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<export-example>
  <doc>
    <id>19020</id>
    <completedYear/>
    <publishedYear>2016</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>183</pageFirst>
    <pageLast>190</pageLast>
    <pageNumber/>
    <edition/>
    <issue>2</issue>
    <volume>1</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2017-03-07</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Chronic ethanol treatment depletes glutathione regeneration capacity in hepatoma cell line HepG2</title>
    <parentTitle language="eng">Journal of Cellular Biotechnology</parentTitle>
    <identifier type="issn">2352-3697</identifier>
    <identifier type="issn">2352-3689</identifier>
    <identifier type="doi">10.3233/JCB-15019</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <author>
      <firstName>S.</firstName>
      <lastName>Kade</lastName>
    </author>
    <submitter>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </submitter>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Kai-Uwe</firstName>
      <lastName>Schmidtke</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>19021</id>
    <completedYear/>
    <publishedYear>2016</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>341</pageFirst>
    <pageLast>353</pageLast>
    <pageNumber/>
    <edition/>
    <issue>3</issue>
    <volume>40</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2017-03-07</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Primary like human hepatocytes genetically engineered to obtain proliferation competence display liver biotransformation activity in 2D and 3D culture systems</title>
    <parentTitle language="eng">Cell Biology International</parentTitle>
    <identifier type="issn">1095-8355</identifier>
    <identifier type="issn">1065-6995</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <submitter>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </submitter>
    <author>
      <firstName>Max</firstName>
      <lastName>Hansen</lastName>
    </author>
    <author>
      <firstName>Sebastian</firstName>
      <lastName>Miethbauer</lastName>
    </author>
    <author>
      <firstName>Kai-Uwe</firstName>
      <lastName>Schmidtke</lastName>
    </author>
    <author>
      <firstName>Ursula</firstName>
      <lastName>Anderer</lastName>
    </author>
    <author>
      <firstName>Amelie</firstName>
      <lastName>Lupp</lastName>
    </author>
    <author>
      <firstName>Sebastian</firstName>
      <lastName>Sperling</lastName>
    </author>
    <author>
      <firstName>Daniel</firstName>
      <lastName>Seehofer</lastName>
    </author>
    <author>
      <firstName>Georg</firstName>
      <lastName>Damm</lastName>
    </author>
    <author>
      <firstName>Katrin</firstName>
      <lastName>Scheibner</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>19024</id>
    <completedYear/>
    <publishedYear>2015</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>15</pageFirst>
    <pageLast>26</pageLast>
    <pageNumber/>
    <edition/>
    <issue>1</issue>
    <volume>1</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2017-03-07</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Generation of cytochrome P450 3A4-overexpressing HepG2 cell clones for standardization of hepatocellular testosterone 6β-hydroxylation activity</title>
    <parentTitle language="eng">Journal of Cellular Biotechnology</parentTitle>
    <identifier type="doi">10.3233/JCB-15002</identifier>
    <identifier type="issn">2352-3697</identifier>
    <identifier type="issn">2352-3689</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <submitter>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </submitter>
    <author>
      <firstName>Nadine</firstName>
      <lastName>Katzenberger</lastName>
    </author>
    <author>
      <firstName>Frank</firstName>
      <lastName>Martin</lastName>
    </author>
    <author>
      <firstName>Kai-Uwe</firstName>
      <lastName>Schmidtke</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>22843</id>
    <completedYear/>
    <publishedYear>2018</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>37</pageFirst>
    <pageLast>47</pageLast>
    <pageNumber/>
    <edition/>
    <issue/>
    <volume>412</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2018-12-10</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Metabolic activity testing can underestimate acute drug cytotoxicity as revealed by HepG2 cell clones overexpressing cytochrome P450 2C19 and 3A4</title>
    <parentTitle language="eng">Toxicology</parentTitle>
    <identifier type="doi">10.1016/j.tox.2018.11.008</identifier>
    <identifier type="issn">0300-483X</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <author>
      <firstName>Susanne</firstName>
      <lastName>Steinbrecht</lastName>
    </author>
    <submitter>
      <firstName>sarah</firstName>
