ArticleBritish journal of pharmacology2017
Modulation of K
Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Intracellular Binding of Terfenadine Competes with Its Access to Pancreatic ß-cell ATP-Sensitive KThe Journal of membrane biology · 2023Article
- Pharmacological activation of the hERG KJournal of arrhythmia · 2022Review
- Cardiac hERG KHandbook of experimental pharmacology · 2021Article
- Modulation of hERG potassium channels by a novel small molecule activator.British journal of pharmacology · 2017Article
- Modulation of KBritish journal of pharmacology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeActivators of K EXPERIMENTAL APPROACH: Conventional electrophysiological methods were used to assess the effects of ITP-2 on hERG1a and hERG1a/1b channels expressed heterologously in HEK-293 cells. KEY
resultsITP-2 selectively increased test pulse currents (EC CONCLUSIONS AND IMPLICATIONS: ITP-2 may serve as another novel lead molecule for designing robust activators of hERG channels. hERG1a/1b gating kinetics were differentially modulated by ITP-2 leading to altered sensitivity. ITP-2 is capable of activating an LQT2 mutant and may be potentially useful in the development of LQT2 therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.