scholarly journals Perspective of Ion Channels in Prostate Cancer

Author(s):  
Nnodim Johnkennedy ◽  
Bako Hauwa ◽  
Ezekwesiri Cletus

Ion channels are membrane proteins, which play a great role in regulating cellular excitability. Alteration of ion channel may contribute to prostate cancer. This could be linked to inherited mutations of ion channel genes which alter channel’s biophysical properties, in a prostate cancer. It is an observed fact that genomic instability is the main cause as well as the major characteristics of prostate cancer. Prostate cancer cell genotypes are mainly characterized by uncontrolled metastasis, resistance to programmed cell death, sustained angiogenesis as well as tissue invasion and metastasis. It is known that genes encoding ion channels are affected in prostate cancer. The Membrane proteins which is involved in signaling in cell and among cells, for coupling of extracellular events with intracellular responses, and for maintaining intracellular ionic homeostasis ion channels which contribute to some extents to pathophysiological features of each prostate cancer.

Author(s):  
Nnodim Johnkennedy ◽  
Bako Hauwa ◽  
Ezekwesiri Cletus

Ion channels are membrane proteins, which play a great role in regulating cellular excitability. Alteration of ion channel may contribute to prostate cancer. This could be linked to inherited mutations of ion channel genes which alter channel’s biophysical properties, in a prostate cancer. It is an observed fact that genomic instability is the main cause as well as the major characteristics of prostate cancer. Prostate cancer cell genotypes are mainly characterized by uncontrolled metastasis, resistance to programmed cell death, sustained angiogenesis as well as tissue invasion and metastasis. It is known that genes encoding ion channels are affected in prostate cancer. The Membrane proteins which is involved in signaling in cell and among cells, for coupling of extracellular events with intracellular responses, and for maintaining intracellular ionic homeostasis ion channels which contribute to some extents to pathophysiological features of each prostate cancer.


2018 ◽  
Vol 98 (2) ◽  
pp. 559-621 ◽  
Author(s):  
Natalia Prevarskaya ◽  
Roman Skryma ◽  
Yaroslav Shuba

Genomic instability is a primary cause and fundamental feature of human cancer. However, all cancer cell genotypes generally translate into several common pathophysiological features, often referred to as cancer hallmarks. Although nowadays the catalog of cancer hallmarks is quite broad, the most common and obvious of them are 1) uncontrolled proliferation, 2) resistance to programmed cell death (apoptosis), 3) tissue invasion and metastasis, and 4) sustained angiogenesis. Among the genes affected by cancer, those encoding ion channels are present. Membrane proteins responsible for signaling within cell and among cells, for coupling of extracellular events with intracellular responses, and for maintaining intracellular ionic homeostasis ion channels contribute to various extents to pathophysiological features of each cancer hallmark. Moreover, tight association of these hallmarks with ion channel dysfunction gives a good reason to classify them as special type of channelopathies, namely oncochannelopathies. Although the relation of cancer hallmarks to ion channel dysfunction differs from classical definition of channelopathies, as disease states causally linked with inherited mutations of ion channel genes that alter channel's biophysical properties, in a broader context of the disease state, to which pathogenesis ion channels essentially contribute, such classification seems absolutely appropriate. In this review the authors provide arguments to substantiate such point of view.


2016 ◽  
Author(s):  
◽  
Autoosa Salari

Ion channels are the building blocks of cellular excitability, controlling the most basic functions necessary for life to the most complex behaviors. The research presented here addresses questions about the mechanisms by which different ion channels function, as well as, how various toxins from venomous animals can alter ion channel behavior. This was done using a combination of molecular biology, electrophysiology, and computational techniques. The results shed light on the specific structures of a channel required for proper function, and target by pharmacological agents. Importantly, these results have significance in developing animal toxins as research tools and as future therapeutic agents for ion channel associated diseases. Lastly, we demonstrate for the first time, a system to study a protein required for high temperature avoidance in fruit flies. This opens the door to addressing detailed questions about the most poorly understood of the five senses, temperature sensation.


