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Book ; Online: Expansionsoptimierung in einer Kompressorantriebs-Modellturbine

Engelmann, David / Polklas, Thomas

Abschlussbericht ; Forschungsvorhaben COORETEC-turbo ; Verbundprojekt: CO2-Reduktions-Technologien ; Vorhaben-Nr. 4.2.4 A ; Zeitraum: 01.04.2008 - 31.12.2012

2013

Title variant	Expansion optimization in a test rig steam turbine as compressor driver
Author's details	Autoren/Projektleitung: Thomas Polklas (MAN Diesel & Turbo SE); Bearb.: David Engelmann (Ruhr-Universität Bochum)
Language	German ; English
Size	Online-Ressource (PDF-Datei: 57 S., 8.031 KB), Ill., graph. Darst.
Publisher	Technische Informationsbibliothek u. Universitätsbibliothek ; Ruhr-Univ., Lehrstuhl für Thermische Turbomaschinen u.a.
Publishing place	Hannover ; Bochum
Document type	Book ; Online
Note	Zsfassung in dt. u. engl. Sprache ; Förderkennzeichen BMWi 0327787A. - Verbund-Nr. 01056932. - Engl. Berichtsbl. u.d.T.: Expansion optimization in a test rig steam turbine as compressor driver ; Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Book ; Online ; Thesis: Strömungsmechanische Untersuchung einer Industriedampfturbine mit Fokus auf die Rückführung von Leckagedampf

Engelmann, David

2013

Author's details	von David Engelmann
Language	German
Size	Online-Ressource (PDF-Datei: 153 S., 13,4 MB)
Publisher	Univ.-Bibliothek
Publishing place	Bochum
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Bochum, 2013
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Book ; Thesis: Strömungsmechanische Untersuchung einer Industriedampfturbine mit Fokus auf die Rückführung von Leckagedampf

Engelmann, David

2013

Author's details	von David Engelmann
Language	German
Size	XVII, 132 S.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Bochum, 2013
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Emerging from the shade of p53 mutants: N-terminally truncated variants of the p53 family in EMT signaling and cancer progression.

Engelmann, David / Pützer, Brigitte M

Science signaling

2014 Volume 7, Issue 345, Page(s) re9

Abstract: The prevailing view has been that N-terminally truncated p53 family isoforms (ΔNp53, ΔNp63, and DNp73) predominantly counteract cell cycle arrest and apoptosis. Recent progress in the field extend these well-known functions and place these isoforms in ... ...

Abstract	The prevailing view has been that N-terminally truncated p53 family isoforms (ΔNp53, ΔNp63, and DNp73) predominantly counteract cell cycle arrest and apoptosis. Recent progress in the field extend these well-known functions and place these isoforms in the center of a comprehensive regulatory network controlling major epithelial-to-mesenchymal transition (EMT)-relevant signaling pathways [such as transforming growth factor-β (TGF-β), wingless-int (WNT), insulin-like growth factor (IGF), and signal transducer and activator of transcription (STAT)], microRNAs, and EMT-associated transcription factors that promote invasion, loss of tumor cell polarity, and metastatic behavior in conjunction with a chemoresistant phenotype. These observations add new weight to the concept that currently underappreciated truncated forms of this tumor suppressor family play an equally important role in promoting cancer aggressiveness as do mutant p53 proteins, and illustrate how the consequences of ΔN/DN expression depend on cellular contexts. The tumor microenvironment contributes to the emergence of these variants, thereby linking inflammation to the activation of the mesenchymal program. In addition, molecular connections between ΔN/DN forms and self-renewal have arisen, suggesting their potential function in the generation of cancer stem cells (CSCs) from bulk tumor cells. These intriguing insights provoke a new understanding of the acquisition of aggressive traits by carcinoma cells in the absence of p53 mutations, and may help direct the development of new therapies for a broad range of cancers.
MeSH term(s)	Carcinoma/genetics ; Carcinoma/physiopathology ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Models, Biological ; Multigene Family/genetics ; Protein Isoforms/genetics ; Signal Transduction/genetics ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Protein Isoforms ; Tumor Suppressor Protein p53
Language	English
Publishing date	2014-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.2005699
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: E2F1 apoptosis counterattacked: evil strikes back.

