The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform

Christopher J Chang - One of the best experts on this subject based on the ideXlab platform.

  • activity based ratiometric fret probe reveals oncogene driven changes in labile copper pools induced by altered Glutathione Metabolism
    Proceedings of the National Academy of Sciences of the United States of America, 2019
    Co-Authors: Clive Yiksham Chung, Jessica M Posimo, Tiffany Tsang, Julianne M Davis, Donita C Brady, Christopher J Chang
    Abstract:

    Copper is essential for life, and beyond its well-established ability to serve as a tightly bound, redox-active active site cofactor for enzyme function, emerging data suggest that cellular copper also exists in labile pools, defined as loosely bound to low-molecular-weight ligands, which can regulate diverse transition metal signaling processes spanning neural communication and olfaction, lipolysis, rest–activity cycles, and kinase pathways critical for oncogenic signaling. To help decipher this growing biology, we report a first-generation ratiometric fluorescence resonance energy transfer (FRET) copper probe, FCP-1, for activity-based sensing of labile Cu(I) pools in live cells. FCP-1 links fluorescein and rhodamine dyes through a Tris[(2-pyridyl)methyl]amine bridge. Bioinspired Cu(I)-induced oxidative cleavage decreases FRET between fluorescein donor and rhodamine acceptor. FCP-1 responds to Cu(I) with high metal selectivity and oxidation-state specificity and facilitates ratiometric measurements that minimize potential interferences arising from variations in sample thickness, dye concentration, and light intensity. FCP-1 enables imaging of dynamic changes in labile Cu(I) pools in live cells in response to copper supplementation/depletion, differential expression of the copper importer CTR1, and redox stress induced by manipulating intracellular Glutathione levels and reduced/oxidized Glutathione (GSH/GSSG) ratios. FCP-1 imaging reveals a labile Cu(I) deficiency induced by oncogene-driven cellular transformation that promotes fluctuations in Glutathione Metabolism, where lower GSH/GSSG ratios decrease labile Cu(I) availability without affecting total copper levels. By connecting copper dysregulation and Glutathione stress in cancer, this work provides a valuable starting point to study broader cross-talk between metal and redox pathways in health and disease with activity-based probes.

  • activity based ratiometric fret probe reveals oncogene driven changes in labile copper pools induced by altered Glutathione Metabolism
    bioRxiv, 2019
    Co-Authors: Clive Yiksham Chung, Jessica M Posimo, Tiffany Tsang, Julianne M Davis, Donita C Brady, Christopher J Chang
    Abstract:

    Copper is essential for life, and beyond its well-established ability to serve as a tightly-bound, redox-active active site cofactor for enzyme function, emerging data suggest that cellular copper also exists in labile pools, defined as loosely bound to low molecular weight ligands, which can regulate diverse transition metal signaling processes spanning neural communication and olfaction, lipolysis, rest-activity cycles, and kinase pathways critical for oncogenic signaling. To help decipher this growing biology, we report a first-generation ratiometric fluorescence resonance energy transfer (FRET) copper probe, FCP-1, for activity-based sensing of labile Cu(I) pools in live cells. FCP-1 links fluorescein and rhodamine dyes through a tris[(2-pyridyl)methyl]amine (TPA) bridge. Bioinspired Cu(I)-induced oxidative cleavage decreases FRET between fluorescein donor and rhodamine acceptor. FCP-1 responds to Cu(I) with high metal selectivity and oxidation-state specificity and facilitates ratiometric measurements that minimize potential interferences arising from variations in sample thickness, dye concentration, and light intensity. FCP-1 enables imaging of dynamic changes in labile Cu(I) pools in live cells in response to copper supplementation/depletion, differential expression of the copper importer CTR1, and redox stress induced by manipulating intracellular Glutathione levels and GSH/GSSG ratios. FCP-1 imaging reveals a labile Cu(I) deficiency induced by oncogene-driven cellular transformation that promotes fluctuations in Glutathione Metabolism, where lower GSH/GSSG ratios decrease labile Cu(I) availability without affecting total copper levels. By connecting copper dysregulation and Glutathione stress in cancer, this work provides a valuable starting point to study broader crosstalk between metal and redox pathways in health and disease with activity-based probes.nnSignificanceCopper is a required metal nutrient for life, yet its altered homeostasis is associated with many diseases. Thus, to develop new methods to help decipher copper biology, we present an activity-based ratiometric FRET probe that exploits a biomimetic, copper(I)-dependent cleavage reaction to enable imaging of loosely-bound, labile copper pools in cells with metal and oxidation state selectivity and a self-calibrating ratiometric response. Application of this technology to cellular models of cancer reveals that oncogene-driven changes in the Metabolism of Glutathione, a major cellular redox buffer, leads to a labile copper(I) deficiency. This work establishes the relevance of copper dysregulation to cancer Metabolism and presages further opportunities for activity-based sensing in studies of metal biology.

