-N-(benzimidazol-2-yl)-1,2,3,4-tetrahydro-1-naphthylamine (NS8593) depends on residues in the inner pore vestibule: pharmacological evidence of deep-pore gating of K(Ca)2 channels.

David Paul Jenkins, Dorte Strøbæk, Charlotte Hougaard, Marianne L Jensen, Rene Hummel, Ulrik S Sørensen, Palle Christophersen, Heike Wulff

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  3. KJournal of neuroscience research · 2023
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  5. KCurrent neuropharmacology · 2023
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  17. Identity and function of a cardiac mitochondrial small conductance CaBiochimica et biophysica acta. Bioenergetics · 2017
    Article
  18. Molecular mechanisms of Slo2 KThe Journal of physiology · 2017
    Article
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

David Paul JenkinsDepartment of Pharmacology, University of California, Davis, CA 95616, USA.
Dorte Strøbæk
Charlotte Hougaard
Marianne L Jensen
Rene Hummel
Ulrik S Sørensen
Palle Christophersen
Heike Wulff
NeuroSearch (Denmark) · DKUniversity of California, Davis · US

Funding

UC DAVIS CLINICAL AND TRANSLATIONAL SCIENCE CENTER: BPCAUL1RR024146 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2006 to 2011
$27.0M
Optimization of KCa2 Channel Activators as Neuroscience Tools and Potential DrugsR21NS072585 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2011 to 2012
$440k
NCRR NIH HHS UL1 RR024146NCRR NIH HHS UL1-RR024146NINDS NIH HHS R21 NS072585
6 · The paper itself

Abstract

Acting as a negative gating modulator, (R)-N-(benzimidazol-2-yl)-1,2,3,4-tetrahydro-1-naphthylamine (NS8593) shifts the apparent Ca(2+)-dependence of the small-conductance Ca(2+)-activated K(+) channels K(Ca)2.1-2.3 to higher Ca(2+) concentrations. Similar to the positive K(Ca) channel-gating modulators 1-ethyl-2-benzimidazolinone (1-EBIO) and cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methylpyrimidin-4-yl]-amine (CyPPA), the binding site for NS8593 has been assumed to be located in the C-terminal region, in which these channels interact with their Ca(2+) sensor calmodulin. However, by using a progressive chimeric approach, we were able to localize the site-of-action of NS8593 to the K(Ca)2 pore. For example, when we transferred the C terminus from the NS8593-insensitive intermediate-conductance K(Ca)3.1 channel to K(Ca)2.3, the chimeric channel remained as sensitive to NS8593 as wild-type K(Ca)2.3. In contrast, when we transferred the K(Ca)2.3 pore to K(Ca)3.1, the channel became sensitive to NS8593. Using site-directed mutagenesis, we subsequently identified two specific residues in the inner vestibule of K(Ca)2.3 (Ser507 and Ala532) that determined the effect of NS8593. Mutation of these residues to the corresponding residues in K(Ca)3.1 (Thr250 and Val275) made K(Ca)2.3 insensitive to NS8593, whereas introduction of serine and alanine into K(Ca)3.1 was sufficient to render this channel highly sensitive to NS8593. It is noteworthy that the same two residue positions have been found previously to mediate sensitivity of K(Ca)3.1 to clotrimazole and 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34). The location of Ser507 in the pore-loop near the selectivity filter and Ala532 in an adjacent position in S6 are within the region predicted to contain the K(Ca)2 channel gate. Hence, we propose that NS8593-mediated gating modulation occurs via interaction with gating structures at a position deep within the inner pore vestibule.

Indexed as

1-NaphthylamineAmino Acid SequenceBase SequenceCell LineDNA PrimersHumansIon Channel GatingMolecular Sequence DataPatch-Clamp TechniquesSequence Homology, Amino AcidSmall-Conductance Calcium-Activated Potassium Channels1-NaphthylamineDNA Primers(R)-N-(benzimidazol-2-yl)-1,2,3,4-tetrahydro-1-naphthylamineSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID21363929
PMCPMC3102549
OpenAlexW2158980611

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.