Evidence map›Paper›PMID 18755741›Full record

ArticleThe Journal of physiology2008

Internalized Kv1.5 traffics via Rab-dependent pathways.

Alireza Dehghani Zadeh, Hongjian Xu, Matthew E Loewen, Geoffrey P Noble, David F Steele, David Fedida

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 14% 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, 48 citations in OpenAlex.

  1. Rab10 plays a protective role in the development of pathological cardiac hypertrophy.Journal of molecular and cellular cardiology plus · 2025
    Article
  2. Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022
    Review
  3. KInternational journal of molecular sciences · 2021
    Article
  4. Review
  5. Article
  6. Fluvastatin inhibits Rab5-mediated IKs internalization caused by chronic CaJournal of molecular and cellular cardiology · 2019
    Article
  7. Article
  8. Article
  9. Angiotensin II reduces the surface abundance of KThe Journal of physiology · 2017
    Article
  10. Article
  11. Article
  12. Shear stress triggers insertion of voltage-gated potassium channels from intracellular compartments in atrial myocytes.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  13. Article
  14. Article
  15. Trafficking of an endogenous potassium channel in adult ventricular myocytes.American journal of physiology. Cell physiology · 2012
    Article
  16. Novel molecular targets for atrial fibrillation therapy.Nature reviews. Drug discovery · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. Rab11 supports amphetamine-stimulated norepinephrine transporter trafficking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Alireza Dehghani ZadehDepartment of Anaesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada.
Hongjian Xu
Matthew E Loewen
Geoffrey P Noble
David F Steele
David Fedida
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Little is known about the postinternalization trafficking of surface-expressed voltage-gated potassium channels. Here, for the first time, we investigate into which of four major trafficking pathways a voltage-gated potassium channel is targeted after internalization. In both a cardiac myoblast cell line and in HEK293 cells, channels were found to internalize and to recycle quickly. Upon internalization, Kv1.5 rapidly associated with Rab5-and Rab4-positive endosomes, suggesting that the channel is internalized via a Rab5-dependent pathway and rapidly targeted for recycling to the plasma membrane. Nevertheless, as indicated by colocalization with Rab7, a fraction of the channels are targeted for degradation. Recycling through perinuclear endosomes is limited; colocalization with Rab11 was evident only after 24 h postsurface labelling. Expression of dominant negative (DN) Rab constructs significantly increased Kv1.5 functional expression. In the myoblast line, Rab5DN increased Kv1.5 current densities to 1305 +/- 213 pA pF(-1) from control 675 +/- 81.6 pA pF(-1). Rab4DN similarly increased Kv1.5 currents to 1382 +/- 155 pA pF(-1) from the control 522 +/- 82.7 pA pF(-1) at +80 mV. Expression of the Rab7DN increased Kv1.5 currents 2.5-fold in HEK293 cells but had no significant effect in H9c2 myoblasts, and, unlike the other Rab GTPases tested, over-expression of wild-type Rab7 decreased Kv1.5 currents in the myoblast line. Densities fell to 573 +/- 96.3 pA pF(-1) from the control 869 +/- 135.5 pA pF(-1). The Rab11DN was slow to affect Kv1.5 currents but had comparable effects to other dominant negative constructs after 48 h. With the exception of Rab11DN and nocodazole, the effects of interference with microtubule-dependent trafficking by nocodazole or p50 overexpression were not additive with the Rab dominant negatives. The Rab GTPases thus constitute dynamic targets by which cells may modulate Kv1.5 functional expression.

Indexed as

Cell LineHumansIon Channel GatingKidneyKv1.5 Potassium ChannelMyocytes, CardiacProtein Transportrab GTP-Binding ProteinsSignal TransductionKv1.5 Potassium Channelrab GTP-Binding Proteins

Identifiers

PMID18755741
PMCPMC2614053
OpenAlexW1510126127

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.