Zongsuo Liang - One of the best experts on this subject based on the ideXlab platform.

  • nitric oxide is involved in the regulation of ascorbate and Glutathione Metabolism in agropyron cristatum leaves under water stress
    Biologia Plantarum, 2011
    Co-Authors: Changjuan Shan, F He, G Xu, Zongsuo Liang
    Abstract:

    This study investigated the regulation of ascorbate and Glutathione Metabolism by nitric oxide in Agropyron cristatum leaves under water stress. The activities of ascorbate peroxidase (APX), Glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), L-galactono-1,4-lactone dehydrogenase (GalLDH) and γ-glutamylcysteine synthetase (γ-ECS), and the contents of NO, reduced ascorbic acid (AsA), reduced Glutathione (GSH), total ascorbate and total Glutathione increased under water stress. These increases were suppressed by pretreatments with NO synthesis inhibitors N G-nitro-L-arginine methyl ester (L-NAME) and 4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO). However, application of L-NAME and cPTIO to plants sufficiently supplied with water did not affect the activities of above mentioned enzymes and the contents of NO and above mentioned antioxidants. Pretreatments with L-NAME and cPTIO increased the malondialdehyde (MDA) content and electrolyte leakage of plants under water stress. Our results suggested that water stress-induced NO is a signal that leads to the upregulation of ascorbate and Glutathione Metabolism and has important role for acquisition of water stress tolerance.

  • jasmonic acid regulates ascorbate and Glutathione Metabolism in agropyron cristatum leaves under water stress
    Plant Science, 2010
    Co-Authors: Changjuan Shan, Zongsuo Liang
    Abstract:

    This study investigated the regulation of ascorbate and Glutathione Metabolism by jasmonic acid (JA) in Agropyron cristatum leaves under water stress induced by 10% PEG 6000. The results showed that JA level, the transcript levels and activities of APX, GR, MDHAR, DHAR, GalLDH and g-ECS, and the contents of AsA, GSH, total ascorbate and total Glutathione were increased by water stress. Above increases except for total Glutathione content and the transcript level and activity of g-ECS were suppressed by application of JA biosynthesis inhibitor ibuprofen (IBU), a lipoxygenase inhibitor, for 12 h before water stress treatment. Application of JA to IBU-inhibited plants prevented the reduction in the transcript levels and activities of GalLDH, APX, GR, DHAR and MDHAR, and the contents of AsA, GSH, total ascorbate induced by IBU under water stress. Meanwhile, pretreatment with IBU increased the malondialdehyde content and electrolyte leakage of plants and these increases were suppressed by application of JA under water stress. Our results suggested that water stress-induced JA is a signal that leads to the regulation of ascorbate and Glutathione Metabolism and has important role for acquisition of water stress tolerance in A. cristatum.

Clive Yiksham Chung - One of the best experts on this subject based on the ideXlab platform.

  • activity based ratiometric fret probe reveals oncogene driven changes in labile copper pools induced by altered Glutathione Metabolism
    Proceedings of the National Academy of Sciences of the United States of America, 2019
    Co-Authors: Clive Yiksham Chung, Jessica M Posimo, Tiffany Tsang, Julianne M Davis, Donita C Brady, Christopher J Chang
    Abstract:

