scholarly journals Effects of Bisphenol A on ion channels: Experimental evidence and molecular mechanisms

Steroids ◽  
2016 ◽  
Vol 111 ◽  
pp. 12-20 ◽  
Author(s):  
Sergi Soriano ◽  
Cristina Ripoll ◽  
Paloma Alonso-Magdalena ◽  
Esther Fuentes ◽  
Ivan Quesada ◽  
...  
Keyword(s):  
Ion Channels ◽  
Bisphenol A ◽  
Experimental Evidence ◽  
Molecular Mechanisms

Ligand-gated ion channels as targets of neuroactive insecticides

2021 ◽  
Author(s):  
Makoto Ihara
Keyword(s):  
Ion Channels ◽  
Molecular Mechanisms ◽  
Functional Expression ◽  
X Ray ◽  
Acetylcholine Binding Protein ◽  
Site Selectivity ◽  
Future Drug ◽  
Cl Channels ◽  
Gated Ion Channels ◽  
Ligand Gated Ion Channels

Abstract The Cys-loop superfamily of ligand-gated ion channels (Cys-loop receptors) is one of the most ubiquitous ion channel families in vertebrates and invertebrates. Despite their ubiquity, they are targeted by several classes of pesticides, including neonicotinoids, phenylpyrazols, and macrolides such as ivermectins. The current commercialized compounds have high target site selectivity, which contributes to the safety of insecticide use. Structural analyses have accelerated progress in this field; notably, the X-ray crystal structures of acetylcholine binding protein and glutamate-gated Cl channels revealed the details of the molecular interactions between insecticides and their targets. Recently, the functional expression of the insect nicotinic acetylcholine receptor (nAChR) has been described, and detailed evaluations using the insect nAChR have emerged. This review discusses the basic concepts and the current insights into the molecular mechanisms of neuroactive insecticides targeting the ligand-gated ion channels, particularly Cys-loop receptors, and presents insights into target-based selectivity, resistance, and future drug design.

scholarly journals Molecular mechanisms of taste transduction

2002 ◽  
Vol 74 (7) ◽  
pp. 1125-1133 ◽  
Author(s):  
Robert F. Margolskee
Keyword(s):  
Ion Channels ◽  
Molecular Cloning ◽  
G Proteins ◽  
Molecular Mechanisms ◽  
Transmembrane Helix ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Chemical Diversity ◽  
Chemical Information ◽  
Taste Transduction

Taste transduction is a specialized form of signal transduction by which taste receptor cells (TRCs) encode at the cellular level information about chemical substances encountered in the oral environment (so-called tastants). Bitter and sweet taste transduction pathways convert chemical information into a cellular second messenger code utilizing cyclic nucleotides, inositol trisphosphate, and/or diacyl glycerol. These messengers are components of signaling cascades that lead to TRC depolarization and Ca++ release. Bitter and sweet taste transduction pathways typically utilize taste-specific or taste-selective seven transmembrane-helix receptors, G proteins, effector enzymes, second messengers, and ion channels. The structural and chemical diversity of tastants has led to the need for multiple transduction mechanisms. Through molecular cloning and data mining, many of the receptors, G proteins, and effector enzymes involved in transducing responses to bitter and sweet compounds are now known. New insights into taste transduction and taste coding underlying sweet and bitter taste qualities have been gained from molecular cloning of the transduction elements, biochemical elucidation of the transduction pathways, electrophysiological analysis of the function of taste cell ion channels, and behavioral analysis of transgenic and knockout models.

scholarly journals Hydrogen, Bicarbonate, and Their Associated Exchangers in Cell Volume Regulation

2021 ◽  
Vol 9 ◽  
Author(s):  
Yizeng Li ◽  
Xiaohan Zhou ◽  
Sean X. Sun
Keyword(s):  
Ion Channels ◽  
Cell Volume ◽  
Volume Regulation ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Water Flux ◽  
Cell Volume Regulation ◽  
Sodium Potassium ◽  
Before And After

