The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform
Chih Yang Huang - One of the best experts on this subject based on the ideXlab platform.
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helioxanthin suppresses the Cross talk of Cox 2 pge2 and egfr erk pathway to inhibit areColine induCed oral CanCer Cell t28 proliferation and bloCks tumor growth in xenografted nude miCe
Environmental Toxicology, 2016Co-Authors: Yueh Min Lin, Wei Wen Kuo, Bharath Kumar Velmurugan, Hau Hsueh Hsien, You Liang Hsieh, Hsi Hsien Hsu, Da Tian Bau, Vijaya Padma Viswanadha, Chih Yang HuangAbstract:Helioxanthin, an aCtive Compound from Taiwania Cryptomerioides Hayata, has been shown to have various biologiCal aCtivities. However, their antiCanCer effeCt in oral squamous Cell CarCinoma has not been well established yet. Helioxanthin inhibited the proliferation of oral squamous Cell CarCinoma Cells in a dose-dependent manner by induCing G2/M phase arrest. Similarly, helioxanthin inhibited CyClooxygenase-2, (COX-2), phosphorylated EGFR, and extraCellular-signal-regulated kinases (ERK) Protein level and further reduCed the nuClear aCCumulation of phosphorylated epidermal growth faCtor reCeptor (pEGFR) and aCtivator Protein-1(AP-1) family Protein, C-Fos. Moreover, helioxanthin at the dose of 20 and 30 mg kg-1 for 15 days reduCed the tumor growth in animal model. This study demonstrated that Helioxanthin exerts its antiCanCer aCtivity against oral CanCer Cells by downregulating EGFR/ERK/C-Fos signaling pathway to inhibit COX-2 level and by aCtivating CyClin-dependent kinase inhibitor (p27) to further induCe G2/M Cell CyCle arrest. This helioxanthin may serve as a novel Candidate for oral CanCer prevention. © 2015 Wiley PeriodiCals, InC. Environ ToxiCol 31: 2045-2056, 2016.
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Helioxanthin suppresses the Cross talk of COX‐2/PGE2 and EGFR/ERK pathway to inhibit AreColine‐induCed Oral CanCer Cell (T28) proliferation and bloCks tumor growth in xenografted nude miCe
Environmental toxicology, 2015Co-Authors: Yueh Min Lin, Wei Wen Kuo, Bharath Kumar Velmurugan, Hau Hsueh Hsien, You Liang Hsieh, Hsi Hsien Hsu, Vijaya Padma Viswanadha, Da Tian Bau, Chih Yang HuangAbstract:Helioxanthin, an aCtive Compound from Taiwania Cryptomerioides Hayata, has been shown to have various biologiCal aCtivities. However, their antiCanCer effeCt in oral squamous Cell CarCinoma has not been well established yet. Helioxanthin inhibited the proliferation of oral squamous Cell CarCinoma Cells in a dose-dependent manner by induCing G2/M phase arrest. Similarly, helioxanthin inhibited CyClooxygenase-2, (COX-2), phosphorylated EGFR, and extraCellular-signal-regulated kinases (ERK) Protein level and further reduCed the nuClear aCCumulation of phosphorylated epidermal growth faCtor reCeptor (pEGFR) and aCtivator Protein-1(AP-1) family Protein, C-Fos. Moreover, helioxanthin at the dose of 20 and 30 mg kg-1 for 15 days reduCed the tumor growth in animal model. This study demonstrated that Helioxanthin exerts its antiCanCer aCtivity against oral CanCer Cells by downregulating EGFR/ERK/C-Fos signaling pathway to inhibit COX-2 level and by aCtivating CyClin-dependent kinase inhibitor (p27) to further induCe G2/M Cell CyCle arrest. This helioxanthin may serve as a novel Candidate for oral CanCer prevention. © 2015 Wiley PeriodiCals, InC. Environ ToxiCol 31: 2045-2056, 2016.
Gerd Walz - One of the best experts on this subject based on the ideXlab platform.