      <lastName>Kammerer</lastName>
    </submitter>
    <author>
      <firstName>Rosalie</firstName>
      <lastName>König</lastName>
    </author>
    <author>
      <firstName>Kai-Uwe</firstName>
      <lastName>Schmidtke</lastName>
    </author>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Katrin</firstName>
      <lastName>Scheibner</lastName>
    </author>
    <author>
      <firstName>Anne</firstName>
      <lastName>Krüger-Genge</lastName>
    </author>
    <author>
      <firstName>Friedrich</firstName>
      <lastName>Jung</lastName>
    </author>
    <author>
      <firstName>Sarah</firstName>
      <lastName>Kammerer</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <collection role="institutes" number="2111">FG Enzymtechnologie</collection>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>24829</id>
    <completedYear/>
    <publishedYear>2020</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>155</pageFirst>
    <pageLast>159</pageLast>
    <pageNumber/>
    <edition/>
    <issue/>
    <volume>319</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2019-12-06</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">HepG2-1A2 C2 and C7: Lentivirus vector-mediated stable and functional overexpression of cytochrome P450 1A2 in human hepatoblastoma cells</title>
    <abstract language="eng">Novel HepG2 cell clones 1A2 C2 and 1A2 C7 were independently generated by lentiviral transduction to functionally overexpress cytochrome P450 1A2 (CYP1A2). We found similar and stable CYP1A2 transcript and protein levels in both cell clones leading to specific enzyme activities of about 370 pmol paracetamol x min-1 x&#13;
mg-1 protein analyzed by phenacetin conversion. Both clones showed dramatically increased sensitivity to the hepatotoxic compound aflatoxin B1 (EC50&lt;100 nM) when compared to parental HepG2 cells (EC50 ∼5 μM). Thus, newly established cell lines are an appropriate tool to study metabolism and toxicity of substances depending on conversion by CYP1A2.</abstract>
    <parentTitle language="eng">Toxicology Letters</parentTitle>
    <identifier type="doi">10.1016/j.toxlet.2019.11.006</identifier>
    <identifier type="issn">0378-4274</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <enrichment key="Fprofil">2 Gesundheit und Lifes Sciences / Health and Life Sciences</enrichment>
    <enrichment key="Fprofil">3 Globaler Wandel und Transformationsprozesse / Global Change and Transformation Processes</enrichment>
    <author>
      <firstName>Susanne</firstName>
      <lastName>Steinbrecht</lastName>
    </author>
    <submitter>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </submitter>
    <author>
      <firstName>Nadine</firstName>
      <lastName>Pfeifer</lastName>
    </author>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Nadine</firstName>
      <lastName>Katzenberger</lastName>
    </author>
    <author>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </author>
    <author>
      <firstName>Sarah</firstName>
      <lastName>Kammerer</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>HepG2</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>CYP1A2</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Cytochrome P450</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Liver metabolism</value>
    </subject>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>26338</id>
    <completedYear/>
    <publishedYear>2020</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>1210</pageFirst>
    <pageLast>1218</pageLast>
    <pageNumber/>
    <edition/>
    <issue>7</issue>
    <volume>10</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2020-11-13</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Modeling atrial fibrosis in vitro - Generation and characterization of a novel human atrial fibroblast cell line</title>
    <abstract language="eng">Atrial fibrillation (AF) is regularly accompanied by cardiac fibrosis and concomitant heart failure. Due to the heterogeneous nature and complexity of fibrosis, the knowledge about the underlying mechanisms is limited, which prevents effective pharmacotherapy. A deeper understanding of cardiac fibroblasts is essential to meet this need. We previously described phenotypic and functional differences between atrial fibroblasts from patients in sinus rhythm and with AF. Herein, we established and characterized a novel human atrial fibroblast line, which displays typical fibroblast morphology and function comparable to primary cells but with improved proliferation capacity and low spontaneous myofibroblast differentiation. These traits make our model suitable for the study of fibrosis mechanisms and for drug screening aimed at developing effective antifibrotic pharmacotherapy.</abstract>
    <parentTitle language="eng">FEBS Open Bio</parentTitle>
    <identifier type="doi">10.1002/2211-5463.12896</identifier>