    Copper is essential for life, and beyond its well-established ability to serve as a tightly bound, redox-active active site cofactor for enzyme function, emerging data suggest that cellular copper also exists in labile pools, defined as loosely bound to low-molecular-weight ligands, which can regulate diverse transition metal signaling processes spanning neural communication and olfaction, lipolysis, rest–activity cycles, and kinase pathways critical for oncogenic signaling. To help decipher this growing biology, we report a first-generation ratiometric fluorescence resonance energy transfer (FRET) copper probe, FCP-1, for activity-based sensing of labile Cu(I) pools in live cells. FCP-1 links fluorescein and rhodamine dyes through a Tris[(2-pyridyl)methyl]amine bridge. Bioinspired Cu(I)-induced oxidative cleavage decreases FRET between fluorescein donor and rhodamine acceptor. FCP-1 responds to Cu(I) with high metal selectivity and oxidation-state specificity and facilitates ratiometric measurements that minimize potential interferences arising from variations in sample thickness, dye concentration, and light intensity. FCP-1 enables imaging of dynamic changes in labile Cu(I) pools in live cells in response to copper supplementation/depletion, differential expression of the copper importer CTR1, and redox stress induced by manipulating intracellular Glutathione levels and reduced/oxidized Glutathione (GSH/GSSG) ratios. FCP-1 imaging reveals a labile Cu(I) deficiency induced by oncogene-driven cellular transformation that promotes fluctuations in Glutathione Metabolism, where lower GSH/GSSG ratios decrease labile Cu(I) availability without affecting total copper levels. By connecting copper dysregulation and Glutathione stress in cancer, this work provides a valuable starting point to study broader cross-talk between metal and redox pathways in health and disease with activity-based probes.

  • activity based ratiometric fret probe reveals oncogene driven changes in labile copper pools induced by altered Glutathione Metabolism
    bioRxiv, 2019
    Co-Authors: Clive Yiksham Chung, Jessica M Posimo, Tiffany Tsang, Julianne M Davis, Donita C Brady, Christopher J Chang
    Abstract:

    Copper is essential for life, and beyond its well-established ability to serve as a tightly-bound, redox-active active site cofactor for enzyme function, emerging data suggest that cellular copper also exists in labile pools, defined as loosely bound to low molecular weight ligands, which can regulate diverse transition metal signaling processes spanning neural communication and olfaction, lipolysis, rest-activity cycles, and kinase pathways critical for oncogenic signaling. To help decipher this growing biology, we report a first-generation ratiometric fluorescence resonance energy transfer (FRET) copper probe, FCP-1, for activity-based sensing of labile Cu(I) pools in live cells. FCP-1 links fluorescein and rhodamine dyes through a tris[(2-pyridyl)methyl]amine (TPA) bridge. Bioinspired Cu(I)-induced oxidative cleavage decreases FRET between fluorescein donor and rhodamine acceptor. FCP-1 responds to Cu(I) with high metal selectivity and oxidation-state specificity and facilitates ratiometric measurements that minimize potential interferences arising from variations in sample thickness, dye concentration, and light intensity. FCP-1 enables imaging of dynamic changes in labile Cu(I) pools in live cells in response to copper supplementation/depletion, differential expression of the copper importer CTR1, and redox stress induced by manipulating intracellular Glutathione levels and GSH/GSSG ratios. FCP-1 imaging reveals a labile Cu(I) deficiency induced by oncogene-driven cellular transformation that promotes fluctuations in Glutathione Metabolism, where lower GSH/GSSG ratios decrease labile Cu(I) availability without affecting total copper levels. By connecting copper dysregulation and Glutathione stress in cancer, this work provides a valuable starting point to study broader crosstalk between metal and redox pathways in health and disease with activity-based probes.nnSignificanceCopper is a required metal nutrient for life, yet its altered homeostasis is associated with many diseases. Thus, to develop new methods to help decipher copper biology, we present an activity-based ratiometric FRET probe that exploits a biomimetic, copper(I)-dependent cleavage reaction to enable imaging of loosely-bound, labile copper pools in cells with metal and oxidation state selectivity and a self-calibrating ratiometric response. Application of this technology to cellular models of cancer reveals that oncogene-driven changes in the Metabolism of Glutathione, a major cellular redox buffer, leads to a labile copper(I) deficiency. This work establishes the relevance of copper dysregulation to cancer Metabolism and presages further opportunities for activity-based sensing in studies of metal biology.

Changjuan Shan - One of the best experts on this subject based on the ideXlab platform.

