Evidence map›Paper›PMID 24981229›Full record

ArticleThe Journal of general physiology2014

Determinants of ligand selectivity in a cyclic nucleotide-regulated potassium channel.

João Pessoa, Fátima Fonseca, Simone Furini, João H Morais-Cabral

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 45% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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

4 authors at 3 institutions in 3 countries.

João PessoaInstituto de Biologia Molecular e Celular and Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4150-180 Porto, PortugalInstituto de Biologia Molecular e Celular and Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4150-180 Porto, Portugal.
Fátima FonsecaInstituto de Biologia Molecular e Celular and Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4150-180 Porto, Portugal.
Simone FuriniDepartment of Medical Biotechnologies, University of Siena, 53100 Siena, Italy.
João H Morais-CabralInstituto de Biologia Molecular e Celular and Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4150-180 Porto, Portugal jcabral@ibmc.up.pt.
Universidade do Porto · PTInstituto de Biologia Molecular e CelularUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclic nucleotide-binding (CNB) domains regulate the activity of channels, kinases, exchange factors, and transcription factors. These proteins are highly variable in their ligand selectivity; some are highly selective for either cAMP or cGMP, whereas others are not. Several molecular determinants of ligand selectivity in CNB domains have been defined, but these do not provide a complete view of the selectivity mechanism. We performed a thorough analysis of the ligand-binding properties of mutants of the CNB domain from the MlotiK1 potassium channel. In particular, we defined which residues specifically favor cGMP or cAMP. Inversion of ligand selectivity, from favoring cAMP to favoring cGMP, was only achieved through a combination of three mutations in the ligand-binding pocket. We determined the x-ray structure of the triple mutant bound to cGMP and performed molecular dynamics simulations and a biochemical analysis of the effect of the mutations. We concluded that the increase in cGMP affinity and selectivity does not result simply from direct interactions between the nucleotide base and the amino acids introduced in the ligand-binding pocket residues. Rather, tighter cGMP binding over cAMP results from the polar chemical character of the mutations, from greater accessibility of water molecules to the ligand in the bound state, and from an increase in the structural flexibility of the mutated binding pocket.

Indexed as

AnimalsCell LineCyclic AMPCyclic GMPLigandsPotassium ChannelsProtein BindingProtein Structure, SecondaryCyclic AMPCyclic GMPLigandsPotassium Channels

Identifiers

PMID24981229
PMCPMC4076524
OpenAlexW2078118004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.