The Experts below are selected from a list of 1605 Experts worldwide ranked by ideXlab platform
Monica M Bertagnolli - One of the best experts on this subject based on the ideXlab platform.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated β-catenin, dissociation of β-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and β-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc+/+ wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and β-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated β-catenin. Thus, the ApcMin allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including β-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress β-catenin tyrosine phosphorylation.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated beta-catenin. Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
Adelaide M Carothers - One of the best experts on this subject based on the ideXlab platform.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated β-catenin, dissociation of β-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and β-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc+/+ wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and β-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated β-catenin. Thus, the ApcMin allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including β-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress β-catenin tyrosine phosphorylation.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated beta-catenin. Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
Amy E Moran - One of the best experts on this subject based on the ideXlab platform.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated β-catenin, dissociation of β-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and β-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc+/+ wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and β-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated β-catenin. Thus, the ApcMin allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including β-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress β-catenin tyrosine phosphorylation.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated beta-catenin. Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
Chathur Acharya - One of the best experts on this subject based on the ideXlab platform.
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Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium
2016Co-Authors: Vivek Mishra, Rachel Cline, Pawan Noel, Catherine J. Baty, Lidiya Orlichenko, Krutika Patel, Sohail Z. Husain, Jenny Karlsson, Ram Narayan Trivedi, Chathur AcharyaAbstract:Several deleterious intra-acinar phenomena are simultaneously triggered on initiating acute pancreatitis. These culminate in acinar injury or inflammatory mediator generation in vitro and parenchymal damage in vivo. Supraphysiologic caerulein is one such initiator which simultaneously activates numerous signaling pathways including non-receptor tyrosine kinases such as of the Src family. It also causes a sustained increase in cytosolic calcium- a player thought to be crucial in regulating deleterious phenomena. We have shown Src to be involved in caerulein induced actin remodeling, and caerulein induced changes in the Golgi and post-Golgi trafficking to be involved in trypsinogen activation, which initiates acinar cell injury. However, it remains unclear whether an increase in cytosolic calcium is necessary to initiate acinar injury or if injury can be initiated at basal cytosolic calcium levels by an alternate pathway. To study the interplay between tyrosine kinase signaling and calcium, we treated mouse pancreatic acinar cells with the tyrosine phosphatase inhibitor Pervanadate. We studied the effect of the clinically used Src inhibitor Dasatinib (BMS-354825) on Pervanadate or caerulein induced changes in Src activation, trypsinogen activation, cell injury, upstream cytosolic calcium, actin and Golgi morphology. Pervanadate, like supraphysiologic caerulein, induced Src activation, redistribution of the F-actin from its normal location in the sub-apica
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Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium
PloS one, 2013Co-Authors: Vivek Mishra, Rachel Cline, Pawan Noel, Jenny M. Karlsson, Catherine J. Baty, Lidiya Orlichenko, Krutika Patel, Ram N. Trivedi, Sohail Z. Husain, Chathur AcharyaAbstract:Several deleterious intra-acinar phenomena are simultaneously triggered on initiating acute pancreatitis. These culminate in acinar injury or inflammatory mediator generation in vitro and parenchymal damage in vivo. Supraphysiologic caerulein is one such initiator which simultaneously activates numerous signaling pathways including non-receptor tyrosine kinases such as of the Src family. It also causes a sustained increase in cytosolic calcium- a player thought to be crucial in regulating deleterious phenomena. We have shown Src to be involved in caerulein induced actin remodeling, and caerulein induced changes in the Golgi and post-Golgi trafficking to be involved in trypsinogen activation, which initiates acinar cell injury. However, it remains unclear whether an increase in cytosolic calcium is necessary to initiate acinar injury or if injury can be initiated at basal cytosolic calcium levels by an alternate pathway. To study the interplay between tyrosine kinase signaling and calcium, we treated mouse pancreatic acinar cells with the tyrosine phosphatase inhibitor Pervanadate. We studied the effect of the clinically used Src inhibitor Dasatinib (BMS-354825) on Pervanadate or caerulein induced changes in Src activation, trypsinogen activation, cell injury, upstream cytosolic calcium, actin and Golgi morphology. Pervanadate, like supraphysiologic caerulein, induced Src activation, redistribution of the F-actin from its normal location in the sub-apical area to the basolateral areas, and caused antegrade fragmentation of the Golgi. These changes, like those induced by supraphysiologic caerulein, were associated with trypsinogen activation and acinar injury, all of which were prevented by Dasatinib. Interestingly, however, Pervanadate did not cause an increase in cytosolic calcium, and the caerulein induced increase in cytosolic calcium was not affected by Dasatinib. These findings suggest that intra-acinar deleterious phenomena may be initiated independent of an increase in cytosolic calcium. Other players resulting in acinar injury along with the Src family of tyrosine kinases remain to be explored.