  • nitric oxide acts downstream of hydrogen peroxide in the regulation of ascorbate and Glutathione Metabolism by jasmonic acid in agropyron cristatum leaves
    Biologia Plantarum, 2017
    Co-Authors: Changjuan Shan, T Yang
    Abstract:

    The relationship between hydrogen peroxide (H2O2) and nitric oxide (NO) in the regulation of ascorbate and Glutathione Metabolism by jasmonic acid (JA) in Agropyron cristatum leaves were studied. Results showed that JA increased the production of H2O2 and NO, the activities of ascorbate peroxidase (APX), Glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), L-galactono-1,4-lactone dehydrogenase (GalLDH), and γ-glutamylcysteine synthetase (γ-ECS) as well as transcription of the respective genes and also the content of reduced ascorbic acid (AsA) and reduced Glutathione (GSH). Above increases were suppressed by pre-treatments with H2O2 synthesis inhibitor diphenylene iodonium (DPI), H2O2 scavenger dimethylthiourea (DMTU), NO synthesis inhibitor NG-nitro-L-Arg methyl ester (L-NAME), and NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO). Pre-treatments with DPI and DMTU reduced H2O2 and NO production. Pre-treatments with L-NAME and cPTIO reduced NO production, but did not reduce the H2O2 production induced by JA. Our results suggested that NO acted downstream of H2O2 in JA signalling in the up-regulation of ascorbate and Glutathione Metabolism in A. cristatum leaves.

  • nitric oxide is involved in the regulation of ascorbate and Glutathione Metabolism in agropyron cristatum leaves under water stress
    Biologia Plantarum, 2011
    Co-Authors: Changjuan Shan, F He, G Xu, Zongsuo Liang
    Abstract:

    This study investigated the regulation of ascorbate and Glutathione Metabolism by nitric oxide in Agropyron cristatum leaves under water stress. The activities of ascorbate peroxidase (APX), Glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), L-galactono-1,4-lactone dehydrogenase (GalLDH) and γ-glutamylcysteine synthetase (γ-ECS), and the contents of NO, reduced ascorbic acid (AsA), reduced Glutathione (GSH), total ascorbate and total Glutathione increased under water stress. These increases were suppressed by pretreatments with NO synthesis inhibitors N G-nitro-L-arginine methyl ester (L-NAME) and 4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO). However, application of L-NAME and cPTIO to plants sufficiently supplied with water did not affect the activities of above mentioned enzymes and the contents of NO and above mentioned antioxidants. Pretreatments with L-NAME and cPTIO increased the malondialdehyde (MDA) content and electrolyte leakage of plants under water stress. Our results suggested that water stress-induced NO is a signal that leads to the upregulation of ascorbate and Glutathione Metabolism and has important role for acquisition of water stress tolerance.

  • effects of exogenous hydrogen sulfide on the ascorbate and Glutathione Metabolism in wheat seedlings leaves under water stress
    Acta Physiologiae Plantarum, 2011
    Co-Authors: Changjuan Shan, Shengli Zhang, Yuanzeng Zhao, Xueliang Tian, Xinliang Zhao, Xiuying Wei, Runqiang Liu
    Abstract:

    This study investigated the effects of exogenous hydrogen sulfide on the ascorbate and Glutathione Metabolism in wheat seedlings leaves under water stress. The results showed that pretreatment with sodium hydrosulfide (NaHS), hydrogen sulfide donor, increased the activities of ascorbate peroxidase, Glutathione reductase, dehydroascorbate reductase and gamma-glutamylcysteine synthetase, and the contents of reduced ascorbic acid, reduced Glutathione, total ascorbate and total Glutathione under water stress, compared to control and water stress without NaHS. Meanwhile, pretreatment with NaHS decreased the malondialdehyde content and electrolyte leakage induced by water stress in plants, compared to control and water stress without NaHS. Our results suggested that exogenous hydrogen sulfide alleviated oxidative damage by regulating the ascorbate and Glutathione Metabolism in wheat seedlings under water stress.

  • jasmonic acid regulates ascorbate and Glutathione Metabolism in agropyron cristatum leaves under water stress
    Plant Science, 2010
    Co-Authors: Changjuan Shan, Zongsuo Liang
    Abstract:

    This study investigated the regulation of ascorbate and Glutathione Metabolism by jasmonic acid (JA) in Agropyron cristatum leaves under water stress induced by 10% PEG 6000. The results showed that JA level, the transcript levels and activities of APX, GR, MDHAR, DHAR, GalLDH and g-ECS, and the contents of AsA, GSH, total ascorbate and total Glutathione were increased by water stress. Above increases except for total Glutathione content and the transcript level and activity of g-ECS were suppressed by application of JA biosynthesis inhibitor ibuprofen (IBU), a lipoxygenase inhibitor, for 12 h before water stress treatment. Application of JA to IBU-inhibited plants prevented the reduction in the transcript levels and activities of GalLDH, APX, GR, DHAR and MDHAR, and the contents of AsA, GSH, total ascorbate induced by IBU under water stress. Meanwhile, pretreatment with IBU increased the malondialdehyde content and electrolyte leakage of plants and these increases were suppressed by application of JA under water stress. Our results suggested that water stress-induced JA is a signal that leads to the regulation of ascorbate and Glutathione Metabolism and has important role for acquisition of water stress tolerance in A. cristatum.