    <identifier type="issn">2211-5463</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">false</enrichment>
    <enrichment key="Fprofil">2 Gesundheit und Lifes Sciences / Health and Life Sciences</enrichment>
    <enrichment key="Fprofil">3 Globaler Wandel und Transformationsprozesse / Global Change and Transformation Processes</enrichment>
    <author>
      <firstName>Stephan R.</firstName>
      <lastName>Künzel</lastName>
    </author>
    <submitter>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </submitter>
    <author>
      <firstName>Johanna S. E.</firstName>
      <lastName>Rausch</lastName>
    </author>
    <author>
      <firstName>Charlotte</firstName>
      <lastName>Schäffer</lastName>
    </author>
    <author>
      <firstName>Maximilian</firstName>
      <lastName>Hoffmann</lastName>
    </author>
    <author>
      <firstName>Karolina</firstName>
      <lastName>Künzel</lastName>
    </author>
    <author>
      <firstName>Erik</firstName>
      <lastName>Klapproth</lastName>
    </author>
    <author>
      <firstName>Theresa</firstName>
      <lastName>Kant</lastName>
    </author>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <author>
      <firstName>Kristina</firstName>
      <lastName>Lorenz</lastName>
    </author>
    <author>
      <firstName>Svenja</firstName>
      <lastName>Dudek</lastName>
    </author>
    <author>
      <firstName>Ramona</firstName>
      <lastName>Emig</lastName>
    </author>
    <author>
      <firstName>Ursula</firstName>
      <lastName>Ravens</lastName>
    </author>
    <author>
      <firstName>Eva A.</firstName>
      <lastName>Rog‐Zielinska</lastName>
    </author>
    <author>
      <firstName>Rémi</firstName>
      <lastName>Peyronnet</lastName>
    </author>
    <author>
      <firstName>Ali</firstName>
      <lastName>El-Armouche</lastName>
    </author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>cardiovascular disease</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>cell culture</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>cell lines</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>fibroblasts</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>fibrosis</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>heart</value>
    </subject>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>28197</id>
    <completedYear/>
    <publishedYear>2021</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>804</pageFirst>
    <pageLast>820</pageLast>
    <pageNumber/>
    <edition/>
    <issue>8</issue>
    <volume>129</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2021-12-17</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Diminished PLK2 Induces Cardiac Fibrosis and Promotes Atrial Fibrillation</title>
    <abstract language="eng">Rationale:&#13;
Fibrosis promotes the maintenance of atrial fibrillation (AF), making it resistant to therapy. Improved understanding of the molecular mechanisms leading to atrial fibrosis will open new pathways toward effective antifibrotic therapies.&#13;
&#13;
Objective:&#13;
This study aims to decipher the mechanistic interplay between PLK2 (polo-like kinase 2) and the profibrotic cytokine OPN (osteopontin) in the pathogenesis of atrial fibrosis and AF.&#13;
&#13;
Methods and Results:&#13;
Atrial PLK2 mRNA expression was 10-fold higher in human fibroblasts than in cardiomyocytes. Compared with sinus rhythm, right atrial appendages and isolated right atrial fibroblasts from patients with AF showed downregulation of PLK2 mRNA and protein, along with increased PLK2 promotor methylation. Genetic deletion as well as pharmacological inhibition of PLK2 induced profibrotic phenotype conversion in cardiac fibroblasts and led to a striking de novo secretion of OPN. Accordingly, PLK2-deficient (PLK2 knockout) mice showed cardiac fibrosis and were prone to experimentally induced AF. In line with these findings, OPN plasma levels were significantly higher only in patients with AF with atrial low-voltage zones (surrogates of fibrosis) compared with sinus rhythm controls. Mechanistically, we identified ERK1/2 as the relevant downstream mediator of PLK2 leading to increased OPN expression. Finally, oral treatment with the clinically available drug mesalazine, known to inhibit ERK1/2, prevented cardiac OPN overexpression and reversed the pathological PLK2 knockout phenotype in PLK2 knockout mice.&#13;
&#13;
Conclusions:&#13;
Abnormal PLK2/ERK1/2/OPN axis function critically contributes to AF-related atrial fibrosis, suggesting reinforcing PLK2 activity and/or OPN inhibition as innovative targets to prevent fibrosis progression in AF. Mesalazine derivatives may be used as lead compounds for the development of novel anti-AF agents targeting fibrosis.</abstract>
    <parentTitle language="eng">Circulation Research</parentTitle>
