Evidence map›Paper›PMID 25944904›Full record

ArticleThe Journal of biological chemistry2015

Role of Dynamics in the Autoinhibition and Activation of the Hyperpolarization-activated Cyclic Nucleotide-modulated (HCN) Ion Channels.

Bryan VanSchouwen, Madoka Akimoto, Maryam Sayadi, Federico Fogolari, Giuseppe Melacini

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

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  10. Mechanism of cAMP Partial Agonism in Protein Kinase G (PKG).The Journal of biological chemistry · 2015
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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 2 institutions in 2 countries.

Bryan VanSchouwenDepartments of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario L8S 4M1, Canada.
Madoka AkimotoDepartments of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario L8S 4M1, Canada.
Maryam SayadiDepartments of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario L8S 4M1, Canada.
Federico FogolariDepartment of Biomedical Science and Technology, University of Udine, Piazzale Kolbe 4, 33100 Udine, Italy.
Giuseppe MelaciniDepartments of Chemistry and Chemical Biology, McMaster University, Hamilton, Ontario L8S 4M1, Canada; Departments of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario L8S 4M1, Canada. Electronic address: melacin@mcmaster.ca.
McMaster University · CAUniversity of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hyperpolarization-activated cyclic nucleotide-modulated (HCN) ion channels control rhythmicity in neurons and cardiomyocytes. Cyclic AMP allosterically modulates HCN through the cAMP-dependent formation of a tetrameric gating ring spanning the intracellular region (IR) of HCN, to which cAMP binds. Although the apo versus holo conformational changes of the cAMP-binding domain (CBD) have been previously mapped, only limited information is currently available on the HCN IR dynamics, which have been hypothesized to play a critical role in the cAMP-dependent gating of HCN. Here, using molecular dynamics simulations validated and complemented by experimental NMR and CD data, we comparatively analyze HCN IR dynamics in the four states of the thermodynamic cycle arising from the coupling between cAMP binding and tetramerization equilibria. This extensive set of molecular dynamics trajectories captures the active-to-inactive transition that had remained elusive for other CBDs, and it provides unprecedented insight on the role of IR dynamics in HCN autoinhibition and its release by cAMP. Specifically, the IR tetramerization domain becomes more flexible in the monomeric states, removing steric clashes that the apo-CDB structure would otherwise impose. Furthermore, the simulations reveal that the active/inactive structural transition for the apo-monomeric CBD occurs through a manifold of pathways that are more divergent than previously anticipated. Upon cAMP binding, these pathways become disallowed, pre-confining the CBD conformational ensemble to a tetramer-compatible state. This conformational confinement primes the IR for tetramerization and thus provides a model of how cAMP controls HCN channel gating.

Indexed as

Cyclic AMPHumansHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMolecular Dynamics SimulationMuscle ProteinsPotassium ChannelsProtein ConformationProtein MultimerizationThermodynamicsCyclic AMPHCN4 protein, humanHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMuscle ProteinsPotassium Channelsallosteric regulationcAMPcell signalinggatingHCNmolecular dynamicsnuclear magnetic resonance (NMR)

Identifiers

PMID25944904
PMCPMC4505013
OpenAlexW1857393839

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.