Evidence map›Paper›PMID 18768480›Full record

ArticleThe Journal of biological chemistry2008

Novel mechanism for suppression of hyperpolarization-activated cyclic nucleotide-gated pacemaker channels by receptor-like tyrosine phosphatase-alpha.

Jianying Huang, Aijie Huang, Qi Zhang, Yen-Chang Lin, Han-Gang Yu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.8field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. PP2 prevents β-adrenergic stimulation of cardiac pacemaker activity.Journal of cardiovascular pharmacology · 2014
    Article
  8. Article
  9. Defective calcium inactivation causes long QT in obese insulin-resistant rat.American journal of physiology. Heart and circulatory physiology · 2012
    Article
  10. Article
  11. Downregulation of dendritic HCN channel gating in epilepsy is mediated by altered phosphorylation signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  12. Inactivation of L-type calcium channel modulated by HCN2 channel.American journal of physiology. Cell physiology · 2010
    Article
  13. Article
  14. Non-proteolytic HCN2 in the heart.The Journal of biological chemistry · 2009
    Article
  15. Article
  16. Article
  17. Article
  18. 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

5 authors at 1 institution in 1 country.

Jianying HuangCenter for Interdisciplinary Research in Cardiovascular Sciences, Department of Physiology and Pharmacology, West Virginia University School of Medicine, Morgantown, West Virginia 26506, USA.
Aijie Huang
Qi Zhang
Yen-Chang Lin
Han-Gang Yu
West Virginia University · US

Funding

Tyrosine Phosphorylation Mechanism of Pacemaker ChannelsR01HL075023 · NHLBI · WEST VIRGINIA UNIVERSITY · PI YU, HAN-GANG · 2004 to 2007
$1.2M
NHLBI NIH HHS HL075023NHLBI NIH HHS R01 HL075023
6 · The paper itself

Abstract

We have previously reported an important role of increased tyrosine phosphorylation activity by Src in the modulation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. Here we provide evidence showing a novel mechanism of decreased tyrosine phosphorylation on HCN channel properties. We found that the receptor-like protein-tyrosine phosphatase-alpha (RPTPalpha) significantly inhibited or eliminated HCN2 channel expression in HEK293 cells. Biochemical evidence showed that the surface expression of HCN2 was remarkably reduced by RPTPalpha, which was in parallel to the decreased tyrosine phosphorylation of the channel protein. Confocal imaging confirmed that the membrane surface distribution of the HCN2 channel was inhibited by RPTPalpha. Moreover, we detected the presence of RPTPalpha proteins in cardiac ventricles with expression levels changed during development. Inhibition of tyrosine phosphatase activity by phenylarsine oxide or sodium orthovanadate shifted ventricular hyperpolarization-activated current (I(f), generated by HCN channels) activation from nonphysiological voltages into physiological voltages associated with accelerated activation kinetics. In conclusion, we showed a critical role RPTPalpha plays in HCN channel function via tyrosine dephosphorylation. These findings are also important to neurons where HCN and RPTPalpha are richly expressed.

Indexed as

Gene Expression RegulationAnimalsArsenicalsCell LineDNA, ComplementaryGlycosylationHumansMiceMicroscopy, ConfocalModels, BiologicalNeuronsPhosphorylationRatsReceptor Protein-Tyrosine KinasesVanadatesArsenicalsDNA, ComplementaryoxophenylarsineReceptor Protein-Tyrosine KinasesRyk protein, mouseVanadates

Identifiers

PMID18768480
PMCPMC2573077
OpenAlexW2079037835

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.