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  1. AU="Lallet-Daher, Helene"
  2. AU="Greenblatt, M"
  3. AU="Patwa, Ajay K"
  4. AU=Mastaglia F L
  5. AU="De Croock, Femke"
  6. AU=Robinson Michael J
  7. AU=Singh Romil
  8. AU="Martin, S J"
  9. AU="Szendrői, Miklós"
  10. AU="Moncel, Marie-Hélène"
  11. AU=Otu Akaninyene AU=Otu Akaninyene
  12. AU="Chiba, Kentaro"
  13. AU="Zhou, Jihua"
  14. AU="Ronald Bartels"
  15. AU="Liñares, J"
  16. AU="Valle, Valentina"
  17. AU="Tóth, András"
  18. AU="Pawar, Atul Darasing"
  19. AU="Semper, Chelsea"
  20. AU="Kraus, Joanne F"

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Treffer 1 - 4 von insgesamt 4

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  1. Artikel ; Online: Caspase-2 regulates oncogene-induced senescence.

    Gitenay, Delphine / Lallet-Daher, Hélène / Bernard, David

    Oncotarget

    2014  Band 5, Heft 14, Seite(n) 5845–5847

    Abstract: Cellular senescence is activated by numerous cellular insults, in particular those driving cancer formation, resulting in stable proliferation arrest and acquisition of specific features. By self-opposing to oncogenic stimulation, senescence is ... ...

    Abstract Cellular senescence is activated by numerous cellular insults, in particular those driving cancer formation, resulting in stable proliferation arrest and acquisition of specific features. By self-opposing to oncogenic stimulation, senescence is considered as a failsafe program, allowing, when functional, to inhibit cancers occurrence. Compelling evidences suggest a tumor suppressive activity of caspase-2, eventually independently of its effect on cell death. The original results described here demonstrate that this tumor suppressive activity of caspase-2 is mediated, at least in part, by its pro-senescing activity. Indeed, we have demonstrated in vitro and in vivo that loss of function of caspase-2 allows to escape oncogenic stress induced senescence. These results are discussed in the context of known tumor suppressive activity of caspase-2.
    Mesh-Begriff(e) Caspase 2/genetics ; Caspase 2/metabolism ; Cellular Senescence/genetics ; Cysteine Endopeptidases/genetics ; Cysteine Endopeptidases/metabolism ; DNA Damage ; Humans ; Mammary Glands, Human/enzymology ; Oncogenes ; RNA, Small Interfering/administration & dosage ; RNA, Small Interfering/genetics
    Chemische Substanzen RNA, Small Interfering ; CASP2 protein, human (EC 3.4.22.-) ; Caspase 2 (EC 3.4.22.-) ; Cysteine Endopeptidases (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2014-08-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.2286
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Endoplasmic reticulum calcium release through ITPR2 channels leads to mitochondrial calcium accumulation and senescence.

    Wiel, Clotilde / Lallet-Daher, Hélène / Gitenay, Delphine / Gras, Baptiste / Le Calvé, Benjamin / Augert, Arnaud / Ferrand, Mylène / Prevarskaya, Natalia / Simonnet, Hélène / Vindrieux, David / Bernard, David

    Nature communications

    2014  Band 5, Seite(n) 3792

    Abstract: Senescence is involved in various pathophysiological conditions. Besides loss of retinoblastoma and p53 pathways, little is known about other pathways involved in senescence. Here we identify two calcium channels; inositol 1,4,5-trisphosphate receptor, ... ...

    Abstract Senescence is involved in various pathophysiological conditions. Besides loss of retinoblastoma and p53 pathways, little is known about other pathways involved in senescence. Here we identify two calcium channels; inositol 1,4,5-trisphosphate receptor, type 2 (ITPR2) (also known as inositol 1,4,5-triphosphate receptor 2 (IP3R2)) and mitochondrial calcium uniporter (MCU) as new senescence regulators in a loss-of-function genetic screen. We show that loss of ITPR2, known to mediate endoplasmic reticulum (ER) calcium release, as well as loss of MCU, necessary for mitochondrial calcium uptake, enable escape from oncogene-induced senescence (OIS). During OIS, ITPR2 triggers calcium release from the ER, followed by mitochondrial calcium accumulation through MCU channels. Mitochondrial calcium accumulation leads to a subsequent decrease in mitochondrial membrane potential, reactive oxygen species accumulation and senescence. This ER-mitochondria calcium transport is not restricted to OIS, but is also involved in replicative senescence. Our results show a functional role of calcium release by the ITPR2 channel and its subsequent accumulation in the mitochondria.
    Mesh-Begriff(e) Calcium/metabolism ; Cellular Senescence ; Endoplasmic Reticulum/metabolism ; Humans ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Membrane Potential, Mitochondrial ; Mitochondria/metabolism ; Oncogenes ; Oxidative Stress
    Chemische Substanzen ITPR2 protein, human ; Inositol 1,4,5-Trisphosphate Receptors ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2014-05-06
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2041-1723
    ISSN (online) 2041-1723
    DOI 10.1038/ncomms4792
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Potassium channel KCNA1 modulates oncogene-induced senescence and transformation.

