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  1. AU="Ciro Zanca"
  2. AU="Edward Itelman"
  3. AU="Emma Gardner"
  4. AU="Pawlak, Mathias" AU="Pawlak, Mathias"
  5. AU=Evcili Funda
  6. AU="Cochran, Christina J"
  7. AU="Moossavi, Shahab"
  8. AU="M Mathieu Morin"
  9. AU="Angione, Katie"
  10. AU="Abdela, Abdurezak Ahmed"
  11. AU="Sanda, Miloslav"
  12. AU="Srinivas Ramishetti"
  13. AU="Chen, Yaoqing"
  14. AU="Cotton, Anitria"
  15. AU="Bayer, Adrian E."
  16. AU="Boerke, A"
  17. AU="Brown, Guy C."
  18. AU=Ford Caleb A.
  19. AU="Hussain, Muhammad Afaq"
  20. AU="Werner Henkel"
  21. AU=Zellweger M J
  22. AU="Marasco, Michelangelo"
  23. AU="Landa-Moreno, Cinthia"
  24. AU="Kuntner, Matjaz"
  25. AU="Lemes, Robertha Mariana Rodrigues"
  26. AU="Riccioni, M E"
  27. AU="Traer, Colin J"
  28. AU="Cao, Xuejie"
  29. AU="Chen, Zishuo"
  30. AU="Kalachikov, Sergey"
  31. AU="Das, Tilak"
  32. AU="Bessat, Cécile"
  33. AU="Galina Velikova"
  34. AU="Greene, Sharrell"
  35. AU="Chen, Kallie J"
  36. AU="Schwab, Jörg O."
  37. AU="Ke Chen"
  38. AU="Hewei Liang"
  39. AU="Abreu, Cristina"
  40. AU="Mamani Ortiz, Yercin"
  41. AU="Castro, Lucíola de Fátima Albuquerque Almeida Peixoto"
  42. AU="Šimůnek, Tomáš"
  43. AU="Ong, Lizhen"
  44. AU="Chai, Chaoqing"
  45. AU="Maheswaran Kesavan"
  46. AU="Mehta, Mrunal"
  47. AU=Paredes Sergio D
  48. AU=Ghosh Nilanjan AU=Ghosh Nilanjan
  49. AU="Hofmann, Alexander"
  50. AU="Radici, Marco"
  51. AU="Noro, Fabrizia"
  52. AU="Wang, Jianzhao"
  53. AU="Divya Jeyam"
  54. AU="Wolf, Lisette"
  55. AU="Marjanovic, Nemanja Despot"
  56. AU="Jitxin, Lim"

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  1. Artikel ; Online: Correction

    Jorge A. Benitez / Jianhui Ma / Matteo D’Antonio / Antonia Boyer / Maria Fernanda Camargo / Ciro Zanca / Stephen Kelly / Alireza Khodadadi-Jamayran / Nathan M. Jameson / Michael Andersen / Hrvoje Miletic / Shahram Saberi / Kelly A. Frazer / Webster K. Cavenee / Frank B. Furnari

    Nature Communications, Vol 9, Iss 1, Pp 1-

    Publisher Correction: PTEN regulates glioblastoma oncogenesis through chromatin-associated complexes of DAXX and histone H3.3

    2018  Band 1

    Abstract: Nature Communications 8:15223 doi: (2017); Published 12 May 2017; Updated 25 May 2018 The originally published version of this Article contained an error in Fig. 1. In panel d, the uppermost western blot was inadvertently inverted during typesetting of ... ...

    Abstract Nature Communications 8:15223 doi: (2017); Published 12 May 2017; Updated 25 May 2018 The originally published version of this Article contained an error in Fig. 1. In panel d, the uppermost western blot was inadvertently inverted during typesetting of the figure. This has now been corrected in boththe PDF and HTML versions of the Article.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-05-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: PTEN regulates glioblastoma oncogenesis through chromatin-associated complexes of DAXX and histone H3.3

    Jorge A. Benitez / Jianhui Ma / Matteo D’Antonio / Antonia Boyer / Maria Fernanda Camargo / Ciro Zanca / Stephen Kelly / Alireza Khodadadi-Jamayran / Nathan M. Jameson / Michael Andersen / Hrvoje Miletic / Shahram Saberi / Kelly A. Frazer / Webster K. Cavenee / Frank B. Furnari

    Nature Communications, Vol 8, Iss 1, Pp 1-

    2017  Band 15

    Abstract: PTEN mutations are frequent in glioblastoma and often are associated with therapeutic resistance. Here, the authors demonstrate that PTEN regulates gene expression at the chromatin level by interacting with the histone chaperone DAXX and H3.3, and that ... ...

    Abstract PTEN mutations are frequent in glioblastoma and often are associated with therapeutic resistance. Here, the authors demonstrate that PTEN regulates gene expression at the chromatin level by interacting with the histone chaperone DAXX and H3.3, and that DAXX inhibition inhibits PTEN-deficient GBM growth in vivo.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2017-05-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel: Cancer-Associated Protein Kinase C Mutations Reveal Kinase’s Role as Tumor Suppressor

    Antal, Corina E / Andrew M. Hudson / Emily Kang / Ciro Zanca / Christopher Wirth / Natalie L. Stephenson / Eleanor W. Trotter / Lisa L. Gallegos / Crispin J. Miller / Frank B. Furnari / Tony Hunter / John Brognard / Alexandra C. Newton

    Cell. 2015 Jan. 29, v. 160

    2015  

    Abstract: Protein kinase C (PKC) isozymes have remained elusive cancer targets despite the unambiguous tumor promoting function of their potent ligands, phorbol esters, and the prevalence of their mutations. We analyzed 8% of PKC mutations identified in human ... ...

