Evidence map›Paper›PMID 21525363›Full record

ArticleJournal of neurophysiology2011

Optogenetic photochemical control of designer K+ channels in mammalian neurons.

Doris L Fortin, Timothy W Dunn, Alexis Fedorchak, Duane Allen, Rachel Montpetit, Matthew R Banghart, Dirk Trauner, John P Adelman, Richard H Kramer

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Modular architecture of KEMBO reports · 2025
    Review
  3. Development of covalent chemogenetic KCell chemical biology · 2024
    Article
  4. Development of covalent chemogenetic KbioRxiv : the preprint server for biology · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Reversible Photocontrolled Nanopore Assembly.Journal of the American Chemical Society · 2019
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

9 authors at 3 institutions in 2 countries.

Doris L FortinDepartment of Molecular and Cell Biology, University of California, Berkeley, California 94720-3200, USA.
Timothy W Dunn
Alexis Fedorchak
Duane Allen
Rachel Montpetit
Matthew R Banghart
Dirk Trauner
John P Adelman
Richard H Kramer
University of California, Berkeley · USVollum Institute · USLudwig-Maximilians-Universität München · DE

Funding

NDC for the Optical Control of Biological FunctionPN2EY018241 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI ISACOFF, EHUD · 2006 to 2015
$37.5M
Light-activated ion chanenls for remote control of neuronal activityR01EY018957 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI KRAMER, RICHARD H · 2008 to 2011
$1.6M
A universal photoswitch system for optical control of neuronal receptorsR01MH088484 · NIMH · UNIVERSITY OF CALIFORNIA BERKELEY · PI KRAMER, RICHARD H · 2009 to 2012
$1.2M
NEI NIH HHS EY-018957NEI NIH HHS PN2 EY018241NEI NIH HHS PN2-EY-018241NIMH NIH HHS MH-088484NIMH NIH HHS R01 MH088484
6 · The paper itself

Abstract

Currently available optogenetic tools, including microbial light-activated ion channels and transporters, are transforming systems neuroscience by enabling precise remote control of neuronal firing, but they tell us little about the role of indigenous ion channels in controlling neuronal function. Here, we employ a chemical-genetic strategy to engineer light sensitivity into several mammalian K(+) channels that have different gating and modulation properties. These channels provide the means for photoregulating diverse electrophysiological functions. Photosensitivity is conferred on a channel by a tethered ligand photoswitch that contains a cysteine-reactive maleimide (M), a photoisomerizable azobenzene (A), and a quaternary ammonium (Q), a K(+) channel pore blocker. Using mutagenesis, we identify the optimal extracellular cysteine attachment site where MAQ conjugation results in pore blockade when the azobenzene moiety is in the trans but not cis configuration. With this strategy, we have conferred photosensitivity on channels containing Kv1.3 subunits (which control axonal action potential repolarization), Kv3.1 subunits (which contribute to rapid-firing properties of brain neurons), Kv7.2 subunits (which underlie "M-current"), and SK2 subunits (which are Ca(2+)-activated K(+) channels that contribute to synaptic responses). These light-regulated channels may be overexpressed in genetically targeted neurons or substituted for native channels with gene knockin technology to enable precise optopharmacological manipulation of channel function.

Indexed as

Photochemical ProcessesProtein EngineeringAmino Acid SequenceAzo CompoundsHEK293 CellsHumansIon Channel GatingKCNQ2 Potassium ChannelKv1.3 Potassium ChannelMaleimidesMolecular Sequence DataNeuronsPotassium Channels, Calcium-ActivatedQuaternary Ammonium CompoundsazobenzeneAzo CompoundsKCNQ2 Potassium ChannelKv1.3 Potassium ChannelmaleimideMaleimidesPotassium Channels, Calcium-ActivatedQuaternary Ammonium Compounds

Identifiers

PMID21525363
PMCPMC3129715
OpenAlexW2094154412

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.