The Experts below are selected from a list of 81342 Experts worldwide ranked by ideXlab platform
Hana Sychrová - One of the best experts on this subject based on the ideXlab platform.
-
yarrowia lipolytica possesses two plasma membrane alkali metal cation h antiporters with different functions in Cell Physiology
FEBS Letters, 2006Co-Authors: Klara Papouskova, Hana SychrováAbstract:The family of Nha antiporters mediating the efflux of alkali metal cations in exchange for protons across the plasma membrane is conserved in all yeast species. Yarrowia lipolytica is a dimorphic yeast, phylogenetically very distant from the model yeast Saccharomyces cerevisiae. A search in its sequenced genome revealed two genes (designated as YlNHA1 and YlNHA2) with homology to the S. cerevisiae NHA1 gene, which encodes a plasma membrane alkali metal cation/H+ antiporter. Upon heterologous expression of both YlNHA genes in S. cerevisiae, we showed that Y. lipolytica antiporters differ not only in length and sequence, but also in their affinity for individual substrates. While the YlNha1 protein mainly increased Cell tolerance to potassium, YlNha2p displayed a remarkable transport capacity for sodium. Thus, Y. lipolytica is the first example of a yeast species with two plasma membrane alkali metal cation/H+ antiporters differing in their putative functions in Cell Physiology; Cell detoxification vs. the maintenance of stable intraCellular pH, potassium content and Cell volume.
-
Yarrowia lipolytica possesses two plasma membrane alkali metal cation/H+ antiporters with different functions in Cell Physiology.
FEBS Letters, 2006Co-Authors: Klara Papouskova, Hana SychrováAbstract:Abstract The family of Nha antiporters mediating the efflux of alkali metal cations in exchange for protons across the plasma membrane is conserved in all yeast species. Yarrowia lipolytica is a dimorphic yeast, phylogenetically very distant from the model yeast Saccharomyces cerevisiae. A search in its sequenced genome revealed two genes (designated as YlNHA1 and YlNHA2) with homology to the S. cerevisiae NHA1 gene, which encodes a plasma membrane alkali metal cation/H+ antiporter. Upon heterologous expression of both YlNHA genes in S. cerevisiae, we showed that Y. lipolytica antiporters differ not only in length and sequence, but also in their affinity for individual substrates. While the YlNha1 protein mainly increased Cell tolerance to potassium, YlNha2p displayed a remarkable transport capacity for sodium. Thus, Y. lipolytica is the first example of a yeast species with two plasma membrane alkali metal cation/H+ antiporters differing in their putative functions in Cell Physiology; Cell detoxification vs. the maintenance of stable intraCellular pH, potassium content and Cell volume.
Mitchell P. Fink - One of the best experts on this subject based on the ideXlab platform.
-
Red blood Cell Physiology in critical illness.
Critical Care Medicine, 2003Co-Authors: Marion Scharte, Mitchell P. FinkAbstract:ObjectiveReduction in red blood Cell mass, as well as structural and functional alterations of erythrocytes, occurs in critical illness. This review discusses these changes in red blood Cell Physiology, emphasizing the pathogenesis of anemia in intensive care unit patients.Data SourceStudies publish
-
Red blood Cell Physiology in critical illness.
Critical care medicine, 2003Co-Authors: Marion Scharte, Mitchell P. FinkAbstract:Reduction in red blood Cell mass, as well as structural and functional alterations of erythrocytes, occurs in critical illness. This review discusses these changes in red blood Cell Physiology, emphasizing the pathogenesis of anemia in intensive care unit patients. Studies published in biomedical journals. Anemia in intensive care unit patients resembles the anemia of chronic disease, being characterized by diminished erythropoietin production relative to decreased hematocrit, altered iron metabolism, and impaired proliferation and differentiation of erythroid progenitors in the bone marrow. Inflammatory mediators play a major role in the development of insufficient erythropoiesis and altered iron metabolism. Furthermore, a proinflammatory milieu promotes structural and functional alterations of erythrocytes, impairing their deformability and possibly impairing microvascular perfusion. Collectively, these changes in red blood Cell Physiology can impair oxygen transport to tissues and, thereby, might contribute to the development of multiple organ failure in critical illness.
Klara Papouskova - One of the best experts on this subject based on the ideXlab platform.
-
yarrowia lipolytica possesses two plasma membrane alkali metal cation h antiporters with different functions in Cell Physiology
FEBS Letters, 2006Co-Authors: Klara Papouskova, Hana SychrováAbstract:The family of Nha antiporters mediating the efflux of alkali metal cations in exchange for protons across the plasma membrane is conserved in all yeast species. Yarrowia lipolytica is a dimorphic yeast, phylogenetically very distant from the model yeast Saccharomyces cerevisiae. A search in its sequenced genome revealed two genes (designated as YlNHA1 and YlNHA2) with homology to the S. cerevisiae NHA1 gene, which encodes a plasma membrane alkali metal cation/H+ antiporter. Upon heterologous expression of both YlNHA genes in S. cerevisiae, we showed that Y. lipolytica antiporters differ not only in length and sequence, but also in their affinity for individual substrates. While the YlNha1 protein mainly increased Cell tolerance to potassium, YlNha2p displayed a remarkable transport capacity for sodium. Thus, Y. lipolytica is the first example of a yeast species with two plasma membrane alkali metal cation/H+ antiporters differing in their putative functions in Cell Physiology; Cell detoxification vs. the maintenance of stable intraCellular pH, potassium content and Cell volume.
-
Yarrowia lipolytica possesses two plasma membrane alkali metal cation/H+ antiporters with different functions in Cell Physiology.