    <identifier type="url">https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.121.319425</identifier>
    <identifier type="doi">10.1161/CIRCRESAHA.121.319425</identifier>
    <identifier type="issn">1524-4571</identifier>
    <identifier type="issn">0009-7330</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <enrichment key="opus.source">publish</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">false</enrichment>
    <enrichment key="Fprofil">2 Gesundheit und Lifes Sciences / Health and Life Sciences</enrichment>
    <enrichment key="Fprofil">3 Globaler Wandel und Transformationsprozesse / Global Change and Transformation Processes</enrichment>
    <author>
      <firstName>Stephan R.</firstName>
      <lastName>Künzel</lastName>
    </author>
    <submitter>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </submitter>
    <author>
      <firstName>Maximilian</firstName>
      <lastName>Hoffmann</lastName>
    </author>
    <author>
      <firstName>Silvio</firstName>
      <lastName>Weber</lastName>
    </author>
    <author>
      <firstName>Karolina</firstName>
      <lastName>Künzel</lastName>
    </author>
    <author>
      <firstName>Susanne</firstName>
      <lastName>Kämmerer</lastName>
    </author>
    <author>
      <firstName>Mario</firstName>
      <lastName>Günscht</lastName>
    </author>
    <author>
      <firstName>Erik</firstName>
      <lastName>Klapproth</lastName>
    </author>
    <author>
      <firstName>Johanna S. E.</firstName>
      <lastName>Rausch</lastName>
    </author>
    <author>
      <firstName>Mirna S.</firstName>
      <lastName>Sadek</lastName>
    </author>
    <author>
      <firstName>Tomasz</firstName>
      <lastName>Kolanowski</lastName>
    </author>
    <author>
      <firstName>Stefanie</firstName>
      <lastName>Meyer-Roxlau</lastName>
    </author>
    <author>
      <firstName>Christopher</firstName>
      <lastName>Piorkowski</lastName>
    </author>
    <author>
      <firstName>Sems M.</firstName>
      <lastName>Tugtekin</lastName>
    </author>
    <author>
      <firstName>Stefan</firstName>
      <lastName>Rose-John</lastName>
    </author>
    <author>
      <firstName>Xiaoke</firstName>
      <lastName>Yin</lastName>
    </author>
    <author>
      <firstName>Manuel</firstName>
      <lastName>Mayr</lastName>
    </author>
    <author>
      <firstName>Jan Dominik</firstName>
      <lastName>Kuhlmann</lastName>
    </author>
    <author>
      <firstName>Pauline</firstName>
      <lastName>Wimberger</lastName>
    </author>
    <author>
      <firstName>Konrad</firstName>
      <lastName>Grützmann</lastName>
    </author>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <author>
      <firstName>Molly</firstName>
      <lastName>O’Reilly</lastName>
    </author>
    <author>
      <firstName>S. Nashitha</firstName>
      <lastName>Kabir</lastName>
    </author>
    <author>
      <firstName>Laura C.</firstName>
      <lastName>Sommerfeld</lastName>
    </author>
    <author>
      <firstName>Kaomei</firstName>
      <lastName>Guan</lastName>
    </author>
    <author>
      <firstName>Ben</firstName>
      <lastName>Wielockx</lastName>
    </author>
    <author>
      <firstName>Larissa</firstName>
      <lastName>Fabritz</lastName>
    </author>
    <author>
      <firstName>Stanley</firstName>
      <lastName>Nattel</lastName>
    </author>
    <author>
      <firstName>Ursula</firstName>
      <lastName>Ravens</lastName>
    </author>
    <author>
      <firstName>Dobromir</firstName>
      <lastName>Dobrev</lastName>
    </author>
    <author>
      <firstName>Michael</firstName>
      <lastName>Wagner</lastName>
    </author>
    <author>
      <firstName>Ali</firstName>
      <lastName>El-Armouche</lastName>
    </author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>atrial fibrillation</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>fibroblasts</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>fibrosis</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>mesalamine</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>osteopontin</value>
    </subject>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>28198</id>
    <completedYear/>
    <publishedYear>2020</publishedYear>
    <thesisYearAccepted/>
    <language>deu</language>
    <pageFirst/>
    <pageLast/>
    <pageNumber/>
    <edition/>
    <issue/>
    <volume/>
    <type>patent</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2021-12-17</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="deu">Verfahren zur Herstellung von biogenen Stoffen</title>
    <title language="eng">Method for producing biogenic substances</title>
    <identifier type="url">https://patents.google.com/patent/EP3068868B1/de</identifier>
    <enrichment key="Patentnr">EP 3068868 B1</enrichment>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <enrichment key="opus.source">publish</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">false</enrichment>
