The Experts below are selected from a list of 1200 Experts worldwide ranked by ideXlab platform
Michal Hershfinkel - One of the best experts on this subject based on the ideXlab platform.
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ZnR/GPR39 upregulation of K+/Cl−-cotransporter 3 in tamoxifen resistant breast cancer cells
Cell calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
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znr gpr39 upregulation of k cl cotransporter 3 in tamoxifen resistant breast cancer cells
Cell Calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
Maayan Mero - One of the best experts on this subject based on the ideXlab platform.
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ZnR/GPR39 upregulation of K+/Cl−-cotransporter 3 in tamoxifen resistant breast cancer cells
Cell calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
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znr gpr39 upregulation of k cl cotransporter 3 in tamoxifen resistant breast cancer cells
Cell Calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
Lianne Sheppard - One of the best experts on this subject based on the ideXlab platform.
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positive matrix factorization of a 32 month series of daily pm2 5 speciation data with incorporation of temperature stratification
Atmospheric Environment, 2013Co-Authors: Ricardo Piedrahita, Steven J Dutton, Jana B Milford, Joshua G Hemann, Jennifer L Peel, Shelly L Miller, Sverre Vedal, Lianne Sheppard, Michael P HanniganAbstract:Abstract This study presents source apportionment results for PM2.5 from applying positive matrix factorization (PMF) to a 32-month series of daily PM2.5 compositional data from Denver, CO, including concentrations of sulfate, nitrate, bulk elemental carbon (EC) and organic carbon (OC), and 51 organic molecular markers (OMMs). An optimum 8-factor solution was determined primarily based on the interpretability of the PMF results and rate of matching factors from bootstrapped PMF solutions with those from the base case solution. These eight factors were identified as inorganic ion, n-alkane, EC/sterane, light n-alkane/polycyclic aromatic hydrocarbon (PAH), medium alkane/Alkanoic Acid, PAH, winter/methoxyphenol and summer/odd n-alkane. The inorganic ion factor dominated the reconstructed PM2.5 mass (sulfate + nitrate + EC + OC) in cold periods (daily average temperature 20 °C; 53.1%). The two factors had comparable relative contributions of 26.5% and 27.1% in warm periods with temperatures between 10 °C and 20 °C. Each of the seven factors resolved in a previous study ( Dutton et al., 2010b ) using a 1-year data set from the same location matches one factor from the current work based on comparing factor profiles. Six out of the seven matched pairs of factors are linked to similar source classes as suggested by the strong correlations between factor contributions (r = 0.89–0.98). Temperature-stratified source apportionment was conducted for three subsets of the data in the current study, corresponding to the cold, warm and hot periods mentioned above. The cold period (7-factor) solution exhibited a similar distribution of reconstructed PM2.5 mass as the full data set solution. The factor contributions of the warm period (7-factor) solution were well correlated with those from the full data set solution (r = 0.76–0.99). However, the reconstructed PM2.5 mass was distributed more to inorganic ion, n-alkane and medium alkane/Alkanoic Acid factors in the warm period solution than in the full data set solution. For the hot period (6-factor) solution, PM2.5 mass distribution was quite different from that of the full data set solution, as illustrated by regression slopes as low as 0.2 and as high as 4.8 of each matched pair of factors across the two solutions.