Cells lacking a stiff cell wall, e.g., mammalian cells, must actively regulate their volume to maintain proper cell function. On the time scale that protein production is negligible, water flow in and out of the cell determines the cell volume variation. Water flux follows hydraulic and osmotic gradients; the latter is generated by various ion channels, transporters, and pumps in the cell membrane. Compared to the widely studied roles of sodium, potassium, and chloride in cell volume regulation, the effects of proton and bicarbonate are less understood. In this work, we use mathematical models to analyze how proton and bicarbonate, combined with sodium, potassium, chloride, and buffer species, regulate cell volume upon inhibition of ion channels, transporters, and pumps. The model includes several common, widely expressed ion transporters and focuses on obtaining generic outcomes. Results show that the intracellular osmolarity remains almost constant before and after cell volume change. The steady-state cell volume does not depend on water permeability. In addition, to ensure the stability of cell volume and ion concentrations, cells need to develop redundant mechanisms to maintain homeostasis, i.e., multiple ion channels or transporters are involved in the flux of the same ion species. These results provide insights for molecular mechanisms of cell volume regulation with additional implications for water-driven cell migration.

scholarly journals Ion Channels: New Actors Playing in Chemotherapeutic Resistance

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 376 ◽  
Author(s):  
Philippe Kischel ◽  
Alban Girault ◽  
Lise Rodat-Despoix ◽  
Mohamed Chamlali ◽  
Silviya Radoslavova ◽  
...  
Keyword(s):  
Ion Channels ◽  
Molecular Mechanisms ◽  
Early Stage ◽  
Breast Cancers ◽  
Altered Expression ◽  
Acquired Drug Resistance ◽  
Therapeutic Modalities ◽  
Channel Expression ◽  
Systemic Agents ◽  
Resistance To Chemotherapy

In the battle against cancer cells, therapeutic modalities are drastically limited by intrinsic or acquired drug resistance. Resistance to therapy is not only common, but expected: if systemic agents used for cancer treatment are usually active at the beginning of therapy (i.e., 90% of primary breast cancers and 50% of metastases), about 30% of patients with early-stage breast cancer will have recurrent disease. Altered expression of ion channels is now considered as one of the hallmarks of cancer, and several ion channels have been linked to cancer cell resistance. While ion channels have been associated with cell death, apoptosis and even chemoresistance since the late 80s, the molecular mechanisms linking ion channel expression and/or function with chemotherapy have mostly emerged in the last ten years. In this review, we will highlight the relationships between ion channels and resistance to chemotherapy, with a special emphasis on the underlying molecular mechanisms.

scholarly journals Mechanosensitive ion channels in skeletal muscle: Molecular mechanisms of gating and blockade.

1993 ◽  
Vol 61 ◽  
pp. 41
Author(s):  
Tervl Elam ◽  
Alfredo Franco ◽  
Christine Haws ◽  
Bruce Winegar ◽  
Jeffry B. Lansman
Keyword(s):  
Skeletal Muscle ◽  
Ion Channels ◽  
Molecular Mechanisms ◽  
Mechanosensitive Ion Channels

scholarly journals Author Correction: Molecular mechanisms involved in the non-monotonic effect of bisphenol-a on Ca2+ entry in mouse pancreatic β-cells

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Sabrina Villar-Pazos ◽  
Juan Martinez-Pinna ◽  
Manuel Castellano-Muñoz ◽  
Paloma Alonso-Magdalena ◽  
Laura Marroqui ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Molecular Mechanisms ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals New insights into the functions of Cox-2 in skin and esophageal malignancies

2020 ◽  
Vol 52 (4) ◽  
pp. 538-547 ◽  
Author(s):  
Hyeongsun Moon ◽  
Andrew C. White ◽  
Alexander D. Borowsky
Keyword(s):  
Experimental Evidence ◽  
Molecular Mechanisms ◽  
Genetic Manipulation ◽  
Tumor Development ◽  
Cancer Type ◽  
Tumor Initiation ◽  
Cells Of Origin ◽  
Cox 2 ◽  
Underlying Mechanisms ◽  
Necessary And Sufficient

Abstract Understanding the cellular and molecular mechanisms of tumor initiation and progression for each cancer type is central to making improvements in both prevention and therapy. Identifying the cancer cells of origin and the necessary and sufficient mechanisms of transformation and progression provide opportunities for improved specific clinical interventions. In the last few decades, advanced genetic manipulation techniques have facilitated rapid progress in defining the etiologies of cancers and their cells of origin. Recent studies driven by various groups have provided experimental evidence indicating the cellular origins for each type of skin and esophageal cancer and have identified underlying mechanisms that stem/progenitor cells use to initiate tumor development. Specifically, cyclooxygenase-2 (Cox-2) is associated with tumor initiation and progression in many cancer types. Recent studies provide data demonstrating the roles of Cox-2 in skin and esophageal malignancies, especially in squamous cell carcinomas (SCCs) occurring in both sites. Here, we review experimental evidence aiming to define the origins of skin and esophageal cancers and discuss how Cox-2 contributes to tumorigenesis and differentiation.

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