Evidence map›Paper›PMID 22887933›Full record

ReviewChemMedChem2012

Trafficking of intermediate (KCa3.1) and small (KCa2.x) conductance, Ca(2+)-activated K(+) channels: a novel target for medicinal chemistry efforts?

Corina M Balut, Kirk L Hamilton, Daniel C Devor

Abstract readReview
In one paragraph

Review in ChemMedChem, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Dynamic coupling between TRPV4 and CaAmerican journal of physiology. Renal physiology · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. PKA reduces the rat and human KCa3.1 current, CaM binding, and Ca2+ signaling, which requires Ser332/334 in the CaM-binding C terminus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  19. Article
  20. Review
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 2 countries.

Corina M BalutDepartment of Cell Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Kirk L Hamilton
Daniel C Devor
University of Pittsburgh · USUniversity of Otago · NZ

Funding

Assembly and Trafficking of IK1 and SK3 in EndotheliaR01HL092157 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVOR, DANIEL C · 2009 to 2012
$1.5M
Oxidation and Pharmacologic Activation of IK/SK ChannelsR01HL083060 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEVOR, DANIEL C · 2006 to 2009
$1.4M
NHLBI NIH HHS HL083060NHLBI NIH HHS HL092157NHLBI NIH HHS R01 HL083060NHLBI NIH HHS R01 HL092157
6 · The paper itself

Abstract

Ca(2+)-activated K(+) (KCa) channels play a pivotal role in the physiology of a wide variety of tissues and disease states, including vascular endothelia, secretory epithelia, certain cancers, red blood cells (RBC), neurons, and immune cells. Such widespread involvement has generated an intense interest in elucidating the function and regulation of these channels, with the goal of developing pharmacological strategies aimed at selective modulation of KCa channels in various disease states. Herein we give an overview of the molecular and functional properties of these channels and their therapeutic importance. We discuss the achievements made in designing pharmacological tools that control the function of KCa channels by modulating their gating properties. Moreover, this review discusses the recent advances in our understanding of KCa channel assembly and anterograde trafficking toward the plasma membrane, the micro-domains in which these channels are expressed within the cell, and finally the retrograde trafficking routes these channels take following endocytosis. As the regulation of intracellular trafficking by agonists as well as the protein-protein interactions that modify these events continue to be explored, we anticipate this will open new therapeutic avenues for the targeting of these channels based on the pharmacological modulation of KCa channel density at the plasma membrane.

Indexed as

AnimalsCalmodulinChemistry, PharmaceuticalCystic Fibrosis Transmembrane Conductance RegulatorHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsPotassium Channel BlockersSmall-Conductance Calcium-Activated Potassium ChannelsCalmodulinCystic Fibrosis Transmembrane Conductance RegulatorIntermediate-Conductance Calcium-Activated Potassium ChannelsKCNN4 protein, humanPotassium Channel BlockersSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID22887933
PMCPMC3455125
OpenAlexW1967333038

What OpenQuestion holds

Textmetadata
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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.