Pützer, Brigitte M / Engelmann, David

Trends in molecular medicine

2013 Volume 19, Issue 2, Page(s) 89–98

Abstract: Resistance to genotoxic drugs is the major cause of cancer therapy failure. In the past, E2F1 was recognized as a key regulator of apoptosis, but the latest evidence reveals that this transcription factor is aberrantly high in late-stage cancers and ... ...

Abstract	Resistance to genotoxic drugs is the major cause of cancer therapy failure. In the past, E2F1 was recognized as a key regulator of apoptosis, but the latest evidence reveals that this transcription factor is aberrantly high in late-stage cancers and instead of apoptosis promotes tumor invasion and metastasis. This newly discovered activity of deregulated E2F1 reflects a cell context-dependent loss of its death-inducing function. We highlight the role of E2F1 in drug resistance by focusing on recent advances in elucidating the molecular mechanisms that counteract E2F1-induced apoptosis signaling in damaged cells. These mechanisms explain the paradox of high E2F1 expression in advanced tumors, highlight potential loopholes for cancers to escape from conventional treatment, and imply novel therapeutic strategies.
MeSH term(s)	Animals ; Apoptosis/genetics ; DNA Repair ; Drug Resistance, Neoplasm ; E2F1 Transcription Factor/genetics ; E2F1 Transcription Factor/metabolism ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Protein Binding ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	E2F1 Transcription Factor ; Repressor Proteins ; Tumor Suppressor Protein p53
Language	English
Publishing date	2013-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2012.10.009
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Article ; Online: The dark side of E2F1: in transit beyond apoptosis.

Engelmann, David / Pützer, Brigitte M

Cancer research

2012 Volume 72, Issue 3, Page(s) 571–575

Abstract: E2F1 plays a critical role in cell-cycle progression and the induction of apoptosis in response to DNA damage. The latest evidence has uncovered that this tumor suppressor is most relevant for cancer progression and chemoresistance. Increased abundance ... ...

Abstract	E2F1 plays a critical role in cell-cycle progression and the induction of apoptosis in response to DNA damage. The latest evidence has uncovered that this tumor suppressor is most relevant for cancer progression and chemoresistance. Increased abundance of E2F1 triggers invasion and metastasis by activating growth receptor signaling pathways, which in turn promote an antiapoptotic tumor environment. The data shed light on the molecular mechanisms underlying E2F1-induced prometastatic activity and predict its radical switch from a mediator of cell death toward an accelerator of tumor progression. This raises the perspective of new drug targets at late-stage cancer.
MeSH term(s)	Apoptosis/physiology ; Disease Progression ; Drug Resistance, Neoplasm ; E2F1 Transcription Factor/physiology ; Humans ; Models, Biological ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms/pathology ; Neoplasms/physiopathology ; Tumor Suppressor Proteins/physiology
Chemical Substances	E2F1 Transcription Factor ; Tumor Suppressor Proteins
Language	English
Publishing date	2012-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-11-2575
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Book: Expansionsoptimierung in einer Kompressorantriebs-Modellturbine

Polklas, Thomas / Engelmann, David

Abschlussbericht ; Forschungsvorhaben COORETEC-turbo ; Verbundprojekt: CO2-Reduktions-Technologien ; Vorhaben-Nr. 4.2.4 A ; Zeitraum: 01.04.2008 - 31.12.2012

2013

Title variant	Expansion optimization in a test rig steam turbine as compressor driver
Author's details	Autoren/Projektleitung: Thomas Polklas (MAN Diesel & Turbo SE); Bearb.: David Engelmann (Ruhr-Universität Bochum)
Language	German ; English
Size	56 S., [2] Bl., Ill., graph. Darst.
Publisher	Ruhr-Univ. u.a.
Publishing place	Bochum
Document type	Book
Note	Zsfassung in dt. u. engl. Sprache ; Förderkennzeichen BMWi 0327787A. - Verbund-Nr. 01056932. - Engl. Berichtsbl. u.d.T.: Expansion optimization in a test rig steam turbine as compressor driver ; Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Translating DNA damage into cancer cell death-A roadmap for E2F1 apoptotic signalling and opportunities for new drug combinations to overcome chemoresistance.

