scholarly journals A microbial TRP-like polycystic-kidney-disease-related ion channel gene

2005 ◽  
Vol 387 (1) ◽  
pp. 211-219 ◽  
Author(s):  
Christopher P. PALMER ◽  
Ebru AYDAR ◽  
Mustafa B. A. DJAMGOZ
Keyword(s):  
Cell Wall ◽  
Kidney Disease ◽  
Ion Channel ◽  
Polycystic Kidney Disease ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cell Wall Synthesis ◽  
Polycystic Kidney ◽  
Channel Gene ◽  
Ion Channel Gene

Ion channel genes have been discovered in many microbial organisms. We have investigated a microbial TRP (transient receptor potential) ion channel gene which has most similarity to polycystic-kidney-disease-related ion channel genes. We have shown that this gene (pkd2) is essential for cellular viability, and is involved in cell growth and cell wall synthesis. Expression of this gene increases following damage to the cell wall. This fission yeast pkd2 gene, orthologues of which are found in all eukaryotic cells, appears to be a key signalling component in the regulation of cell shape and cell wall synthesis in yeast through an interaction with a Rho1-GTPase. A model for the mode of action of this Schizosaccharomyces pombe protein in a Ca2+ signalling pathway is hypothesized.

TRP channels and kidney disease: lessons from polycystic kidney disease

2007 ◽  
Vol 35 (1) ◽  
pp. 124-128 ◽  
Author(s):  
S. Qamar ◽  
M. Vadivelu ◽  
R. Sandford
Keyword(s):  
Kidney Disease ◽  
Intracellular Calcium ◽  
Polycystic Kidney Disease ◽  
Primary Cilium ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Polycystic Kidney ◽  
Pkd2 Gene ◽  
Transient Receptor

Important insights in to the function of members of the TRP (transient receptor potential) channel superfamily have been gained from the identification of disease-related mutations. In particular the identification of mutations in the PKD2 gene in autosomal dominant polycystic kidney disease has revealed a link between TRP channel function, mechanosensation and the role of the primary cilium in renal cyst formation. The PKD2 gene encodes TRPP2 (transient receptor potential polycystin 2) that has significant homology to voltage-activated calcium and sodium TRP channels. It interacts with polycystin-1 to form a large membrane-associated complex that is localized to the renal primary cilium. Functional characterization of this polycystin complex reveals that it can respond to mechanical stimuli such as flow, resulting in influx of extracellular calcium and release of calcium from intracellular stores. TRPP2 is expressed in the endoplasmic reticulum/sarcoplasmic reticulum where it also regulates intracellular calcium signalling. Therefore TRPP2 modulates many cellular processes via intracellular calcium-dependent signalling pathways.

scholarly journals Altered Regulation of Ion Channel Activity by EGF in Polycystic Kidney Disease

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Zhi‐Ren Zhang ◽  
Wen‐Feng Chu ◽  
Peter Komlosi ◽  
Courtney J. Haycraft ◽  
Phillip Darwin Bell
Keyword(s):  
Kidney Disease ◽  
Ion Channel ◽  
Polycystic Kidney Disease ◽  
Channel Activity ◽  
Polycystic Kidney ◽  
Altered Regulation

scholarly journals Polycystic Kidney Disease Ryanodine Receptor Domain (PKDRR) Proteins in Oomycetes

Pathogens ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 577
Author(s):  
Limian Zheng ◽  
Barbara Doyle Prestwich ◽  
Patrick T. Harrison ◽  
John J. Mackrill
Keyword(s):  
Kidney Disease ◽  
Cell Surface ◽  
Polycystic Kidney Disease ◽  
Ryanodine Receptor ◽  
Transient Receptor Potential ◽  
Expression System ◽  
Surface Membrane ◽  
Protein Domain ◽  
Polycystic Kidney ◽  
Extracellular Medium

In eukaryotes, two sources of Ca2+ are accessed to allow rapid changes in the cytosolic levels of this second messenger: the extracellular medium and intracellular Ca2+ stores, such as the endoplasmic reticulum. One class of channel that permits Ca2+ entry is the transient receptor potential (TRP) superfamily, including the polycystic kidney disease (PKD) proteins, or polycystins. Channels that release Ca2+ from intracellular stores include the inositol 1,4,5-trisphosphate/ryanodine receptor (ITPR/RyR) superfamily. Here, we characterise a family of proteins that are only encoded by oomycete genomes, that we have named PKDRR, since they share domains with both PKD and RyR channels. We provide evidence that these proteins belong to the TRP superfamily and are distinct from the ITPR/RyR superfamily in terms of their evolutionary relationships, protein domain architectures and predicted ion channel structures. We also demonstrate that a hypothetical PKDRR protein from Phytophthora infestans is produced by this organism, is located in the cell-surface membrane and forms multimeric protein complexes. Efforts to functionally characterise this protein in a heterologous expression system were unsuccessful but support a cell-surface localisation. These PKDRR proteins represent potential targets for the development of new “fungicides”, since they are of a distinctive structure that is only found in oomycetes and not in any other cellular organisms.

scholarly journals EGFR augments cell proliferation in polycystic kidney disease through activation of a novel ion channel

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Zhi‐Ren Zhang ◽  
Wen‐Feng Chu ◽  
Binlin Song ◽  
Monika Gooz ◽  
Aleksander Baldys ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Kidney Disease ◽  
Ion Channel ◽  
Polycystic Kidney Disease ◽  
Polycystic Kidney

scholarly journals Deciphering physiological role of the mechanosensitive TRPV4 channel in the distal nephron

2015 ◽  
Vol 308 (4) ◽  
pp. F275-F286 ◽  
Author(s):  
M. Mamenko ◽  
O. Zaika ◽  
N. Boukelmoune ◽  
R. G. O'Neil ◽  
O. Pochynyuk
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Molecular Mechanisms ◽  
Transient Receptor Potential ◽  
Renal Tubule ◽  
Trp Channels ◽  
Current Evidence ◽  
Distal Nephron ◽  
Polycystic Kidney ◽  
Intracellular Ca

Long-standing experimental evidence suggests that epithelial cells in the renal tubule are able to sense osmotic and pressure gradients caused by alterations in ultrafiltrate flow by elevating intracellular Ca2+ concentration. These responses are viewed as critical regulators of a variety of processes ranging from transport of water and solutes to cellular growth and differentiation. A loss in the ability to sense mechanical stimuli has been implicated in numerous pathologies associated with systemic imbalance of electrolytes and to the development of polycystic kidney disease. The molecular mechanisms conferring mechanosensitive properties to epithelial tubular cells involve activation of transient receptor potential (TRP) channels, such as TRPV4, allowing direct Ca2+ influx to increase intracellular Ca2+ concentration. In this review, we critically analyze the current evidence about signaling determinants of TRPV4 activation by luminal flow in the distal nephron and discuss how dysfunction of this mechanism contributes to the progression of polycystic kidney disease. We also review the physiological relevance of TRPV4-based mechanosensitivity in controlling flow-dependent K+ secretion in the distal renal tubule.

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