    <enrichment key="Fprofil">2 Gesundheit und Lifes Sciences / Health and Life Sciences</enrichment>
    <enrichment key="Fprofil">3 Globaler Wandel und Transformationsprozesse / Global Change and Transformation Processes</enrichment>
    <author>
      <firstName>Katrin</firstName>
      <lastName>Scheibner</lastName>
    </author>
    <submitter>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </submitter>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <author>
      <firstName>Kai-Uwe</firstName>
      <lastName>Schmidtke</lastName>
    </author>
    <author>
      <firstName>Sebastian</firstName>
      <lastName>Miethbauer</lastName>
    </author>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
  <doc>
    <id>29931</id>
    <completedYear/>
    <publishedYear>2022</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst/>
    <pageLast/>
    <pageNumber/>
    <edition/>
    <issue>8</issue>
    <volume>11</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2022-08-09</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Primary-like Human Hepatocytes Genetically Engineered to Obtain Proliferation Competence as a Capable Application for Energy Metabolism Experiments in In Vitro Oncologic Liver Models</title>
    <abstract language="eng">Non-alcoholic fatty liver disease (NAFLD), characterized by lipid accumulation in the liver, is the most common cause of liver diseases in Western countries. NAFLD is a major risk factor for developing hepatocellular carcinoma (HCC); however, in vitro evaluation of hepatic cancerogenesis fails due to a lack of liver models displaying a proliferation of hepatocytes. Originally designed to overcome primary human hepatocyte (PHH) shortages, upcyte hepatocytes were engineered to obtain continuous proliferation and, therefore, could be a suitable tool for HCC research. We generated upcyte hepatocytes, termed HepaFH3 cells, and compared their metabolic characteristics to HepG2 hepatoma cells and PHHs isolated from resected livers. For displaying NAFLD-related HCCs, we induced steatosis in all liver models. Lipid accumulation, lipotoxicity and energy metabolism were characterized using biochemical assays and Western blot analysis. We showed that proliferating HepaFH3 cells resemble HepG2, both showing a higher glucose uptake rate, lactate levels and metabolic rate compared to PHHs. Confluent HepaFH3 cells displayed some similarities to PHHs, including higher levels of the transaminases AST and ALT compared to proliferating HepaFH3 cells. We recommend proliferating HepaFH3 cells as a pre-malignant cellular model for HCC research, while confluent HepaFH3 cells could serve as PHH surrogates for energy metabolism studies.</abstract>
    <parentTitle language="eng">Biology</parentTitle>
    <identifier type="issn">2079-7737</identifier>
    <identifier type="doi">10.3390/biology11081195</identifier>
    <enrichment key="opus.import.date">2023-01-10T13:57:44+00:00</enrichment>
    <enrichment key="opus.source">sword</enrichment>
    <enrichment key="opus.import.user">deepgreen</enrichment>
    <enrichment key="opus.import.file">attachment; filename=deposit.zip</enrichment>
    <enrichment key="opus.import.checksum">ac4602bd461b85bbce65384b28e7e235</enrichment>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <enrichment key="Artikelnummer">1195</enrichment>
    <enrichment key="Publikationsweg">Open Access</enrichment>
    <enrichment key="Fprofil">2 Gesundheit und Lifes Sciences / Health and Life Sciences</enrichment>
    <enrichment key="Fprofil">3 Globaler Wandel und Transformationsprozesse / Global Change and Transformation Processes</enrichment>
    <author>
      <firstName>Andrea</firstName>
      <lastName>Scheffschick</lastName>
    </author>
    <author>
      <firstName>Jonas</firstName>
      <lastName>Babel</lastName>
    </author>
    <author>
      <firstName>Sebastian</firstName>
      <lastName>Sperling</lastName>
    </author>
    <author>
      <firstName>Julia</firstName>
      <lastName>Nerusch</lastName>
    </author>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Daniel</firstName>
      <lastName>Seehofer</lastName>
    </author>
    <author>
      <firstName>Georg</firstName>
      <lastName>Damm</lastName>
    </author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>upcyte hepatocytes</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>primary human hepatocytes</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>HepG2 cells</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>HCC</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>energy metabolism</value>
    </subject>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
    <collection role="Import" number="import">Import</collection>
  </doc>
  <doc>
    <id>32264</id>
    <completedYear/>