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positive matrix factorization of a 32 month series of daily pm2 5 speciation data with incorporation of temperature stratification
Atmospheric Environment, 2013Co-Authors: Mingjie Xie, Ricardo Piedrahita, Steven J Dutton, Jana B Milford, Joshua G Hemann, Jennifer L Peel, Shelly L Miller, Sverre Vedal, Sunyoung Kim, Lianne SheppardAbstract:Abstract This study presents source apportionment results for PM 2.5 from applying positive matrix factorization (PMF) to a 32-month series of daily PM 2.5 compositional data from Denver, CO, including concentrations of sulfate, nitrate, bulk elemental carbon (EC) and organic carbon (OC), and 51 organic molecular markers (OMMs). An optimum 8-factor solution was determined primarily based on the interpretability of the PMF results and rate of matching factors from bootstrapped PMF solutions with those from the base case solution. These eight factors were identified as inorganic ion, n -alkane, EC/sterane, light n -alkane/polycyclic aromatic hydrocarbon (PAH), medium alkane/Alkanoic Acid, PAH, winter/methoxyphenol and summer/odd n -alkane. The inorganic ion factor dominated the reconstructed PM 2.5 mass (sulfate + nitrate + EC + OC) in cold periods (daily average temperature 2.5 mass) whereas the summer/odd n -alkane factor dominated in hot periods (>20 °C; 53.1%). The two factors had comparable relative contributions of 26.5% and 27.1% in warm periods with temperatures between 10 °C and 20 °C. Each of the seven factors resolved in a previous study ( Dutton et al., 2010b ) using a 1-year data set from the same location matches one factor from the current work based on comparing factor profiles. Six out of the seven matched pairs of factors are linked to similar source classes as suggested by the strong correlations between factor contributions ( r = 0.89–0.98). Temperature-stratified source apportionment was conducted for three subsets of the data in the current study, corresponding to the cold, warm and hot periods mentioned above. The cold period (7-factor) solution exhibited a similar distribution of reconstructed PM 2.5 mass as the full data set solution. The factor contributions of the warm period (7-factor) solution were well correlated with those from the full data set solution ( r = 0.76–0.99). However, the reconstructed PM 2.5 mass was distributed more to inorganic ion, n -alkane and medium alkane/Alkanoic Acid factors in the warm period solution than in the full data set solution. For the hot period (6-factor) solution, PM 2.5 mass distribution was quite different from that of the full data set solution, as illustrated by regression slopes as low as 0.2 and as high as 4.8 of each matched pair of factors across the two solutions.
Israel Sekler - One of the best experts on this subject based on the ideXlab platform.
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ZnR/GPR39 upregulation of K+/Cl−-cotransporter 3 in tamoxifen resistant breast cancer cells
Cell calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
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znr gpr39 upregulation of k cl cotransporter 3 in tamoxifen resistant breast cancer cells
Cell Calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
Hila Asraf - One of the best experts on this subject based on the ideXlab platform.
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ZnR/GPR39 upregulation of K+/Cl−-cotransporter 3 in tamoxifen resistant breast cancer cells
Cell calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.
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znr gpr39 upregulation of k cl cotransporter 3 in tamoxifen resistant breast cancer cells
Cell Calcium, 2019Co-Authors: Maayan Mero, Israel Sekler, Hila Asraf, Kathryn Mary Taylor, Michal HershfinkelAbstract:Expression of the zinc receptor, ZnR/GPR39, is increased in higher grade breast cancer tumors and cells. Zinc, its ligand, is accumulated at larger concentrations in the tumor tissue and can therefore activate ZnR/GPR39-dependent Ca2+ signaling leading to tumor progression. The K+/Cl- co-transporters (KCC), activated by intracellular signaling, enhance breast cancer cell migration and invasion. We asked if ZnR/GPR39 enhances breast cancer cell malignancy by activating KCC. Activation of ZnR/GPR39 by Zn2+ upregulated K+/Cl- co-transport activity, measured using NH4+ as a surrogate to K+ while monitoring intracellular pH. Upregulation of NH4+ transport was monitored in tamoxifen resistant cells with functional ZnR/GPR39-dependent Ca2+ signaling but not in MCF-7 cells lacking this response. The NH4+ transport was Na+-independent, and we therefore focused on KCC family members. Silencing of KCC3, but not KCC4, expression abolished Zn2+-dependent K+/Cl- co-transport, suggesting that KCC3 is mediating upregulated NH4+ transport. The ZnR/GPR39-dependent KCC3 activation accelerated scratch closure rate, which was abolished by inhibiting KCC transport with [(DihydroIndenyl) Oxy] Alkanoic Acid (DIOA). Importantly, silencing of either ZnR/GPR39 or KCC3 attenuated Zn2+-dependent scratch closure. Thus, a novel link between KCC3 and Zn2+, via ZnR/GPR39, promotes breast cancer cell migration and proliferation.