Engelmann, David / Pützer, Brigitte M

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

2010 Volume 13, Issue 4-5, Page(s) 119–131

Abstract: The cellular transcription factor E2F1 has been identified as a tumor suppressor regulating the activities of p53 and its homologue TAp73, and promoting apoptosis by the activation of a plethora of death pathways. More than 15 years of experimentation ... ...

Abstract	The cellular transcription factor E2F1 has been identified as a tumor suppressor regulating the activities of p53 and its homologue TAp73, and promoting apoptosis by the activation of a plethora of death pathways. More than 15 years of experimentation recognized E2F1 as the key player in apoptosis induced by DNA damage in all types of human cancer. This occurs by several mechanisms that affect RB-E2F1 interaction, E2F1 stability and its binding to promoters of E2F1-regulated genes. Recent progress has been made in revealing new proapoptotic genes regulated by E2F1 and it seems that many still remain to be discovered. However, whereas in the past one focused mainly on identifying E2F1 target genes translating cellular stress signals into cell death, today the DNA damage-induced regulatory network governing E2F1's ability to induce apoptosis is rapidly gaining attention as well. Notably, the lately uncovered role of pRB and E2F3 in triggering E2F1-dependent apoptosis through chemotherapy gains our understanding of the DNA damage response in normal and tumor cells. In this context a large body of evidence indicates that nuclear cofactors targeting E2F1 seem to have a major impact on its tumor suppressor function. These new findings are discussed in the context of preclinical studies applying E2F1 overexpression in combination with genotoxic anticancer agents - called chemogene therapy, thereby providing new mechanistic links between the E2F1-induced apoptotic programming and advanced cancer phenotype.
MeSH term(s)	Animals ; Antineoplastic Agents/metabolism ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Apoptosis/genetics ; Cell Line, Tumor ; DNA Damage ; Drug Resistance, Neoplasm ; E2F1 Transcription Factor/genetics ; E2F1 Transcription Factor/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Retinoblastoma Protein/genetics ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Antineoplastic Agents ; E2F1 Transcription Factor ; Retinoblastoma Protein ; Tumor Suppressor Protein p53 ; Tumor Suppressor Proteins
Language	English
Publishing date	2010-08
Publishing country	Scotland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1474513-6
ISSN	1532-2084 ; 1368-7646
ISSN (online)	1532-2084
ISSN	1368-7646
DOI	10.1016/j.drup.2010.06.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: MiR-182 promotes cancer invasion by linking RET oncogene activated NF-κB to loss of the HES1/Notch1 regulatory circuit.

Spitschak, Alf / Meier, Claudia / Kowtharapu, Bhavani / Engelmann, David / Pützer, Brigitte M

Molecular cancer

2017 Volume 16, Issue 1, Page(s) 24

Abstract: Background: Dominant-activating mutations in the RET proto-oncogene, a receptor tyrosine kinase, are responsible for the development of medullary thyroid carcinoma (MTC) and causative for multiple endocrine neoplasia (MEN) type 2A and 2B. These tumors ... ...

