ArticleEuropean biophysics journal : EBJ2015
PKD2L1/PKD1L3 channel complex with an alkali-activated mechanism and calcium-dependent inactivation.
Article in European biophysics journal : EBJ, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Polycystin Channel Complexes.Annual review of physiology · 2023Review
- Article
- Ciliated neurons lining the central canal sense both fluid movement and pH through ASIC3.Nature communications · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Polycystic kidney disease-like (PKDL) genes that are expressed in sour taste cells have been proposed to be involved in the transduction of sourness by producing off-responses, which shows a large inward current after withdrawing the acid stimuli. However, the underlying mechanisms of off-responses are still unclear. Here, we demonstrate that an alkali-activated mechanism is responsible for eliciting off-responses, as evidenced by both experimental and theoretical analyses. In addition, we showed that the decaying phase of offset responses in PKD2L1/PKD1L3 channels was substantially accelerated by extracellular Ca(2+).
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