    <publishedYear>2023</publishedYear>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst/>
    <pageLast/>
    <pageNumber/>
    <edition/>
    <issue>17</issue>
    <volume>12</volume>
    <type>articler</type>
    <publisherName/>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>0</belongsToBibliography>
    <completedDate>2024-01-04</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Stable Chinese Hamster Ovary Suspension Cell Lines Harboring Recombinant Human Cytochrome P450 Oxidoreductase and Human Cytochrome P450 Monooxygenases as Platform for In Vitro Biotransformation Studies</title>
    <abstract language="eng">In the liver, phase-1 biotransformation of drugs and other xenobiotics is largely facilitated by enzyme complexes consisting of cytochrome P450 oxidoreductase (CPR) and cytochrome P450 monooxygenases (CYPs). Generated from human liver-derived cell lines, recombinant in vitro cell systems with overexpression of defined phase-1 enzymes are widely used for pharmacological and toxicological drug assessment and laboratory-scale production of drug-specific reference metabolites. Most, if not all, of these cell lines, however, display some background activity of several CYPs, making it difficult to attribute effects to defined CYPs. The aim of this study was to generate cell lines with stable overexpression of human phase-1 enzymes based on Chinese hamster ovary (CHO) suspension cells. Cells were sequentially modified with cDNAs for human CPR in combination with CYP1A2, CYP2B6, or CYP3A4, using lentiviral gene transfer. In parallel, CYP-overexpressing cell lines without recombinant CPR were generated. Successful recombinant expression was demonstrated by mRNA and protein analyses. Using prototypical CYP-substrates, generated cell lines proved to display specific enzyme activities of each overexpressed CYP while we did not find any endogenous activity of those CYPs in parental CHO cells. Interestingly, cell lines revealed some evidence that the dependence of CYP activity on CPR could vary between CYPs. This needs to be confirmed in further studies. Recombinant expression of CPR was also shown to enhance CYP3A4-independent metabolisation of testosterone to androstenedione in CHO cells. We propose the novel serum-free CHO suspension cell lines with enhanced CPR and/or defined CYP activity as a promising “humanised” in vitro model to study the specific effects of those human CYPs. This could be relevant for toxicology and/or pharmacology studies in the pharmaceutical industry or medicine.</abstract>
    <parentTitle language="eng">Cells</parentTitle>
    <identifier type="url">https://www.mdpi.com/2073-4409/12/17/2140#metrics</identifier>
    <identifier type="doi">10.3390/cells12172140</identifier>
    <identifier type="issn">2073-4409</identifier>
    <enrichment key="BTU">an der BTU erstellt / created at BTU</enrichment>
    <enrichment key="Artikelnummer">2140</enrichment>
    <enrichment key="Publikationsweg">Open Access</enrichment>
    <enrichment key="opus.source">publish</enrichment>
    <enrichment key="opus.doi.autoCreate">false</enrichment>
    <enrichment key="opus.urn.autoCreate">false</enrichment>
    <enrichment key="Fprofil">2 Gesundheit und Lifes Sciences / Health and Life Sciences</enrichment>
    <enrichment key="Fprofil">3 Globaler Wandel und Transformationsprozesse / Global Change and Transformation Processes</enrichment>
    <author>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </author>
    <submitter>
      <firstName>Christian</firstName>
      <lastName>Schulz</lastName>
    </submitter>
    <author>
      <firstName>Natalie</firstName>
      <lastName>Herzog</lastName>
    </author>
    <author>
      <firstName>Stefan</firstName>
      <lastName>Kubick</lastName>
    </author>
    <author>
      <firstName>Friedrich</firstName>
      <lastName>Jung</lastName>
    </author>
    <author>
      <firstName>Jan-Heiner</firstName>
      <lastName>Küpper</lastName>
    </author>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>Chinese hamster ovary cells</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>CHO-K1</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>CPR</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>CYP450</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>cytochrome P450 monooxygenase</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>liver</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>NADPH P450 oxidoreductase</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>phase-1 biotransformation</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>serum-free</value>
    </subject>
    <subject>
      <language>eng</language>
      <type>uncontrolled</type>
      <value>suspension cells</value>
    </subject>
    <collection role="institutes" number="2110">FG Molekulare Zellbiologie</collection>
  </doc>
</export-example>
