ArticlePloS one2012
Surface expression and subunit specific control of steady protein levels by the Kv7.2 helix A-B linker.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- MLe-KCNQ2: An Artificial Intelligence Model for the Prognosis of MissenseInternational journal of molecular sciences · 2024Article
- Disruption of a Conservative Motif in the C-Terminal Loop of the KCNQ1 Channel Causes LQT Syndrome.International journal of molecular sciences · 2022Article
- Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of biological chemistry · 2018Article
- Structural basis and energy landscape for the CaProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants.Channels (Austin, Tex.) · 2018Article
- CaChannels (Austin, Tex.) · 2017Article
- Calmodulin confers calcium sensitivity to the stability of the distal intracellular assembly domain of Kv7.2 channels.Scientific reports · 2017Article
- Phosphorylation regulates the sensitivity of voltage-gated Kv7.2 channels towards phosphatidylinositol-4,5-bisphosphate.The Journal of physiology · 2017Article
- Competition of calcified calmodulin N lobe and PIP2 to an LQT mutation site in Kv7.1 channel.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Long QT mutations at the interface between KCNQ1 helix C and KCNE1 disrupt I(KS) regulation by PKA and PIP₂.Journal of cell science · 2014Article
- PIP2 regulation of KCNQ channels: biophysical and molecular mechanisms for lipid modulation of voltage-dependent gating.Frontiers in physiology · 2014Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kv7.2 and Kv7.3 are the main components of the neuronal voltage-dependent M-current, which is a subthreshold potassium conductance that exerts an important control on neuronal excitability. Despite their predominantly intracellular distribution, these channels must reach the plasma membrane in order to control neuronal activity. Thus, we analyzed the amino acid sequence of Kv7.2 to identify intrinsic signals that may control its surface expression. Removal of the interlinker connecting helix A and helix B of the intracellular C-terminus produces a large increase in the number of functional channels at the plasma membrane. Moreover, elimination of this linker increased the steady-state amount of protein, which was not associated with a decrease of protein degradation. The magnitude of this increase was inversely correlated with the number of helix A - helix B linkers present in the tetrameric channel assemblies. In contrast to the remarkable effect on the amount of Kv7.2 protein, removal of the Kv7.2 linker had no detectable impact on the steady-state levels of Kv7.3 protein.
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