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Olivier Boyer - One of the best experts on this subject based on the ideXlab platform.
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AMPK Activation of PGC-1α/NRF-1-Dependent SELENOT Gene Transcription Promotes PACAP-Induced Neuroendocrine Cell Differentiation Through Tolerance to Oxidative Stress
Molecular Neurobiology, 2019Co-Authors: Houssni Abid, Jerome Leprince, Dorthe Cartier, Abdallah Hamieh, Anne-marie François-bellan, Christine Bucharles, Hugo Pothion, Destiny-love Manecka, Sahil Adriouch, Olivier BoyerAbstract:Several cues including pituitary adenylate cyclase-activating polypeptide (PACAP), which acts through cAMP stimulation, specify the conversion of sympathoadrenal (SA) precursors toward different Cell phenotypes by promoting their survival and differentiation. Selenoprotein T (SELENOT) is a PACAP-stimulated ER oxidoreductase that exerts an essential antioxidant activity and whose up-regulation is associated with SA Cell differentiation. In the present study, we investigated the transcriptional cascade elicited by PACAP/cAMP to trigger SELENOT gene transcription during the conversion of Pc12 Cells from SA progenitor-like Cells toward a neuroendocrine phenotype. Unexpectedly, we found that PACAP/cAMP recruits the canonical pathway that regulates mitochondrial function in order to elicit SELENOT gene transcription and the consequent antioxidant response during Pc12 Cell differentiation. This cascade involves LKB1-mediated AMPK activation in order to stimulate SELENOT gene transcription through the PGC1-α/NRF-1 complex, thus allowing SELENOT to promote PACAP-stimulated neuroendocrine Cell survival and differentiation. Our data reveal that a PACAP and cAMP-activated AMPK-PGC-1α/NRF-1 cascade is critical for the coupling of oxidative stress tolerance, via SELENOT gene expression, and mitochondrial biogenesis in order to achieve Pc12 Cell differentiation. The data further highlight the essential role of SELENOT in Cell metabolism during differentiation.
Jerome Leprince - One of the best experts on this subject based on the ideXlab platform.
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AMPK Activation of PGC-1α/NRF-1-Dependent SELENOT Gene Transcription Promotes PACAP-Induced Neuroendocrine Cell Differentiation Through Tolerance to Oxidative Stress
Molecular Neurobiology, 2019Co-Authors: Houssni Abid, Jerome Leprince, Dorthe Cartier, Abdallah Hamieh, Anne-marie François-bellan, Christine Bucharles, Hugo Pothion, Destiny-love Manecka, Sahil Adriouch, Olivier BoyerAbstract:Several cues including pituitary adenylate cyclase-activating polypeptide (PACAP), which acts through cAMP stimulation, specify the conversion of sympathoadrenal (SA) precursors toward different Cell phenotypes by promoting their survival and differentiation. Selenoprotein T (SELENOT) is a PACAP-stimulated ER oxidoreductase that exerts an essential antioxidant activity and whose up-regulation is associated with SA Cell differentiation. In the present study, we investigated the transcriptional cascade elicited by PACAP/cAMP to trigger SELENOT gene transcription during the conversion of Pc12 Cells from SA progenitor-like Cells toward a neuroendocrine phenotype. Unexpectedly, we found that PACAP/cAMP recruits the canonical pathway that regulates mitochondrial function in order to elicit SELENOT gene transcription and the consequent antioxidant response during Pc12 Cell differentiation. This cascade involves LKB1-mediated AMPK activation in order to stimulate SELENOT gene transcription through the PGC1-α/NRF-1 complex, thus allowing SELENOT to promote PACAP-stimulated neuroendocrine Cell survival and differentiation. Our data reveal that a PACAP and cAMP-activated AMPK-PGC-1α/NRF-1 cascade is critical for the coupling of oxidative stress tolerance, via SELENOT gene expression, and mitochondrial biogenesis in order to achieve Pc12 Cell differentiation. The data further highlight the essential role of SELENOT in Cell metabolism during differentiation.
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selenoprotein t is a pacap regulated gene involved in intraCellular ca2 mobilization and neuroendocrine secretion
The FASEB Journal, 2008Co-Authors: Luca Grumolato, Hafida Ghzili, Maite Monterohadjadje, Stephane Gasman, Jean Lesage, Yannick Tanguy, Ludovic Galas, Djida Aitali, Jerome Leprince, Nathalie C GuerineauAbstract:Selenoproteins contain the essential trace element selenium, the deficiency of which is associated with cancer or accelerated aging. Although selenoproteins are thought to be instrumental for the effects of selenium, the biological function of many of these proteins remains unknown. Here, we studied the role of selenoprotein T (SelT), a selenocysteine (Sec) -containing protein with no known function, which we have identified as a novel target gene of the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) during Pc12 Cell differentiation. SelT was found to be ubiquitously expressed throughout embryonic development and in adulthood in rat. Immunocytochemical analysis revealed that SelT is mainly localized to the endoplasmic reticulum through a hydrophobic domain. PACAP and cAMP induced a rapid and long-lasting increase in SelT gene expression in Pc12 Cells, in a Ca2+-dependent manner. These results suggested a possible role of SelT in PACAP signaling during Pc12 Cell differentiation. In...
