Evidence map›Paper›PMID 14638933›Full record

ArticleThe Journal of general physiology2003

Pseudechetoxin binds to the pore turret of cyclic nucleotide-gated ion channels.

R Lane Brown, Leatha L Lynch, Tammie L Haley, Reza Arsanjani

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Interplay between PIP3 and calmodulin regulation of olfactory cyclic nucleotide-gated channels.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  11. Review
  12. 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 1 institution in 1 country.

R Lane BrownNeurological Sciences Institute, OHSU West Campus 505 NW 185th Avenue, Beaverton, OR 97006, USA. brownla@ohsu.edu
Leatha L Lynch
Tammie L Haley
Reza Arsanjani
Oregon Health & Science University · US

Funding

DISSECTING ROD CNG CHANNEL FUNCTION WITH PSEUDECHETOXINR01EY012837 · NEI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI BROWN, RONALD LANE · 2001 to 2003
$952k
NEI NIH HHS EY 12,837NEI NIH HHS R01 EY012837
6 · The paper itself

Abstract

Peptide toxins are invaluable tools for studying the structure and physiology of ion channels. Pseudechetoxin (PsTx) is the first known peptide toxin that targets cyclic nucleotide-gated (CNG) ion channels, which play a critical role in sensory transduction in the visual and olfactory systems. PsTx inhibited channel currents at low nM concentrations when applied to the extracellular face of membrane patches expressing olfactory CNGA2 subunits. Surprisingly, 500 nM PsTx did not inhibit currents through channels formed by the CNGA3 subunit from cone photoreceptors. We have exploited this difference to identify the PsTx-binding site on the extracellular face of CNG channels. Studies using chimeric channels revealed that transplantation of the pore domain from CNGA2 was sufficient to confer high affinity PsTx binding upon a CNGA3 background. To further define the binding site, reciprocal mutations were made at 10 nonidentical amino acid residues in this region. We found that two residues in CNGA2, D316 and Y321, were essential for high-affinity inhibition by PsTx. Furthermore, replacement of both residues was required to confer high-affinity PsTx inhibition upon CNGA3. Several other residues, including E325, also form favorable interactions with PsTx. In the CNGA2-E325K mutant, PsTx affinity was reduced by approximately 5-fold to 120 nM. An electrostatic interaction with D316 does not appear to be the primary determinant of PsTx affinity, as modification of the D316C mutant with a negatively charged methanethiosulfonate reagent did not restore high affinity inhibition. The residues involved in PsTx binding are found within the pore turret and helix, in similar positions to residues that form the receptor for pore-blocking toxins in voltage-gated potassium channels. Furthermore, biophysical properties of PsTx block, including an unfavorable interaction with permeant ions, also suggest that it acts as a pore blocker. In summary, PsTx seems to occlude the entrance to the pore by forming high-affinity contacts with the pore turret, which may be larger than that found in the KcsA structure.

Indexed as

Snake VenomsAmino Acid SequenceAnimalsBinding SitesCell LineCyclic Nucleotide-Gated Cation ChannelsDose-Response Relationship, DrugElapid VenomsHumansIon Channel GatingIon ChannelsMolecular Sequence DataCyclic Nucleotide-Gated Cation ChannelsElapid VenomsIon Channelspseudechetoxin, Pseudechis australisPseudechis venomSnake Venoms

Identifiers

PMID14638933
PMCPMC2229597
OpenAlexW2125409836

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.