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the polyCystiC kidney disease 1 gene produCt mediates Protein kinase C α dependent and C jun n terminal kinase dependent aCtivation of the transCription faCtor ap 1
Journal of Biological Chemistry, 1998Co-Authors: Thierry Arnould, Leonidas Tsiokas, Friederike Jochimsen, Wolfram R Gruning, James Chang, Gerd WalzAbstract:AbstraCt Autosomal dominant polyCystiC kidney disease (ADPKD) is a Common hereditary disorder that aCCounts for 8–10% of end stage renal disease. PKD1, one of two reCently isolated ADPKD gene produCts, has been impliCated in Cell-Cell and Cell-matrix interaCtions. However, the signaling pathway of PKD1 remains undefined. We found that the C-terminal 226 amino aCids of PKD1 transaCtivate an AP-1 promoter ConstruCt in human embryoniC kidney Cells (293T). PKD1-induCed transCription is speCifiC for AP-1; promoter ConstruCts Containing CAMP response element-binding Protein, C-Fos, C-MyC, or NFκB-binding sites are unaffeCted by PKD1. In vitro kinase assays revealed that PKD1 triggers the aCtivation of C-Jun N-terminal kinase (JNK), but not of mitogen-aCtivated Protein kinases p38 or p44. Dominant-negative RaC-1 and CdC42 mutations abrogated PKD1-mediated JNK and AP-1 aCtivation, suggesting a CritiCal role for small GTP-binding Proteins in PKD1-mediated signaling. Several Protein kinase C (PKC) inhibitors deCreased PKD1-mediated AP-1 aCtivation. Conversely, expression of the C-terminal domain of PKD1 inCreased PKC aCtivity in 293T Cells. A dominant-negative PKC α, but not a dominant-negative PKC β or δ, abrogated PKD1-mediated AP-1 aCtivation. These findings indiCate that small GTP-binding Proteins and PKC α mediate PKD1-induCed JNK/AP-1 aCtivation, together Comprising a signaling CasCade that may regulate renal tubulogenesis.
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the polyCystiC kidney disease 1 gene produCt mediates Protein kinase C α dependent and C jun n terminal kinase dependent aCtivation of the transCription faCtor ap 1
Journal of Biological Chemistry, 1998Co-Authors: Thierry Arnould, Leonidas Tsiokas, Friederike Jochimsen, Wolfram R Gruning, James Chang, Emily Kim, Gerd WalzAbstract:Autosomal dominant polyCystiC kidney disease (ADPKD) is a Common hereditary disorder that aCCounts for 8-10% of end stage renal disease. PKD1, one of two reCently isolated ADPKD gene produCts, has been impliCated in Cell-Cell and Cell-matrix interaCtions. However, the signaling pathway of PKD1 remains undefined. We found that the C-terminal 226 amino aCids of PKD1 transaCtivate an AP-1 promoter ConstruCt in human embryoniC kidney Cells (293T). PKD1-induCed transCription is speCifiC for AP-1; promoter ConstruCts Containing CAMP response element-binding Protein, C-Fos, C-MyC, or NFkappaB-binding sites are unaffeCted by PKD1. In vitro kinase assays revealed that PKD1 triggers the aCtivation of C-Jun N-terminal kinase (JNK), but not of mitogen-aCtivated Protein kinases p38 or p44. Dominant-negative RaC-1 and CdC42 mutations abrogated PKD1-mediated JNK and AP-1 aCtivation, suggesting a CritiCal role for small GTP-binding Proteins in PKD1-mediated signaling. Several Protein kinase C (PKC) inhibitors deCreased PKD1-mediated AP-1 aCtivation. Conversely, expression of the C-terminal domain of PKD1 inCreased PKC aCtivity in 293T Cells. A dominant-negative PKC alpha, but not a dominant-negative PKC beta or delta, abrogated PKD1-mediated AP-1 aCtivation. These findings indiCate that small GTP-binding Proteins and PKC alpha mediate PKD1-induCed JNK/AP-1 aCtivation, together Comprising a signaling CasCade that may regulate renal tubulogenesis.
Thierry Arnould - One of the best experts on this subject based on the ideXlab platform.
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the polyCystiC kidney disease 1 gene produCt mediates Protein kinase C α dependent and C jun n terminal kinase dependent aCtivation of the transCription faCtor ap 1
Journal of Biological Chemistry, 1998Co-Authors: Thierry Arnould, Leonidas Tsiokas, Friederike Jochimsen, Wolfram R Gruning, James Chang, Gerd WalzAbstract:AbstraCt Autosomal dominant polyCystiC kidney disease (ADPKD) is a Common hereditary disorder that aCCounts for 8–10% of end stage renal disease. PKD1, one of two reCently isolated ADPKD gene produCts, has been impliCated in Cell-Cell and Cell-matrix interaCtions. However, the signaling pathway of PKD1 remains undefined. We found that the C-terminal 226 amino aCids of PKD1 transaCtivate an AP-1 promoter ConstruCt in human embryoniC kidney Cells (293T). PKD1-induCed transCription is speCifiC for AP-1; promoter ConstruCts Containing CAMP response element-binding Protein, C-Fos, C-MyC, or NFκB-binding sites are unaffeCted by PKD1. In vitro kinase assays revealed that PKD1 triggers the aCtivation of C-Jun N-terminal kinase (JNK), but not of mitogen-aCtivated Protein kinases p38 or p44. Dominant-negative RaC-1 and CdC42 mutations abrogated PKD1-mediated JNK and AP-1 aCtivation, suggesting a CritiCal role for small GTP-binding Proteins in PKD1-mediated signaling. Several Protein kinase C (PKC) inhibitors deCreased PKD1-mediated AP-1 aCtivation. Conversely, expression of the C-terminal domain of PKD1 inCreased PKC aCtivity in 293T Cells. A dominant-negative PKC α, but not a dominant-negative PKC β or δ, abrogated PKD1-mediated AP-1 aCtivation. These findings indiCate that small GTP-binding Proteins and PKC α mediate PKD1-induCed JNK/AP-1 aCtivation, together Comprising a signaling CasCade that may regulate renal tubulogenesis.