Houssni Abid - One of the best experts on this subject based on the ideXlab platform.
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AMPK Activation of PGC-1α/NRF-1-Dependent SELENOT Gene Transcription Promotes PACAP-Induced Neuroendocrine Cell Differentiation Through Tolerance to Oxidative Stress
Molecular Neurobiology, 2019Co-Authors: Houssni Abid, Jerome Leprince, Dorthe Cartier, Abdallah Hamieh, Anne-marie François-bellan, Christine Bucharles, Hugo Pothion, Destiny-love Manecka, Sahil Adriouch, Olivier BoyerAbstract:Several cues including pituitary adenylate cyclase-activating polypeptide (PACAP), which acts through cAMP stimulation, specify the conversion of sympathoadrenal (SA) precursors toward different Cell phenotypes by promoting their survival and differentiation. Selenoprotein T (SELENOT) is a PACAP-stimulated ER oxidoreductase that exerts an essential antioxidant activity and whose up-regulation is associated with SA Cell differentiation. In the present study, we investigated the transcriptional cascade elicited by PACAP/cAMP to trigger SELENOT gene transcription during the conversion of Pc12 Cells from SA progenitor-like Cells toward a neuroendocrine phenotype. Unexpectedly, we found that PACAP/cAMP recruits the canonical pathway that regulates mitochondrial function in order to elicit SELENOT gene transcription and the consequent antioxidant response during Pc12 Cell differentiation. This cascade involves LKB1-mediated AMPK activation in order to stimulate SELENOT gene transcription through the PGC1-α/NRF-1 complex, thus allowing SELENOT to promote PACAP-stimulated neuroendocrine Cell survival and differentiation. Our data reveal that a PACAP and cAMP-activated AMPK-PGC-1α/NRF-1 cascade is critical for the coupling of oxidative stress tolerance, via SELENOT gene expression, and mitochondrial biogenesis in order to achieve Pc12 Cell differentiation. The data further highlight the essential role of SELENOT in Cell metabolism during differentiation.
E L Sabban - One of the best experts on this subject based on the ideXlab platform.
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Endogenous and exogenous ARC in serum withdrawal mediated Pc12 Cell apoptosis: a new pro-apoptotic role for ARC.
Cell death and differentiation, 2001Co-Authors: T A Dowds, E L SabbanAbstract:The role of ARC (Apoptosis Repressor with Caspase Recruitment Domain) in Pc12 Cell serum withdrawal driven apoptosis was studied. A progressive and massive increase in ARC protein occurs during serum withdrawal that correlates with declining survival and processing of caspase-2, previously shown to associate with ARC.1 This accumulation of ARC occurs in a transcriptional and translational independent manner. Additionally, ARC is localized exclusively in the nucleus of Pc12 Cells. Furthermore, transfection of Pc12 Cells with hARC-Flag promotes death and fails to protect the Cells from apoptosis by serum withdrawal. Therefore, ARC functions in a pro-apoptotic manner in Pc12 Cell serum withdrawal induced apoptosis. Cell Death and Differentiation (2001) 8, 640–648
Dorthe Cartier - One of the best experts on this subject based on the ideXlab platform.
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AMPK Activation of PGC-1α/NRF-1-Dependent SELENOT Gene Transcription Promotes PACAP-Induced Neuroendocrine Cell Differentiation Through Tolerance to Oxidative Stress
Molecular Neurobiology, 2019Co-Authors: Houssni Abid, Jerome Leprince, Dorthe Cartier, Abdallah Hamieh, Anne-marie François-bellan, Christine Bucharles, Hugo Pothion, Destiny-love Manecka, Sahil Adriouch, Olivier BoyerAbstract:Several cues including pituitary adenylate cyclase-activating polypeptide (PACAP), which acts through cAMP stimulation, specify the conversion of sympathoadrenal (SA) precursors toward different Cell phenotypes by promoting their survival and differentiation. Selenoprotein T (SELENOT) is a PACAP-stimulated ER oxidoreductase that exerts an essential antioxidant activity and whose up-regulation is associated with SA Cell differentiation. In the present study, we investigated the transcriptional cascade elicited by PACAP/cAMP to trigger SELENOT gene transcription during the conversion of Pc12 Cells from SA progenitor-like Cells toward a neuroendocrine phenotype. Unexpectedly, we found that PACAP/cAMP recruits the canonical pathway that regulates mitochondrial function in order to elicit SELENOT gene transcription and the consequent antioxidant response during Pc12 Cell differentiation. This cascade involves LKB1-mediated AMPK activation in order to stimulate SELENOT gene transcription through the PGC1-α/NRF-1 complex, thus allowing SELENOT to promote PACAP-stimulated neuroendocrine Cell survival and differentiation. Our data reveal that a PACAP and cAMP-activated AMPK-PGC-1α/NRF-1 cascade is critical for the coupling of oxidative stress tolerance, via SELENOT gene expression, and mitochondrial biogenesis in order to achieve Pc12 Cell differentiation. The data further highlight the essential role of SELENOT in Cell metabolism during differentiation.
