Oncogene C Fos

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Julie Y H Chan - One of the best experts on this subject based on the ideXlab platform.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase Cβ niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase C niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

Samuel H H Chan - One of the best experts on this subject based on the ideXlab platform.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase Cβ niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase C niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

Linglin Wang - One of the best experts on this subject based on the ideXlab platform.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase Cβ niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase C niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

Hueyling Tseng - One of the best experts on this subject based on the ideXlab platform.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase Cβ niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

  • upregulation of at1 reCeptor gene on aCtivation of protein kinase C niCotinamide adenine dinuCleotide diphosphate oxidase erk1 2 C Fos signaling CasCade mediates long term pressor effeCt of angiotensin ii in rostral ventrolateral medulla
    Journal of Hypertension, 2007
    Co-Authors: Samuel H H Chan, Linglin Wang, Hueyling Tseng, Julie Y H Chan
    Abstract:

    ObjeCtive Angiotensin II induCes the phosphorylation of p38 mitogen-aCtivated protein kinase (MAPK) and extraCellular signal-regulated kinase (ERK) 1/2 via the aCtivation of niCotinamide adenine dinuCleotide diphosphate (NADPH) oxidase on stimulation of the angiotensin subtype 1 reCeptor (AT 1 R) in the rostral ventrolateral medulla (RVLM), where sympathetiC premotor neurons for the maintenanCe of vasomotor tone and blood pressure are loCated. Angiotensin II-aCtivated p38 MAPK in RVLM promotes a short-term pressor effeCt via augmented glutamatergiC neurotransmission. We tested the hypothesis that the NADPH oxidase-dependent phosphorylation of ERK1/2 after the aCtivation of Conventional protein kinase C (PKC) mediates the AT 1 R-dependent long-term pressor effeCts of angiotensin II via transCriptional induCtion of the proto-OnCogene C-Fos gene in RVLM. Methods and results In Sprague-Dawley rats, a miCroinjeCtion of angiotensin II bilaterally into the RVLM induCed membrane-bound transloCation of the Conventional PKCα, PKCp or PKCγ isoform, phosphorylation of the p47 phox subunit of NADPH oxidase and ERK1/2, followed by phosphorylation of the transCription faCtor CyCliC adenosine monophosphate response element binding protein (CREB), and C-Fos induCtion. The PKC inhibitor antagonized angiotensin II-induCed p47 phox phosphorylation, and an antisense oligonuCleotide (ASON) Complementary to PKCp messenger RNA suppressed angiotensin ll-induCed ERK1/ 2 aCtivation, phosphorylation or DNA binding aCtivity of CREB, and upregulation of C-Fos mRNA expression in the ventrolateral medulla. Furthermore, a miCroinjeCtion of ERK1/2, CREB or C-Fos ASON into the RVLM signifiCantly reduCed the long-term pressor effeCt and augmented AT 1 R expression in the ventrolateral medulla induCed by intraCerebroventriCular infusion of angiotensin II. ConClusion We ConCluded that the PKCp/NADPH oxidase/ ERK1/2/CREB/C-Fos CasCade represents a novel signaling CasCade that mediates the long-term pressor effeCt induCed by angiotensin II in the RVLM.

Shigeru Taketani - One of the best experts on this subject based on the ideXlab platform.

  • map kinase independent induCtion of proto OnCogene C Fos mrna by hemin in human Cells
    Biochemical and Biophysical Research Communications, 1999
    Co-Authors: Yoshiro Masuya, Isamu Kameshita, Hitoshi Fujisawa, Hirao Kohno, Koshiro Hioki, Rikio Tokunaga, Shigeru Taketani
    Abstract:

    Treatment of HeLa Cells or human skin fibroblast Cells with hemin led to a time- and dose-dependent rapid induCtion of C-Fos mRNA. This induCtion was absent in the Cells treated with aCtinomyCin D, indiCating that the C-Fos induCtion by hemin oCCurs at the level of transCription. Metalloporphyrins, inCluding zinC-, Cobalt-, and tin-protoporphyrin, ferriC ion, and protoporphyrin also induCed C-Fos mRNA. Transient reporter assay with the reporter ConstruCts of the human C-Fos gene promoter up to -404 bp ConneCted to the luCiferase gene showed high aCtivity but no induCtion by hemin, suggesting that Cis-aCting elements, inCluding the serum response element loCated about -310 bp upstream of the human C-Fos gene promoter, may not Contribute to the heme-dependent induCtion. With in-gel assay of protein kinases, the aCtivity of the mitogen-aCtivated protein (MAP) kinases suCh as extraCellular signal-regulated kinase 12 or p38 MAP kinase in hemin-treated HeLa Cells was not stimulated. Stimulation of C-Jun N-terminal kinase by hemin was nil. Furthermore, PD58059 and SB203580, inhibitors for MAP kinases, did not affeCt the hemin-dependent C-Fos induCtion. Of the inhibitors for protein kinases so far tested, KN-62, a speCifiC inhibitor for Calmodulin-dependent protein kinase II (CaMK II), inhibited the induCtion of C-Fos mRNA by hemin. Phosphorylation of CaMK II in hemin-treated Cells inCreased. With gel mobility assay, the DNA AP-1 binding aCtivity transiently inCreased when treating HeLa Cells with hemin. Therefore, induCtion of C-Fos led to an aCtivation of AP-1 in the presenCe of hemin. We suggest that Calmodulin-dependent protein kinase II rather than the MAP kinase family regulates the induCtion of the human C-Fos gene expression by hemin.

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