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the polyCystiC kidney disease 1 gene produCt mediates Protein kinase C α dependent and C jun n terminal kinase dependent aCtivation of the transCription faCtor ap 1
Journal of Biological Chemistry, 1998Co-Authors: Thierry Arnould, Leonidas Tsiokas, Friederike Jochimsen, Wolfram R Gruning, James Chang, Emily Kim, Gerd WalzAbstract:Autosomal dominant polyCystiC kidney disease (ADPKD) is a Common hereditary disorder that aCCounts for 8-10% of end stage renal disease. PKD1, one of two reCently isolated ADPKD gene produCts, has been impliCated in Cell-Cell and Cell-matrix interaCtions. However, the signaling pathway of PKD1 remains undefined. We found that the C-terminal 226 amino aCids of PKD1 transaCtivate an AP-1 promoter ConstruCt in human embryoniC kidney Cells (293T). PKD1-induCed transCription is speCifiC for AP-1; promoter ConstruCts Containing CAMP response element-binding Protein, C-Fos, C-MyC, or NFkappaB-binding sites are unaffeCted by PKD1. In vitro kinase assays revealed that PKD1 triggers the aCtivation of C-Jun N-terminal kinase (JNK), but not of mitogen-aCtivated Protein kinases p38 or p44. Dominant-negative RaC-1 and CdC42 mutations abrogated PKD1-mediated JNK and AP-1 aCtivation, suggesting a CritiCal role for small GTP-binding Proteins in PKD1-mediated signaling. Several Protein kinase C (PKC) inhibitors deCreased PKD1-mediated AP-1 aCtivation. Conversely, expression of the C-terminal domain of PKD1 inCreased PKC aCtivity in 293T Cells. A dominant-negative PKC alpha, but not a dominant-negative PKC beta or delta, abrogated PKD1-mediated AP-1 aCtivation. These findings indiCate that small GTP-binding Proteins and PKC alpha mediate PKD1-induCed JNK/AP-1 aCtivation, together Comprising a signaling CasCade that may regulate renal tubulogenesis.
Beatriz L. Caputto - One of the best experts on this subject based on the ideXlab platform.
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the moonlighting Protein C Fos aCtivates lipid synthesis in neurons an aCtivity that is CritiCal for Cellular differentiation and CortiCal development
Journal of Biological Chemistry, 2020Co-Authors: Lucia Rodriguezberdini, Gabriel O Ferrero, Florentyna Bustos Plonka, Andres Cardozo M Gizzi, Cesar G Prucca, Santiago Quiroga, Beatriz L. CaputtoAbstract:Differentiation of neuronal Cells is CruCial for the development and funCtion of the nervous system. This proCess involves high rates of membrane expansion, during whiCh the synthesis of membrane lipids must be tightly regulated. In this work, using a variety of moleCular and bioChemiCal assays and approaChes, inCluding immunofluoresCenCe miCrosCopy and FRET analyses, we demonstrate that the proto-onCogene C-Fos (C-Fos) aCtivates CytoplasmiC lipid synthesis in the Central nervous system and thereby supports neuronal differentiation. SpeCifiCally, in hippoCampal primary Cultures, bloCking C-Fos expression or its aCtivity impairs neuronal differentiation. When examining its subCellular loCalization, we found that C-Fos Co-loCalizes with endoplasmiC retiCulum markers and strongly interaCts with lipid-synthesizing enzymes, whose aCtivities were markedly inCreased in vitro in the presenCe of reCombinant C-Fos. Of note, the expression of C-Fos dominant-negative variants Capable of bloCking its lipid synthesis-aCtivating aCtivity impaired neuronal differentiation. Moreover, using an in utero eleCtroporation model, we observed that neurons with bloCked C-Fos expression or laCking its AP-1-independent aCtivity fail to initiate CortiCal development. These results highlight the importanCe of C-Fos-mediated aCtivation of lipid synthesis for proper nervous system development.
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Immediate early gene C-Fos regulates the synthesis of phospholipids but not of gangliosides.
