ArticleThe Journal of physiology2007
On the physiological roles of PIP(2) at cardiac Na+ Ca2+ exchangers and K(ATP) channels: a long journey from membrane biophysics into cell biology.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Acute phosphatidylinositol 4,5 bisphosphate depletion destabilizes sarcolemmal expression of cardiac L-type CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- From Crosstalk to Synergism: The Combined Effect of Cholesterol and PI(4,5)PAdvances in experimental medicine and biology · 2023Review
- Insights into Cardiac IKs (KCNQ1/KCNE1) Channels Regulation.International journal of molecular sciences · 2020Review
- Dynamics of Phosphoinositide-Dependent Signaling in Sympathetic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Interplay Between Lipid Modulators of Kir2 Channels: Cholesterol and PIP2.Computational and structural biotechnology journal · 2014Article
- Label-free cell phenotypic profiling decodes the composition and signaling of an endogenous ATP-sensitive potassium channel.Scientific reports · 2014Article
- The signaling lipid PI(3,5)P₂ stabilizes V₁-V(o) sector interactions and activates the V-ATPase.Molecular biology of the cell · 2014Article
- Article
- Fitting K(V) potassium channels into the PIP(2) puzzle: Hille group connects dots between illustrious HH groups.The Journal of general physiology · 2012Article
- Characterization of a binding site for anionic phospholipids on KCNQ1.The Journal of biological chemistry · 2011Article
- A genetically encoded tool kit for manipulating and monitoring membrane phosphatidylinositol 4,5-bisphosphate in intact cells.PloS one · 2011Article
- Regulation of Ca2+ entry by inositol lipids in mammalian cells by multiple mechanisms.Cell calcium · 2009Review
- Direct regulation of BK channels by phosphatidylinositol 4,5-bisphosphate as a novel signaling pathway.The Journal of general physiology · 2008Article
- How highly charged anionic lipids bind and regulate ion channels.The Journal of general physiology · 2008Review
- Regulation of ion channels and transporters by phosphatidylinositol 4,5-bisphosphate.The Journal of physiology · 2007Article
- The phosphoinositide sensitivity of the K(v) channel family.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Over the last 10 years we have tried to understand the roles of PIP(2) in regulating cardiac Na(+)-Ca(2+) exchangers and K(ATP) K(+) channels, both of which are directly activated by PIP(2). Up to now, the idea that hormones might physiologically regulate these mechanisms by causing changes of PIP(2) concentrations in the cardiac sarcolemma, either locally or globally, is not well supported. In intact myocardium, but not excised patches, phosphatidylinositol 4-phosphate 5-kinase (PIP5K) activity appears to be Ca(2+) activated and dependent on cardiac activity. Potentially therefore the primary second messenger of the heart, cytoplasmic Ca(2+), may regulate PIP(2) and therewith numerous cardiac membrane processes. In general, however, PIP(2) may simply serve to strongly activate various cardiac channels and transporters when they are inserted in the sarcolemma, while a lack of PIP(2) on internal membranes maintains transporters and channels inactive during trafficking and processing. As in most, if not all, strong regulatory systems of cells, the activating effects of PIP(2) can apparently be countered by strong inactivation mechanisms. In this context, our recent work suggests that internalization of cardiac Na(+)-Ca(2+) exchangers is promoted by increased PIP(2) synthesis, especially in combination with other cell signals. Assuming that multiple adapter-PIP(2) interactions are necessary to initiate the budding of individual membrane vesicles, the dependence of endocytosis on PIP(2) in the surface membrane can potentially be a very steep function. Thus, a better understanding of the regulation of cardiac lipid kinases may be key to understanding when and how cardiac ion transporters and channels are internalized.
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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.