Kim, Ella L.

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Wuestenberg, Robin"],["dc.contributor.author","Leppert, Jan"],["dc.contributor.author","Hanson, Sven"],["dc.contributor.author","Pawlak, E."],["dc.contributor.author","Pettkus, Nadine"],["dc.contributor.author","Giese, A."],["dc.date.accessioned","2018-11-07T09:12:44Z"],["dc.date.available","2018-11-07T09:12:44Z"],["dc.date.issued","2006"],["dc.format.extent","397"],["dc.identifier.isi","000240877301024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27012"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Duke Univ Press"],["dc.publisher.place","Durham"],["dc.relation.conference","7th Congress of the European-Association-for-Neuro-Oncology (EANO)"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","1522-8517"],["dc.title","Activation of the p53 transcriptional response by chloroquine in glioma cells: Unknown side of the known drug"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Richter, Christoph"],["dc.contributor.author","Pilzak, Agatha A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Gunawan, Bastian"],["dc.contributor.author","Schmitz-Salue, Christoph"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Giese, Alf"],["dc.date.accessioned","2018-11-07T11:21:41Z"],["dc.date.available","2018-11-07T11:21:41Z"],["dc.date.issued","2009"],["dc.format.extent","918"],["dc.identifier.isi","000272974100197"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55834"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press Inc"],["dc.publisher.place","Cary"],["dc.relation.conference","3rd Quadrennial Meeting of the World-Federation-of-Neuro-Oncoloyg/6th Meeting of the Asian-Society-for-Neuro-Oncology"],["dc.relation.eventlocation","Yokohama, JAPAN"],["dc.relation.issn","1522-8517"],["dc.title","ESTABLISHMENT AND CHARACTERIZATION OF AN EXPERIMENTAL MODEL OF INVASIVE GLIOMA WITH HIGHLY RADIORESISTANT PHENOTYPE"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Todkar, Kiran"],["dc.contributor.author","Hanson, Sven"],["dc.contributor.author","Schlaffer, S."],["dc.contributor.author","Pettkus, Nadine"],["dc.contributor.author","Pawlak, E."],["dc.contributor.author","Tronnier, Volker M."],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Giese, A."],["dc.date.accessioned","2018-11-07T09:12:47Z"],["dc.date.available","2018-11-07T09:12:47Z"],["dc.date.issued","2006"],["dc.format.extent","402"],["dc.identifier.isi","000240877301043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27023"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Duke Univ Press"],["dc.publisher.place","Durham"],["dc.relation.conference","7th Congress of the European-Association-for-Neuro-Oncology (EANO)"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","1522-8517"],["dc.title","Invasion factor ets-1 is a functional antagonist and negative regulator of tumor suppressor p53"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biochemical Pharmacology"],["dc.bibliographiccitation.lastpage","20"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Giese, Alf"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.date.accessioned","2018-11-07T08:33:53Z"],["dc.date.available","2018-11-07T08:33:53Z"],["dc.date.issued","2009"],["dc.description.abstract","The tumor suppressor p53 controls a broad range of cellular responses. Induction of a transient (cell cycle arrest) or a permanent (senescence) block of cell proliferation, or the activation of cell death pathways in response to genotoxic stress comprise the major arms of the survival-death axis governed by p53. Due to these biological properties, inactivation of p53 is a crucial step in tumor development and progression, reflected by the high incidence of TP53 mutations in different types of human cancers. The remarkable potency of p53 in suppressing tumorigenic outgrowth has promoted the expectation that tumor cells expressing wild-type p53 (wtp53) should be more prone to elimination by cytotoxic treatments than tumor cells expressing mutant p53 (mutp53) with defunct wtp53 activities. However, recent findings yielded somewhat unexpected insights concerning the preponderance of the survival-promoting effects of wtp53 in cancer cells, a rather undesired property from the therapeutic point of view. In this commentary we will discuss the possibility that the developmentally established distinct patterns of wtp53 mediated responses in different tissues are an important factor in determining the ultimate outcome of cellular responses mediated by wtp53 in different types of tumor cells, with a particular focus on the divergent impact of wtp53 in malignant tumors of the central nervous system. We infer that a selective gain of pro-survival