scholarly journals Assessing the Impact of Calmodulinopathic Mutations on Neuronal Ion Channel Regulation

2021 ◽  
Vol 120 (3) ◽  
pp. 155a
Author(s):  
John W. Hussey ◽  
Emily DeMarco ◽  
Deborah DiSilvestre ◽  
Helene H. Jensen ◽  
Mette Nyegaard ◽  
...  
Keyword(s):  
Ion Channel ◽  
Ion Channel Regulation ◽  
Channel Regulation ◽  
The Impact

Ion channel regulation by G proteins

1995 ◽  
Vol 75 (4) ◽  
pp. 865-885 ◽  
Author(s):  
K. Wickman ◽  
D. E. Clapham
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
G Protein ◽  
G Proteins ◽  
Second Messengers ◽  
Channel Activity ◽  
Ion Channel Regulation ◽  
Protein Subunits ◽  
Channel Regulation ◽  
Intracellular Cascades

Ion channels are poised uniquely to initiate, mediate, or regulate such distinct cellular activities as action potential propagation, secretion, and gene transcription. In retrospect, it is not surprising that studies of ion channels have revealed considerable diversities in their primary structures, regulation, and expression. From a functional standpoint, the various mechanisms coopted by cells to regulate channel activity are particularly fascinating. Extracellular ligands, membrane potential, phosphorylation, ions themselves, and diffusible second messengers are all well-established regulators of ion channel activity. Heterotrimeric GTP-binding proteins (G proteins) mediate many of these types of ion channel regulation by stimulating or inhibiting phosphorylation pathways, initiating intracellular cascades leading to elevation of cytosolic Ca2+ or adenosine 3',5'-cyclic monophosphate levels, or by generating various lipid-derived compounds. In some cases, it seems that activated G protein subunits can interact directly with ion channels to elicit regulation. Although there is currently little direct biochemical evidence to support such a mechanism, it is the working hypothesis for the most-studied G protein-regulated ion channels.

scholarly journals Trafficking of TRPP2 by PACS proteins represents a novel mechanism of ion channel regulation

2005 ◽  
Vol 24 (4) ◽  
pp. 705-716 ◽  
Author(s):  
Michael Köttgen ◽  
Thomas Benzing ◽  
Thomas Simmen ◽  
Robert Tauber ◽  
Björn Buchholz ◽  
...  
Keyword(s):  
Ion Channel ◽  
Ion Channel Regulation ◽  
Channel Regulation

Regulation of ion transport by oxidants

2013 ◽  
Vol 305 (9) ◽  
pp. L595-L603 ◽  
Author(s):  
Charles A. Downs ◽  
My N. Helms
Keyword(s):  
Oxidative Stress ◽  
Ion Channels ◽  
Ion Channel ◽  
Redox Regulation ◽  
Experimental Biology ◽  
Cellular Functions ◽  
Ion Channel Regulation ◽  
Channel Regulation ◽  
Made In

Ion channels perform a variety of cellular functions in lung epithelia. Oxidant- and antioxidant-mediated mechanisms (that is, redox regulation) of ion channels are areas of intense research. Significant progress has been made in our understanding of redox regulation of ion channels since the last Experimental Biology report in 2003. Advancements include: 1) identification of nonphagocytic NADPH oxidases as sources of regulated reactive species (RS) production in epithelia, 2) an understanding that excessive treatment with antioxidants can result in greater oxidative stress, and 3) characterization of novel RS signaling pathways that converge upon ion channel regulation. These advancements, as discussed at the 2013 Experimental Biology Meeting in Boston, MA, impact our understanding of oxidative stress in the lung, and, in particular, illustrate that the redox state has profound effects on ion channel and cellular function.

scholarly journals PIP2: A critical regulator of vascular ion channels hiding in plain sight

2020 ◽  
Vol 117 (34) ◽  
pp. 20378-20389 ◽  
Author(s):  
Osama F. Harraz ◽  
David Hill-Eubanks ◽  
Mark T. Nelson
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Intracellular Signaling ◽  
Vascular Function ◽  
Current Knowledge ◽  
Ion Channel Regulation ◽  
Channel Regulation ◽  
Scant Attention ◽  
Blood Flow Control ◽  
Hydrolysis Of

The phosphoinositide, phosphatidylinositol 4,5-bisphosphate (PIP2), has long been established as a major contributor to intracellular signaling, primarily by virtue of its role as a substrate for phospholipase C (PLC). Signaling by Gq-protein–coupled receptors triggers PLC-mediated hydrolysis of PIP2into inositol 1,4,5-trisphosphate and diacylglycerol, which are well known to modulate vascular ion channel activity. Often overlooked, however, is the role PIP2itself plays in this regulation. Although numerous reports have demonstrated that PIP2is critical for ion channel regulation, how it impacts vascular function has received scant attention. In this review, we focus on PIP2as a regulator of ion channels in smooth muscle cells and endothelial cells—the two major classes of vascular cells. We further address the concerted effects of such regulation on vascular function and blood flow control. We close with a consideration of current knowledge regarding disruption of PIP2regulation of vascular ion channels in disease.

scholarly journals Phosphatidylinositol(4,5)bisphosphate: diverse functions at the plasma membrane

2020 ◽  
Vol 64 (3) ◽  
pp. 513-531 ◽  
Author(s):  
Matilda Katan ◽  
Shamshad Cockcroft
Keyword(s):  
Plasma Membrane ◽  
Ion Channel ◽  
Tyrosine Kinases ◽  
Cell Biology ◽  
Second Messengers ◽  
Membrane Dynamics ◽  
Actin Dynamics ◽  
Ion Channel Regulation ◽  
Channel Regulation ◽  
Phosphoinositide 3 Kinase

Abstract Phosphatidylinositol(4,5) bisphosphate (PI(4,5)P2) has become a major focus in biochemistry, cell biology and physiology owing to its diverse functions at the plasma membrane. As a result, the functions of PI(4,5)P2 can be explored in two separate and distinct roles – as a substrate for phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K) and as a primary messenger, each having unique properties. Thus PI(4,5)P2 makes contributions in both signal transduction and cellular processes including actin cytoskeleton dynamics, membrane dynamics and ion channel regulation. Signalling through plasma membrane G-protein coupled receptors (GPCRs), receptor tyrosine kinases (RTKs) and immune receptors all use PI(4,5)P2 as a substrate to make second messengers. Activation of PI3K generates PI(3,4,5)P3 (phosphatidylinositol(3,4,5)trisphosphate), a lipid that recruits a plethora of proteins with pleckstrin homology (PH) domains to the plasma membrane to regulate multiple aspects of cellular function. In contrast, PLC activation results in the hydrolysis of PI(4,5)P2 to generate the second messengers, diacylglycerol (DAG), an activator of protein kinase C and inositol(1,4,5)trisphosphate (IP3/I(1,4,5)P3) which facilitates an increase in intracellular Ca2+. Decreases in PI(4,5)P2 by PLC also impact on functions that are dependent on the intact lipid and therefore endocytosis, actin dynamics and ion channel regulation are subject to control. Spatial organisation of PI(4,5)P2 in nanodomains at the membrane allows for these multiple processes to occur concurrently.

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