Abstract	Background: Dominant-activating mutations in the RET proto-oncogene, a receptor tyrosine kinase, are responsible for the development of medullary thyroid carcinoma (MTC) and causative for multiple endocrine neoplasia (MEN) type 2A and 2B. These tumors are highly aggressive with a high propensity for early metastasis and chemoresistance. This attribute makes this neoplasia an excellent model for probing mechanisms underlying cancer progression. Methods: The expression level of miR-182 was measured in MTC tumor specimens and in TT cells by real-time RT-PCR. TT cells and modified NThy-ori 3.1 that stably express RETM918T were used to investigate RET-dependent regulation of miR-182. Identification and validation of miR-182 targets and pathways was accomplished with luciferase assays, qRT-PCR, Western blotting and immunofluorescence. In vitro, overexpression and knockdown experiments were carried out to examine the impact of miR-182 and HES1 on invasion and migration. Results: We found that miR-182 expression is significantly upregulated in MTC patient samples and tumor-derived cell lines harboring mutated RET. Inhibition of RET oncogenic signaling through a dominant-negative RET∆TK mutant in TT cells reduces miR-182, whereas overexpression of RETM918T in NThy-ori 3.1 cells increases miR-182 levels. We further show that overexpression of this miRNA in NThy.miR-182 cells promotes the invasive and migratory properties without affecting cell proliferation. MiR-182 is upregulated after RET induced NF-κB translocation into the nucleus via binding of NF-κB to the miR-182 promoter. Database analysis revealed that HES1, a repressor of the Notch pathway, is a target of miR-182, whose upregulation correlates with loss of HES1 transcription in MTC tissue samples and mutant RET cell lines. Moreover, we demonstrated that the 3'UTR of the HES1 mRNA bearing the targeting sequence for miR-182 clearly reduced luciferase reporter activity in cells expressing miR-182. Decreased expression of HES1 promotes migration by upregulating Notch1 inhibitor Deltex1 and consequent repression of Notch1. Conclusion: We demonstrate a novel mechanism for MTC aggressiveness in which mutated RET/NF-κB-driven expression of miR-182 impedes HES1 activation in a negative feedback loop. This observation might open new possibilities to treat RET oncogene associated metastatic cancer.
MeSH term(s)	3' Untranslated Regions ; Carcinoma, Neuroendocrine/genetics ; Carcinoma, Neuroendocrine/metabolism ; Carcinoma, Neuroendocrine/pathology ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics ; Models, Biological ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Neoplasm Invasiveness ; Proto-Oncogene Proteins c-ret/genetics ; Proto-Oncogene Proteins c-ret/metabolism ; RNA Interference ; Receptor, Notch1/metabolism ; Signal Transduction ; Thyroid Neoplasms/genetics ; Thyroid Neoplasms/metabolism ; Thyroid Neoplasms/pathology ; Transcription Factor HES-1/metabolism
Chemical Substances	3' Untranslated Regions ; MicroRNAs ; Mirn182 microRNA, human ; NF-kappa B ; Receptor, Notch1 ; Transcription Factor HES-1 ; HES1 protein, human (149348-15-2) ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1)
Language	English
Publishing date	2017-01-26
Publishing country	England
Document type	Journal Article
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/s12943-016-0563-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: LncRNA-SLC16A1-AS1 induces metabolic reprogramming during Bladder Cancer progression as target and co-activator of E2F1.

Logotheti, Stella / Marquardt, Stephan / Gupta, Shailendra K / Richter, Christin / Edelhäuser, Berdien A H / Engelmann, David / Brenmoehl, Julia / Söhnchen, Christoph / Murr, Nico / Alpers, Michael / Singh, Krishna P / Wolkenhauer, Olaf / Heckl, Dirk / Spitschak, Alf / Pützer, Brigitte M

Theranostics

2020 Volume 10, Issue 21, Page(s) 9620–9643

Abstract: Long non-coding RNAs (lncRNAs) have emerged as integral components of E2F1-regulated gene regulatory networks (GRNs), but their implication in advanced or treatment-refractory malignancy is unknown. ...

Abstract	Long non-coding RNAs (lncRNAs) have emerged as integral components of E2F1-regulated gene regulatory networks (GRNs), but their implication in advanced or treatment-refractory malignancy is unknown.
MeSH term(s)	Adenosine Triphosphate/genetics ; Cell Line, Tumor ; Cellular Reprogramming/physiology ; Disease Progression ; E2F1 Transcription Factor/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Glycolysis/genetics ; Humans ; Mitochondria/genetics ; Monocarboxylic Acid Transporters/genetics ; Oxidation-Reduction ; Promoter Regions, Genetic/genetics ; RNA, Long Noncoding/genetics ; Symporters/genetics ; Transcriptional Activation/genetics ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/pathology
Chemical Substances	E2F1 Transcription Factor ; E2F1 protein, human ; Monocarboxylic Acid Transporters ; RNA, Long Noncoding ; Symporters ; monocarboxylate transport protein 1 ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2020-07-29
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.44176
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