functions of wtp53 in cancer cells will confer a survival advantage that counteracts tumor therapy. (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bcp.2008.08.030"],["dc.identifier.isi","261779500002"],["dc.identifier.pmid","18812169"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17697"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0006-2952"],["dc.title","Wild-type p53 in cancer cells: When a guardian turns into a blackguard"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Richter, Christoph"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Pilzak, Agatha A."],["dc.contributor.author","Schmitz-Salue, Christoph"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Giese, Alf"],["dc.date.accessioned","2018-11-07T11:10:44Z"],["dc.date.available","2018-11-07T11:10:44Z"],["dc.date.issued","2008"],["dc.format.extent","905"],["dc.identifier.isi","000259854500533"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53272"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press Inc"],["dc.publisher.place","Cary"],["dc.relation.conference","13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)"],["dc.relation.eventlocation","Las Vegas, NV"],["dc.relation.issn","1522-8517"],["dc.title","BRAIN TUMOUR-INITIATING STEM-LIKE CELLS IN ESTABLISHED GLIOMA CELL LINES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Warneke, Gabi"],["dc.contributor.author","Schmitz-Salue, Christoph"],["dc.contributor.author","Depperr, Wolfgang"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Giese, Alf"],["dc.date.accessioned","2018-11-07T11:10:43Z"],["dc.date.available","2018-11-07T11:10:43Z"],["dc.date.issued","2008"],["dc.format.extent","772"],["dc.identifier.isi","000259854500061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53269"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press Inc"],["dc.publisher.place","Cary"],["dc.relation.conference","13th Annual Meeting of the Society-for-Neuro-Oncology (SNO)"],["dc.relation.eventlocation","Las Vegas, NV"],["dc.relation.issn","1522-8517"],["dc.title","CHLOROQUINE INDUCES DEATH RESPONSE IN GLIOMA CELLS BY P53-DEPENDENT AND P53-INDEPENDENT MECHANISMS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","398"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","407"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Henning, K."],["dc.contributor.author","Heering, Jan"],["dc.contributor.author","Schwanbeck, R."],["dc.contributor.author","Schroeder, T."],["dc.contributor.author","Helmbold, H."],["dc.contributor.author","Schaefer, H."],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Just, U."],["dc.date.accessioned","2018-11-07T11:18:30Z"],["dc.date.available","2018-11-07T11:18:30Z"],["dc.date.issued","2008"],["dc.description.abstract","Signaling mediated by activation of the transmembrane receptor Notch influences cell-fate decisions, differentiation, proliferation, and cell survival. Activated Notch reduces proliferation by altering cell-cycle kinetics and promotes differentiation in hematopoietic progenitor cells. Here, we investigated if the G(1) arrest and differentiation induced by activated mNotch1 are dependent on tumor suppressor p53, a critical mediator of cellular growth arrest. Multipotent wild-type p53-expressing (p53(wt)) and p53-deficient (p53(null)) hematopoietic progenitor cell lines (FDCP-mix) carrying an inducible mNotch1 system were used to investigate the effects of proliferation and differentiation upon mNotch1 signaling. While activated Notch reduced proliferation of p53(wt)-cells, no change was observed in p53(null)-cells. Activated Notch upregulated the p53 target p21(cip/waf) in p53(wt)-cells, but not in p53(null)-cells. Induction of the p21(cip/waf) gene by activated Notch was mediated by increased binding of p53 to p53-binding sites in the p21(cip/waf) promoter and was independent of the canonical RBP-J binding site. Re-expression of p53(wt) in p53(null) cells restored the inhibition of proliferation by activated Notch. Thus, activated Notch inhibits proliferation of multipotent hematopoietic progenitor cells via a p53-dependent pathway. In contrast, myeloid and erythroid differentiation was similarly induced in p53(wt) and p53(null) cells. These data suggest that Notch signaling triggers two distinct pathways, a p53-dependent one leading to a block in proliferation and a p53-independent one promoting differentiation."],["dc.identifier.doi","10.1038/sj.cdd.4402277"],["dc.identifier.isi","000252387900019"],["dc.identifier.pmid","18049480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55047"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1350-9047"],["dc.title","Notch1 activation reduces proliferation in the multipotent hematopoietic