    Abstract Protein kinase C (PKC) isozymes have remained elusive cancer targets despite the unambiguous tumor promoting function of their potent ligands, phorbol esters, and the prevalence of their mutations. We analyzed 8% of PKC mutations identified in human cancers and found that, surprisingly, most were loss of function and none were activating. Loss-of-function mutations occurred in all PKC subgroups and impeded second-messenger binding, phosphorylation, or catalysis. Correction of a loss-of-function PKCβ mutation by CRISPR-mediated genome editing in a patient-derived colon cancer cell line suppressed anchorage-independent growth and reduced tumor growth in a xenograft model. Hemizygous deletion promoted anchorage-independent growth, revealing that PKCβ is haploinsufficient for tumor suppression. Several mutations were dominant negative, suppressing global PKC signaling output, and bioinformatic analysis suggested that PKC mutations cooperate with co-occurring mutations in cancer drivers. These data establish that PKC isozymes generally function as tumor suppressors, indicating that therapies should focus on restoring, not inhibiting, PKC activity.
    Schlagwörter bioinformatics ; catalytic activity ; colorectal neoplasms ; esters ; genome ; humans ; isozymes ; ligands ; loss-of-function mutation ; models ; phosphorylation ; protein kinase C
    Sprache Englisch
    Erscheinungsverlauf 2015-0129
    Umfang p. 489-502.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2015.01.001
    Datenquelle NAL Katalog (AGRICOLA)

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  4. Artikel ; Online: Akt regulates drug-induced cell death through Bcl-w downregulation.

    Michela Garofalo / Cristina Quintavalle / Ciro Zanca / Assunta De Rienzo / Giulia Romano / Mario Acunzo / Loredana Puca / Mariarosaria Incoronato / Carlo M Croce / Gerolama Condorelli

    PLoS ONE, Vol 3, Iss 12, p e

    2008  Band 4070

    Abstract: Akt is a serine threonine kinase with a major role in transducing survival signals and regulating proteins involved in apoptosis. To find new interactors of Akt involved in cell survival, we performed a two-hybrid screening in yeast using human full- ... ...

    Abstract Akt is a serine threonine kinase with a major role in transducing survival signals and regulating proteins involved in apoptosis. To find new interactors of Akt involved in cell survival, we performed a two-hybrid screening in yeast using human full-length Akt c-DNA as bait and a murine c-DNA library as prey. Among the 80 clones obtained, two were identified as Bcl-w. Bcl-w is a member of the Bcl-2 family that is essential for the regulation of cellular survival, and that is up-regulated in different human tumors, such as gastric and colorectal carcinomas. Direct interaction of Bcl-w with Akt was confirmed by immunoprecipitation assays. Subsequently, we addressed the function of this interaction: by interfering with the activity or amount of Akt, we have demonstrated that Akt modulates the amount of Bcl-w protein. We have found that inhibition of Akt activity may promote apoptosis through the downregulation of Bcl-w protein and the consequential reduction in interaction of Bcl-w with pro-apoptotic members of the Bcl-2 family. Our data provide evidence that Bcl-w is a new member of the Akt pathway and that Akt may induce anti-apoptotic signals at least in part through the regulation of the amount and activity of Bcl-w.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel: EGFR Mutation Promotes Glioblastoma through Epigenome and Transcription Factor Network Remodeling

    Liu, Feng / Ah Young Lee / Andrew K. Shiau / Bin Li / Bing Ren / Bowen Wei / Cathy L. Barr / Ciro Zanca / David Jenkins / Frank B. Furnari / Gary C. Hon / Genaro R. Villa / Greg Lucey / Huijun Yang / Kristen M. Turner / Paul S. Mischel / Samantha Kuan / Shiro Ikegami / Timothy C. Gahman /
    Timothy F. Cloughesy / Webster K. Cavenee / Wei Zhang / William H. Yong / Zhen Ye

    Molecular cell. 2015 Oct. 15, v. 60

    2015  

    Abstract: Epidermal growth factor receptor (EGFR) gene amplification and mutations are the most common oncogenic events in glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated ... ...

    Abstract Epidermal growth factor receptor (EGFR) gene amplification and mutations are the most common oncogenic events in glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, genotyped clinical samples, and TCGA data, we show that EGFR mutations remodel the activated enhancer landscape of GBM, promoting tumorigenesis through a SOX9 and FOXG1-dependent transcriptional regulatory network in vitro and in vivo. The most common EGFR mutation, EGFRvIII, sensitizes GBM cells to the BET-bromodomain inhibitor JQ1 in a SOX9, FOXG1-dependent manner. These results identify the role of transcriptional/epigenetic remodeling in EGFR-dependent pathogenesis and suggest a mechanistic basis for epigenetic therapy.
    Schlagwörter carcinogenesis ; epidermal growth factor receptors ; epigenetics ; gene amplification ; genotyping ; mutation ; therapeutics ; transcription (genetics) ; transcription factors ; transcriptome
    Sprache Englisch
    Erscheinungsverlauf 2015-1015
    Umfang p. 307-318.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2015.09.002
    Datenquelle NAL Katalog (AGRICOLA)

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