    Lallet-Daher, Hélène / Wiel, Clotilde / Gitenay, Delphine / Navaratnam, Naveenan / Augert, Arnaud / Le Calvé, Benjamin / Verbeke, Stéphanie / Carling, David / Aubert, Sébastien / Vindrieux, David / Bernard, David

    Cancer research

    2013  Band 73, Heft 16, Seite(n) 5253–5265

    Abstract: Oncogene-induced senescence (OIS) constitutes a failsafe program that restricts tumor development. However, the mechanisms that link oncogenesis to senescence are not completely understood. We carried out a loss-of-function genetic screen that identified ...

    Abstract Oncogene-induced senescence (OIS) constitutes a failsafe program that restricts tumor development. However, the mechanisms that link oncogenesis to senescence are not completely understood. We carried out a loss-of-function genetic screen that identified the potassium channel KCNA1 as a determinant of OIS escape that can license tumor growth. Oncogenic stress triggers an increase in KCNA1 expression and its relocation from the cytoplasm to the membrane. Mechanistically, this relocation is due to a loss of protein kinase A (PKA)-induced phosphorylation at residue S446 of KCNA1. Accordingly, sustaining PKA activity or expressing a KCNA1 phosphomimetic mutant maintained KCNA1 in the cytoplasm and caused escape from OIS. KCNA1 relocation to the membrane induced a change in membrane potential that invariably resulted in cellular senescence. Restoring KCNA1 expression in transformation-competent cells triggered variation in membrane potential and blocked RAS-induced transformation, and PKA activation suppressed both effects. Furthermore, KCNA1 expression was reduced in human cancers, and this decrease correlated with an increase in breast cancer aggressiveness. Taken together, our results identify a novel pathway that restricts oncogenesis through a potassium channel-dependent senescence pathway.
    Mesh-Begriff(e) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Growth Processes/physiology ; Cell Line ; Cell Membrane/genetics ; Cell Membrane/metabolism ; Cell Transformation, Neoplastic/genetics ; Cellular Senescence/genetics ; Cyclic AMP-Dependent Protein Kinases/genetics ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cytoplasm/genetics ; Cytoplasm/metabolism ; Down-Regulation ; Humans ; Kv1.1 Potassium Channel/genetics ; Kv1.1 Potassium Channel/metabolism ; Mammary Glands, Human/metabolism ; Mammary Glands, Human/pathology ; Membrane Potentials/genetics ; Mice ; NIH 3T3 Cells ; Phosphorylation/genetics ; Signal Transduction/genetics
    Chemische Substanzen Kv1.1 Potassium Channel (147173-20-4) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Sprache Englisch
    Erscheinungsdatum 2013-06-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-12-3690
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: PLA2R1 mediates tumor suppression by activating JAK2.

    Vindrieux, David / Augert, Arnaud / Girard, Christophe A / Gitenay, Delphine / Lallet-Daher, Helene / Wiel, Clotilde / Le Calvé, Benjamin / Gras, Baptiste / Ferrand, Mylène / Verbeke, Stéphanie / de Launoit, Yvan / Leroy, Xavier / Puisieux, Alain / Aubert, Sébastien / Perrais, Michael / Gelb, Michael / Simonnet, Hélène / Lambeau, Gérard / Bernard, David

    Cancer research

    2013  Band 73, Heft 20, Seite(n) 6334–6345

    Abstract: Little is known about the physiological role of the phospholipase A2 receptor (PLA2R1). PLA2R1 has been described as regulating the replicative senescence, a telomerase-dependent proliferation arrest. The downstream PLA2R1 signaling and its role in ... ...

    Abstract Little is known about the physiological role of the phospholipase A2 receptor (PLA2R1). PLA2R1 has been described as regulating the replicative senescence, a telomerase-dependent proliferation arrest. The downstream PLA2R1 signaling and its role in cancer are currently unknown. Senescence induction in response to activated oncogenes is a failsafe program of tumor suppression that must be bypassed for tumorigenesis. We now present evidence that PLA2R1 functions in vitro as a tumor suppressor, the depletion of which is sufficient to escape oncogene-induced senescence (OIS), thereby facilitating oncogenic cell transformation. Furthermore, mice that are genetically deficient in PLA2R1 display increased sensitivity to RAS-induced tumorigenesis by facilitating OIS escape, highlighting its physiological role as a tumor suppressor. Unexpectedly, PLA2R1 activated JAK2 and its effector signaling, with PLA2R1-mediated inhibition of cell transformation largely reverted in JAK2-depleted cells. This finding was unexpected as the JAK2 pathway has been associated mainly with protumoral functions and several inhibitors are currently in clinical trials. Taken together, our findings uncover an unanticipated tumor suppressive role for PLA2R1 that is mediated by targeting downstream JAK2 effector signaling.
    Mesh-Begriff(e) Animals ; Cell Culture Techniques ; Cell Growth Processes/physiology ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cellular Senescence/genetics ; Cellular Senescence/physiology ; Enzyme Activation ; Humans ; Immunohistochemistry ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NIH 3T3 Cells ; Receptors, Phospholipase A2/genetics ; Receptors, Phospholipase A2/metabolism ; Skin Neoplasms/enzymology ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Transfection
    Chemische Substanzen PLA2R1 protein, human ; Pla2r1 protein, mouse ; Receptors, Phospholipase A2 ; Janus Kinase 2 (EC 2.7.10.2)
    Sprache Englisch
    Erscheinungsdatum 2013-09-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-13-0318
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.135/5: Hefte anzeigen Standort:
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