Evidence map›Paper›PMID 17596331›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2007

PKA phosphorylation of SUR2B subunit underscores vascular KATP channel activation by beta-adrenergic receptors.

Yun Shi, Zhongying Wu, Ningren Cui, Weiwei Shi, Yang Yang, Xiaoli Zhang, Asheebo Rojas, Binh T Ha, Chun Jiang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. [Exogenous nitric oxide suppresses KSheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026
    Article
  3. Article
  4. Electro-metabolic signaling.The Journal of general physiology · 2024
    Article
  5. Rapid Characterization of the Functional and Pharmacological Consequences of Cantú Syndrome KThe Journal of pharmacology and experimental therapeutics · 2023
    Article
  6. KAmerican journal of physiology. Cell physiology · 2022
    Review
  7. Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022
    Review
  8. Review
  9. The Pharmacology of ATP-Sensitive KHandbook of experimental pharmacology · 2021
    Article
  10. The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020
    Review
  11. Alterations of ATP-sensitive KPflugers Archiv : European journal of physiology · 2018
    Article
  12. Frontiers in pharmacology · 2018
    Article
  13. Article
  14. Review
  15. Review
  16. KATP Channels in the Cardiovascular System.Physiological reviews · 2016
    Review
  17. Article
  18. 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

9 authors at 1 institution in 1 country.

Yun ShiDepartment of Biology, Georgia State University, 24 Peachtree Center Ave., Atlanta, GA 30302, USA.
Zhongying Wu
Ningren Cui
Weiwei Shi
Yang Yang
Xiaoli Zhang
Asheebo Rojas
Binh T Ha
Chun Jiang
Georgia State University · US

Funding

Vascular KATP Channel Modulation in Hypercapnic AcidosisR01HL067890 · NHLBI · GEORGIA STATE UNIVERSITY · PI JIANG, CHUN · 2003 to 2006
$1.2M
NHLBI NIH HHS HL 067890NHLBI NIH HHS R01 HL067890
6 · The paper itself

Abstract

ATP-sensitive K(+) (K(ATP)) channels are activated by several vasodilating hormones and neurotransmitters through the PKA pathway. Here, we show that phosphorylation at Ser1387 of the SUR2B subunit is critical for the channel activation. Experiments were performed in human embryonic kidney (HEK) 293 cells expressing the cloned Kir6.1/SUR2B channel. In whole cell patch, the Kir6.1/SUR2B channel activity was stimulated by isoproterenol via activation of beta(2) receptors. This effect was blocked in the presence of inhibitors for adenylyl cyclase or PKA. Similar channel activation was seen by exposing inside-out patches to the catalytic subunit of PKA. Because none of the previously suggested PKA phosphorylation sites accounted for the channel activation, we performed systematic mutational analysis on Kir6.1 and SUR2B. Two serine residues (Ser1351, Ser1387) located in the NBD2 of SUR2B were critical for the channel activation. In vitro phosphorylation experiments showed that Ser1387 but not Ser1351 was phosphorylated by PKA. The PKA-dependent activation of cell-endogenous K(ATP) channels was observed in acutely dissociated mesenteric smooth myocytes and isolated mesenteric artery rings, where activation of these channels contributed significantly to the isoproterenol-induced vasodilation. Taken together, these results indicate that the Kir6.1/SUR2B channel is a target of beta(2) receptors and that the channel activation relies on PKA phosphorylation of SUR2B at Ser1387.

Indexed as

Adrenergic beta-AgonistsAmino Acid SequenceAnimalsATP-Binding Cassette TransportersBlood VesselsCell LineColforsinCyclic AMP-Dependent Protein KinasesHumansIn Vitro TechniquesIsoproterenolMolecular Sequence DataMuscle, Smooth, VascularPatch-Clamp TechniquesPhosphorylationPotassium ChannelsAdrenergic beta-AgonistsATP-Binding Cassette TransportersColforsinCyclic AMP-Dependent Protein KinasesIsoproterenolmitochondrial K(ATP) channelPotassium ChannelsPotassium Channels, Inwardly RectifyingReceptors, Adrenergic, betaReceptors, DrugSulfonylurea Receptors

Identifiers

PMID17596331
PMCPMC2258221
OpenAlexW2000007129

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.