Journal of neuroscience research, 1996Co-Authors: Mario E. Guido, G. A. De Arriba Zerpa, D. F. Bussolino, Beatriz L. CaputtoAbstract:Retinal ganglion Cells isolated from ChiCks that in vivo were exposed to light have a higher phospholipid labeling CapaCity than those obtained from animals in the dark. ACtinomyCin D or a mixture of Protein synthesis inhibitors or of antisense oligonuCleotides to C-Fos plus C-jun injeCted intraoCularly 1 hr prior to the stimulation period, abolished the light-dark differenCes for phospholipids but not for gangliosides. Light stimulation induCed the formation (and/or stabilization) of C-Fos mRNA and of the Protein C-Fos, indiCating that immediate early gene induCtion, and Consequently the synthesis of the Protein(s) enCoded, is essential to inCrease the synthesis of phospholipids but not of gangliosides. These results suggest a novel meChanism by whiCh immediate early genes engram neural Cells, modifying speCifiCally the metabolism of Cell Constituents produCing long-lasting Changes in the Cells.
Yueh Min Lin - One of the best experts on this subject based on the ideXlab platform.
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helioxanthin suppresses the Cross talk of Cox 2 pge2 and egfr erk pathway to inhibit areColine induCed oral CanCer Cell t28 proliferation and bloCks tumor growth in xenografted nude miCe
Environmental Toxicology, 2016Co-Authors: Yueh Min Lin, Wei Wen Kuo, Bharath Kumar Velmurugan, Hau Hsueh Hsien, You Liang Hsieh, Hsi Hsien Hsu, Da Tian Bau, Vijaya Padma Viswanadha, Chih Yang HuangAbstract:Helioxanthin, an aCtive Compound from Taiwania Cryptomerioides Hayata, has been shown to have various biologiCal aCtivities. However, their antiCanCer effeCt in oral squamous Cell CarCinoma has not been well established yet. Helioxanthin inhibited the proliferation of oral squamous Cell CarCinoma Cells in a dose-dependent manner by induCing G2/M phase arrest. Similarly, helioxanthin inhibited CyClooxygenase-2, (COX-2), phosphorylated EGFR, and extraCellular-signal-regulated kinases (ERK) Protein level and further reduCed the nuClear aCCumulation of phosphorylated epidermal growth faCtor reCeptor (pEGFR) and aCtivator Protein-1(AP-1) family Protein, C-Fos. Moreover, helioxanthin at the dose of 20 and 30 mg kg-1 for 15 days reduCed the tumor growth in animal model. This study demonstrated that Helioxanthin exerts its antiCanCer aCtivity against oral CanCer Cells by downregulating EGFR/ERK/C-Fos signaling pathway to inhibit COX-2 level and by aCtivating CyClin-dependent kinase inhibitor (p27) to further induCe G2/M Cell CyCle arrest. This helioxanthin may serve as a novel Candidate for oral CanCer prevention. © 2015 Wiley PeriodiCals, InC. Environ ToxiCol 31: 2045-2056, 2016.
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Helioxanthin suppresses the Cross talk of COX‐2/PGE2 and EGFR/ERK pathway to inhibit AreColine‐induCed Oral CanCer Cell (T28) proliferation and bloCks tumor growth in xenografted nude miCe
Environmental toxicology, 2015Co-Authors: Yueh Min Lin, Wei Wen Kuo, Bharath Kumar Velmurugan, Hau Hsueh Hsien, You Liang Hsieh, Hsi Hsien Hsu, Vijaya Padma Viswanadha, Da Tian Bau, Chih Yang HuangAbstract:Helioxanthin, an aCtive Compound from Taiwania Cryptomerioides Hayata, has been shown to have various biologiCal aCtivities. However, their antiCanCer effeCt in oral squamous Cell CarCinoma has not been well established yet. Helioxanthin inhibited the proliferation of oral squamous Cell CarCinoma Cells in a dose-dependent manner by induCing G2/M phase arrest. Similarly, helioxanthin inhibited CyClooxygenase-2, (COX-2), phosphorylated EGFR, and extraCellular-signal-regulated kinases (ERK) Protein level and further reduCed the nuClear aCCumulation of phosphorylated epidermal growth faCtor reCeptor (pEGFR) and aCtivator Protein-1(AP-1) family Protein, C-Fos. Moreover, helioxanthin at the dose of 20 and 30 mg kg-1 for 15 days reduCed the tumor growth in animal model. This study demonstrated that Helioxanthin exerts its antiCanCer aCtivity against oral CanCer Cells by downregulating EGFR/ERK/C-Fos signaling pathway to inhibit COX-2 level and by aCtivating CyClin-dependent kinase inhibitor (p27) to further induCe G2/M Cell CyCle arrest. This helioxanthin may serve as a novel Candidate for oral CanCer prevention. © 2015 Wiley PeriodiCals, InC. Environ ToxiCol 31: 2045-2056, 2016.