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Dasatinib reduces Pervanadate and caerulein induced trypsinogen activation and acinar cell injury.
2013Co-Authors: Vivek Mishra, Rachel Cline, Pawan Noel, Catherine J. Baty, Lidiya Orlichenko, Krutika Patel, Sohail Z. Husain, Jenny Karlsson, Ram Narayan Trivedi, Chathur AcharyaAbstract:Trypsin activity is increased in cell homogenates from acini treated with 100 µM Pervanadate (PV) (A), 100 nM caerulein (CER) (B) for 30 minutes. Lactate dehydrogenase (LDH) leakage is increased from acini treated with 100 µM Pervanadate (PV) (C), 100 nM caerulein (D) for 4 hours. Preincubation with 10 µM Dasatinib (DAS) prevents these phenomena in response to both Pervanadate and caerulein (A, B, C, D). BAS; Basal conditions. p-values mentioned in the figure were calculated using the Student’s t-test. Each bar representing mean ± SEM, was calculated from at least 3 different experiments.
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Pervanadate induced F-actin reorganization and antegrade Golgi fragmentation is inhibited by Dasatinib.
2013Co-Authors: Vivek Mishra, Rachel Cline, Pawan Noel, Catherine J. Baty, Lidiya Orlichenko, Krutika Patel, Sohail Z. Husain, Jenny Karlsson, Ram Narayan Trivedi, Chathur AcharyaAbstract:Fluorescence imaging of acini under basal conditions (Basal, A, E), after stimulation with 100 µM Pervanadate (PV) for 10 minutes (B,F) or Pervanadate treated acini in the presence of Dasatinib (PV+DAS, C,G) showing F-actin (Red), the Golgi marker GM130 (green) and nuclei (Blue). Under basal conditions F-actin (A) is enriched in the sub-apical area, and the stacks of Golgi (E) in the supranuclear area occupying
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Src is activated by Pervanadate and supramaximal Caerulein.
2013Co-Authors: Vivek Mishra, Rachel Cline, Pawan Noel, Catherine J. Baty, Lidiya Orlichenko, Krutika Patel, Sohail Z. Husain, Jenny Karlsson, Ram Narayan Trivedi, Chathur AcharyaAbstract:Western-blot of immunoprecipitated Src after treatment of acini with 100 µM Pervanadate (PV) for various times (A), 2 minutes of 100 µM Pervanadate with or without pre-incubation with 10 µM Dasatinib (DAS) (B) or 100 nM caerulein (CER) with or without pre-incubation with 10 µM Dasatinib (Das) (C). These were blotted for antibodies to Src PY416 (i.e. active Src, upper panel), and then stripped and blotted for Total Src (SC-18, Lower panel). Corresponding graphs shown on the right show active Src levels (PY-416) as a ratio to total Src (SC-18) depicted as fold change over basal (BAS). Each data point was calculated from 3 or more experiments. For figure 1A, the graph depicts fold increase over BAS at the time of adding the stimulus and the asterisks in the graph depict a p value of ≤0.02. p values for the graphs corresponding to figure 1B, C are mentioned above these.
Michael J Weyant - One of the best experts on this subject based on the ideXlab platform.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated β-catenin, dissociation of β-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and β-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc+/+ wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and β-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated β-catenin. Thus, the ApcMin allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including β-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress β-catenin tyrosine phosphorylation.
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carnosol inhibits β catenin tyrosine phosphorylation and prevents adenoma formation in the c57bl 6j min min mouse
Cancer Research, 2005Co-Authors: Amy E Moran, Adelaide M Carothers, Michael J Weyant, Mark Redston, Monica M BertagnolliAbstract:Carnosol, a constituent of the herb, rosemary, has shown beneficial medicinal and antitumor effects. Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%. Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes. Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate. Moreover, treatment of WT intestine with the phosphatase inhibitor, Pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue. Pretreatment of WT tissue with carnosol inhibited the Pervanadate-inducible expression of tyrosine-phosphorylated beta-catenin. Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin. Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.