progenitor cell line FDCP-mix through a p53-dependent pathway but Notch1 effects on myeloid and erythroid differentiation are independent of p53"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Hanson, Sven"],["dc.contributor.author","Todkar, Kiran"],["dc.contributor.author","Schmitz-Salue, Christoph"],["dc.contributor.author","Warnecke, Gabriele"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Giese, Alf"],["dc.date.accessioned","2018-11-07T11:21:42Z"],["dc.date.available","2018-11-07T11:21:42Z"],["dc.date.issued","2009"],["dc.format.extent","958"],["dc.identifier.isi","000272974100386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55838"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press Inc"],["dc.publisher.place","Cary"],["dc.relation.conference","3rd Quadrennial Meeting of the World-Federation-of-Neuro-Oncoloyg/6th Meeting of the Asian-Society-for-Neuro-Oncology"],["dc.relation.eventlocation","Yokohama, JAPAN"],["dc.relation.issn","1522-8517"],["dc.title","THE CELLULAR ONCOGENE ETS-1 COUNTERACTS P53 TUMOR SUPPRFSSOR ACTIVITY BY AFFECTING THE LEVEL OF P53 PROTEIN"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2185"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","2190"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Deppert, Wolfgang R."],["dc.date.accessioned","2018-11-07T11:03:17Z"],["dc.date.available","2018-11-07T11:03:17Z"],["dc.date.issued","2007"],["dc.description.abstract","Since the very early days of p53 research, the gain of oncogenic activities by some mutant p53 proteins had been suspected as an important factor contributing to cancer progression. Considerable progress towards understanding the biology of mutant p53 has been made during the last years, the quintessence being the realization that the impact of mutant p53 proteins on the transcriptome of a tumor cell is much more global than previously thought. The emerging role of mutant p53 proteins in coordinating oncogenic signaling and chromatin modifying activities reveals an until now unsuspected function of these proteins as important modifiers of the oncogenic transcriptional response. Notwithstanding the fact that the sequence specific DNA binding activity of mutant p53 proteins is impaired, they are still able to associate with specific loci on DNA by utilizing different mechanisms. The ability to associate with DNA appears to be crucial for the master role of mutant p53 proteins in coordinating oncogenic transcriptional responses."],["dc.identifier.doi","10.1038/sj.onc.1210312"],["dc.identifier.isi","000245394800007"],["dc.identifier.pmid","17401427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51580"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","Interactions of mutant p53 with DNA: guilt by association"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","307"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","324"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Kim, Ella L."],["dc.contributor.author","Bielanska, Joanna"],["dc.contributor.author","Giese, Alf"],["dc.contributor.author","Mortensen, Lena Suenke"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2018-11-07T09:26:43Z"],["dc.date.available","2018-11-07T09:26:43Z"],["dc.date.issued","2013"],["dc.description.abstract","Glioma-initiating cells (GICs) represent a potential important therapeutic target because they are likely to account for the frequent recurrence of malignant gliomas; however, their identity remains unsolved. Here, we characterized the cellular lineage fingerprint of GICs through a combination of electrophysiology, lineage marker expression, and differentiation assays of 5 human patient-derived primary GIC lines. Most GICs coexpressed nestin, NG2 proteoglycan, platelet-derived growth factor receptor-alpha, and glial fibrillary acidic protein. Glioma-initiating cells could be partially differentiated into astrocytic but not oligodendroglial or neural lineages. We also demonstrate that GICs have a characteristic electrophysiologic profile distinct from that of well-characterized tumor bulk cells. Together, our results suggest that GICs represent a unique type of cells reminiscent of an immature phenotype that closely resembles but is not identical to NG2 glia with respect to marker expression and functional membrane properties."],["dc.identifier.doi","10.1097/NEN.0b013e31828afdbd"],["dc.identifier.isi","000316944200004"],["dc.identifier.pmid","23481707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30362"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Human Glioma-Initiating Cells Show a Distinct Immature Phenotype Resembling but Not Identical to NG2 Glia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]