Wenbiao Shen - One of the best experts on this subject based on the ideXlab platform.

  • transcriptome analysis reveals insight into molecular hydrogen induced cadmium tolerance in alfalfa the prominent role of sulfur and homo Glutathione Metabolism
    BMC Plant Biology, 2020
    Co-Authors: Weiti Cui, Ping Yao, Jincheng Pan, Chen Dai, Hong Cao, Zhiyu Chen, Shiting Zhang, Wenbiao Shen
    Abstract:

    Hydrogen gas (H2) is hypothesised to play a role in plants that are coping with stresses by regulating signal transduction and gene expression. Although the beneficial role of H2 in plant tolerance to cadmium (Cd) has been investigated previously, the corresponding mechanism has not been elucidated. In this report, the transcriptomes of alfalfa seedling roots under Cd and/or hydrogen-rich water (HRW) treatment were first analysed. Then, the sulfur Metabolism pathways were focused on and further investigated by pharmacological and genetic approaches. A total of 1968 differentially expressed genes (DEGs) in alfalfa seedling roots under Cd and/or HRW treatment were identified by RNA-Seq. The DEGs were classified into many clusters, including Glutathione (GSH) Metabolism, oxidative stress, and ATP-binding cassette (ABC) transporters. The results validated by RT-qPCR showed that the levels of relevant genes involved in sulfur Metabolism were enhanced by HRW under Cd treatment, especially the genes involved in (homo)Glutathione Metabolism. Additional experiments carried out with a Glutathione synthesis inhibitor and Arabidopsis thaliana cad2–1 mutant plants suggested the prominent role of Glutathione in HRW-induced Cd tolerance. These results were in accordance with the effects of HRW on the contents of (homo)Glutathione and (homo)phytochelatins and in alleviating oxidative stress under Cd stress. In addition, the HRW-induced alleviation of Cd toxicity might also be caused by a decrease in available Cd in seedling roots, achieved through ABC transporter-mediated secretion. Taken together, the results of our study indicate that H2 regulated the expression of genes relevant to sulfur and Glutathione Metabolism and enhanced Glutathione Metabolism which resulted in Cd tolerance by activating antioxidation and Cd chelation. These results may help to elucidate the mechanism governing H2-induced Cd tolerance in alfalfa.

  • carbon monoxide alleviates cadmium induced oxidative damage by modulating Glutathione Metabolism in the roots of medicago sativa
    New Phytologist, 2008
    Co-Authors: Yi Han, Jing Zhang, Xiaoyue Chen, Zhaozhou Gao, Wei Xuan, Xiao Ding, Wenbiao Shen
    Abstract:

    Summary • Using pharmacological and biochemical approaches, the role of cadmium (Cd)-induced carbon monoxide (CO) release and the relationship between CO and oxidative stress conferred by Cd exposure in the root tissues of alfalfa (Medicago sativa) plants were investigated. • Cd treatments showed a dose-dependent enhancement in lipid peroxidation. Both 100 and 200 µm CdCl2 treatments caused the increase of CO release, which is consistent with the changes in the activity of the CO synthetic enzyme heme oxygenase (HO) and its HO-1 transcript. • A 100 µm CdCl2 exposure enhanced the formation of nonprotein thiols (NPT), and reduced Glutathione (GSH) to oxidized Glutathione (GSSG), which was potentiated by the pretreatment of CO scavenger hemoglobin (Hb). Plants pretreated for 6 h with 50% CO-saturated aqueous solution, which induced the rapid endogenous CO release followed by a gradual decrease when subsequently exposed to 100 µm CdCl2 for 72 h, effectively decreased oxidative damage. Meanwhile, CO pretreatment modulated several enzymes responsible for GSH Metabolism, thus resulting in the partial restoration of GSH : GSSG ratio, which was significantly blocked by Hb. • These results are suggestive of a role for CO release as a signal element for the alleviation of Cd-induced oxidative damage by modulating Glutathione Metabolism.