Physiology ◽  
1997 ◽  
Vol 12 (3) ◽  
pp. 105-112
Author(s):  
F Lehmann-Horn ◽  
R Rudel

Since 1990, many mutations in genes encoding voltage-dependent sodium, potassium, calcium, and chloride channels have been discovered to cause disorders of heart, skeletal muscle, brain, or kidney. Study of the defective gene products has furthered our knowledge not only of pathology but also of ion-channel function.


2020 ◽  
Vol 37 (5) ◽  
pp. 703-716
Author(s):  
Saumya Bajaj ◽  
Seow Theng Ong ◽  
K. George Chandy

Natural products harnessed from the diverse universe of compounds within the bioenvironment are being used to modulate ion channels, a vast super-family of membrane proteins that play critical physiological roles in excitable and non-excitable cells.


2020 ◽  
Vol 318 (6) ◽  
pp. H1357-H1370
Author(s):  
Hassan Musa ◽  
Cherisse A. Marcou ◽  
Todd J. Herron ◽  
Michael A. Makara ◽  
David J. Tester ◽  
...  

The gene encoding SAP97 ( DLG1) joins a growing list of genes encoding ion channel interacting proteins (ChIPs) identified as potential channelopathy-susceptibility genes because of their ability to regulate the trafficking, targeting, and modulation of ion channels that are critical for the generation and propagation of the cardiac electrical impulse. In this study we provide the first data supporting DLG1-encoded SAP97’s candidacy as a minor Brugada syndrome susceptibility gene.


2008 ◽  
Vol 88 (4) ◽  
pp. 1407-1447 ◽  
Author(s):  
Helene Vacher ◽  
Durga P. Mohapatra ◽  
James S. Trimmer

The intrinsic electrical properties and the synaptic input-output relationships of neurons are governed by the action of voltage-dependent ion channels. The localization of specific populations of ion channels with distinct functional properties at discrete sites in neurons dramatically impacts excitability and synaptic transmission. Molecular cloning studies have revealed a large family of genes encoding voltage-dependent ion channel principal and auxiliary subunits, most of which are expressed in mammalian central neurons. Much recent effort has focused on determining which of these subunits coassemble into native neuronal channel complexes, and the cellular and subcellular distributions of these complexes, as a crucial step in understanding the contribution of these channels to specific aspects of neuronal function. Here we review progress made on recent studies aimed to determine the cellular and subcellular distribution of specific ion channel subunits in mammalian brain neurons using in situ hybridization and immunohistochemistry. We also discuss the repertoire of ion channel subunits in specific neuronal compartments and implications for neuronal physiology. Finally, we discuss the emerging mechanisms for determining the discrete subcellular distributions observed for many neuronal ion channels.


2010 ◽  
pp. 160-168 ◽  
Author(s):  
Frances M. Ashcroft

Ion channels are membrane proteins that act as gated pathways for the movement of ions across cell membranes. They are found in both surface and intracellular membranes, and play essential roles in the physiology of all cell types. An ever-increasing number of human diseases are found to be caused by defects in ion channel function. Ion channel diseases may arise in a number of different ways:...


Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2417
Author(s):  
Camille E. Blandin ◽  
Basile J. Gravez ◽  
Stéphane N. Hatem ◽  
Elise Balse

Both inherited and acquired cardiac arrhythmias are often associated with the abnormal functional expression of ion channels at the cellular level. The complex machinery that continuously traffics, anchors, organizes, and recycles ion channels at the plasma membrane of a cardiomyocyte appears to be a major source of channel dysfunction during cardiac arrhythmias. This has been well established with the discovery of mutations in the genes encoding several ion channels and ion channel partners during inherited cardiac arrhythmias. Fibrosis, altered myocyte contacts, and post-transcriptional protein changes are common factors that disorganize normal channel trafficking during acquired cardiac arrhythmias. Channel availability, described notably for hERG and KV1.5 channels, could be another potent arrhythmogenic mechanism. From this molecular knowledge on cardiac arrhythmias will emerge novel antiarrhythmic strategies.


Sign in / Sign up

Export Citation Format

Share Document