FEBS Letters, 2006Co-Authors: Klara Papouskova, Hana SychrováAbstract:Abstract The family of Nha antiporters mediating the efflux of alkali metal cations in exchange for protons across the plasma membrane is conserved in all yeast species. Yarrowia lipolytica is a dimorphic yeast, phylogenetically very distant from the model yeast Saccharomyces cerevisiae. A search in its sequenced genome revealed two genes (designated as YlNHA1 and YlNHA2) with homology to the S. cerevisiae NHA1 gene, which encodes a plasma membrane alkali metal cation/H+ antiporter. Upon heterologous expression of both YlNHA genes in S. cerevisiae, we showed that Y. lipolytica antiporters differ not only in length and sequence, but also in their affinity for individual substrates. While the YlNha1 protein mainly increased Cell tolerance to potassium, YlNha2p displayed a remarkable transport capacity for sodium. Thus, Y. lipolytica is the first example of a yeast species with two plasma membrane alkali metal cation/H+ antiporters differing in their putative functions in Cell Physiology; Cell detoxification vs. the maintenance of stable intraCellular pH, potassium content and Cell volume.
Perolof Berggren - One of the best experts on this subject based on the ideXlab platform.
-
The Role of Voltage-Gated Calcium Channels in Pancreatic β-Cell Physiology and PathoPhysiology
Endocrine reviews, 2006Co-Authors: Shaonian Yang, Perolof BerggrenAbstract:Voltage-gated calcium (CaV) channels are ubiquitously expressed in various Cell types throughout the body. In principle, the molecular identity, biophysical profile, and pharmacological property of CaV channels are independent of the Cell type where they reside, whereas these channels execute unique functions in different Cell types, such as muscle contraction, neurotransmitter release, and hormone secretion. At least six CaValpha1 subunits, including CaV1.2, CaV1.3, CaV2.1, CaV2.2, CaV2.3, and CaV3.1, have been identified in pancreatic beta-Cells. These pore-forming subunits complex with certain auxiliary subunits to conduct L-, P/Q-, N-, R-, and T-type CaV currents, respectively. beta-Cell CaV channels take center stage in insulin secretion and play an important role in beta-Cell Physiology and pathoPhysiology. CaV3 channels become expressed in diabetes-prone mouse beta-Cells. Point mutation in the human CaV1.2 gene results in excessive insulin secretion. Trinucleotide expansion in the human CaV1.3 and CaV2.1 gene is revealed in a subgroup of patients with type 2 diabetes. beta-Cell CaV channels are regulated by a wide range of mechanisms, either shared by other Cell types or specific to beta-Cells, to always guarantee a satisfactory concentration of Ca2+. Inappropriate regulation of beta-Cell CaV channels causes beta-Cell dysfunction and even death manifested in both type 1 and type 2 diabetes. This review summarizes current knowledge of CaV channels in beta-Cell Physiology and pathoPhysiology.
-
the role of voltage gated calcium channels in pancreatic β Cell Physiology and pathoPhysiology
Endocrine Reviews, 2006Co-Authors: Shaonian Yang, Perolof BerggrenAbstract:Voltage-gated calcium (CaV) channels are ubiquitously expressed in various Cell types throughout the body. In principle, the molecular identity, biophysical profile, and pharmacological property of CaV channels are independent of the Cell type where they reside, whereas these channels execute unique functions in different Cell types, such as muscle contraction, neurotransmitter release, and hormone secretion. At least six CaVα1 subunits, including CaV1.2, CaV1.3, CaV2.1, CaV2.2, CaV2.3, and CaV3.1, have been identified in pancreatic β-Cells. These pore-forming subunits complex with certain auxiliary subunits to conduct L-, P/Q-, N-, R-, and T-type CaV currents, respectively. β-Cell CaV channels take center stage in insulin secretion and play an important role in β-Cell Physiology and pathoPhysiology. CaV3 channels become expressed in diabetes-prone mouse β-Cells. Point mutation in the human CaV1.2 gene results in excessive insulin secretion. Trinucleotide expansion in the human CaV1.3 and CaV2.1 gene is r...
Marion Scharte - One of the best experts on this subject based on the ideXlab platform.
-
Red blood Cell Physiology in critical illness.
Critical Care Medicine, 2003Co-Authors: Marion Scharte, Mitchell P. FinkAbstract:ObjectiveReduction in red blood Cell mass, as well as structural and functional alterations of erythrocytes, occurs in critical illness. This review discusses these changes in red blood Cell Physiology, emphasizing the pathogenesis of anemia in intensive care unit patients.Data SourceStudies publish
-
Red blood Cell Physiology in critical illness.
Critical care medicine, 2003Co-Authors: Marion Scharte, Mitchell P. FinkAbstract:Reduction in red blood Cell mass, as well as structural and functional alterations of erythrocytes, occurs in critical illness. This review discusses these changes in red blood Cell Physiology, emphasizing the pathogenesis of anemia in intensive care unit patients. Studies published in biomedical journals. Anemia in intensive care unit patients resembles the anemia of chronic disease, being characterized by diminished erythropoietin production relative to decreased hematocrit, altered iron metabolism, and impaired proliferation and differentiation of erythroid progenitors in the bone marrow. Inflammatory mediators play a major role in the development of insufficient erythropoiesis and altered iron metabolism. Furthermore, a proinflammatory milieu promotes structural and functional alterations of erythrocytes, impairing their deformability and possibly impairing microvascular perfusion. Collectively, these changes in red blood Cell Physiology can impair oxygen transport to tissues and, thereby, might contribute to the development of multiple organ failure in critical illness.