Journal articles: 'Proteinexpression'

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Maelicke, Alfred. "Proteinexpression und -faltung." Nachrichten aus Chemie, Technik und Laboratorium 43, no. 11 (November 1995): 1197–98. http://dx.doi.org/10.1002/nadc.19950431114.

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Huber, R., D. Ritter, T. Hering, F. Kensy, L. Wang, and J. Büchs. "Optimierung der Proteinexpression im Hochdurchsatz." Chemie Ingenieur Technik 81, no. 8 (August 2009): 1248. http://dx.doi.org/10.1002/cite.200950023.

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End, Caroline, Christian Walczuch, and Matthias Buntru. "Zellfreie Proteinexpression für Forschung und Produktion." BIOspektrum 20, no. 1 (February 2014): 70–72. http://dx.doi.org/10.1007/s12268-014-0411-8.

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Dietzsch, C., O. Spadiut, D. Zalai, and C. Herwig. "Effiziente Bioprozessentwicklung für rekombinante Proteinexpression in Pichia pastoris." Chemie Ingenieur Technik 84, no. 8 (July 25, 2012): 1341. http://dx.doi.org/10.1002/cite.201250281.

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Stenzel, I., M. P�sl, H. Ritzel, M. Hentz, M. Werner, and G. Delling. "Zellproliferation bei Knochentumoren Immunhistologische Untersuchung zur Ki-67-Proteinexpression*." Der Pathologe 17, no. 1 (January 1, 1996): 56–62. http://dx.doi.org/10.1007/s002920050135.

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Hinkelbein, J., A. Kalenka, and R. E. Feldmann Jr. "Frühzeitige Veränderungen der Proteinexpression im Gehirn der Ratte bei Sepsis." Der Anaesthesist 58, no. 2 (December 14, 2008): 134–43. http://dx.doi.org/10.1007/s00101-008-1488-6.

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Schraml. "Onkogene, Motoren der Krebszelle." Praxis 93, no. 22 (May 1, 2004): 957–59. http://dx.doi.org/10.1024/0369-8394.93.22.957.

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Nach dem heutigen Wissensstand der Krebsforschung tragen DNA-Veränderungen entscheidend zur Entstehung eines Tumors bei. Dabei werden Gene betroffen, deren Produkte bei der Regulation des Zellzyklus eine entscheidende Rolle spielen. Bei Onkogenen führen Mutationen häufig zu einer abnormen Genaktivierung und damit zu einer massiven Proteinexpression. Die starke Expression und andauernde Präsenz von Onkoproteinen in Tumorzellen veranlassen diese sich unkontrolliert zu teilen, was mit der Zeit Krebs hervorrufen kann. Neuartige Medikamente, welche spezifisch die Funktion von Onkoproteinen hemmen können, lassen in Zukunft auf effizientere Krebstherapien hoffen.

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Ohlendieck, K. "Proteomforschung und molekulare Mechanismen bei Muskelanpassungen und Muskelerkrankungen." Nervenheilkunde 32, no. 06 (2013): 389–94. http://dx.doi.org/10.1055/s-0038-1628512.

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ZusammenfassungBiomedizinische Untersuchungen mit global ausgerichteten Forschungsansätzen haben erhebliche Erfolge bei der Erforschung der physiologischen Muskelanpassung und der molekularen Pathogenese von Muskelerkrankungen erzielt. Die Proteomanalyse mittels 2D-Gelelektrophorese, Flüssigkeitschromatografie und Massenspektrometrie wurde gezielt für die Erforschung pathobiochemischer Veränderungen bei der zeitlichen Abfolge der Proteinexpression und der posttranslationalen Modifizierung eingesetzt sowie zur Bestimmung von abnormalen Wechselwirkungen zwischen Muskelproteinen. Die differenzielle Proteomanalyse wurde erfolgreich angewendet zum Vergleich der Expressionsprofile von gesundem menschlichem Muskelgewebe und Muskelbiopsien von Patienten mit Einschlusskörpermyositis, Adipositas, Diabetes mellitus und Sarkopenie. Die zelluläre Plastizität von Muskelfasern wurde bestimmt bei der Muskelanpassung an Ausdauertraining und an Hypoxie. Weiterhin haben Proteomstudien an Modellorganismen mit Muskelerkrankungen zur Identifizierung von potenziell veränderten Reaktionskaskaden bei bestimmten Formen der Muskeldystrophie, Myotonie, Muskelatrophie und der amyotrophen Lateralsklerose geführt.

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Ohlendieck, K. "Biomarkeridentifizierung und Anwendung bei der Muskeldystrophie Typ Duchenne." Nervenheilkunde 34, no. 01/02 (2015): 77–82. http://dx.doi.org/10.1055/s-0038-1627549.

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ZusammenfassungObwohl die zur Muskeldystrophie vom Typ Duchenne führenden primären Defekte im Dystrophingen schon seit über zwei Jahrzehnten bekannt sind, haben diese biomedizinischen Erkenntnisse noch nicht zu einer erfolgreichen Therapie des progredienten Muskelschwundes geführt. Möglicherweise können jetzt Impulse gesetzt werden durch neue Einsichten in die molekulare Pathogenese der Muskeldystrophie, welche auf der vergleichenden Proteomanalyse beruhen. Mithilfe der Massenspektrometrie wurden diskrete Veränderungen bei der zeitlichen Abfolge der Proteinexpression im dystrophischen Muskelgewebe ermittelt. Systematische Proteomstudien von Muskelgewebe und Körperflüssigkeiten von Patienten und Modellorganismen haben neue potenzielle Biomarker identifiziert, welche involviert sind in die Muskelkontraktion, die Regulierung der Ionenhomöostase, den Energiestoffwechsel und die zelluläre Stressreaktion sowie die Dynamik des Zytoskeletts und der extrazellulären Matrix. Die Etablierung neuer diagnostischer Biomarker verspricht eine verbesserte klinische Beurteilung von experimentellen Ansätzen wie der Antisensetherapie.

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Giarnieril, E., G. De Francesco, C. Amanti, B. Bucci, V. Catracchia, V. Moscarolis, M. Lo Russ, and M. Giovagnoli. "P4 Evaluation of Msh2, MIh1, Brca1 and Fhit proteinexpression in T1 NO MO breast cancer." Breast 14 (February 2005): S15—S16. http://dx.doi.org/10.1016/s0960-9776(05)80043-8.

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Baghai, T. C., D. Eser, C. Schüle, R. Rupprecht, P. Zill, and B. Bondy. "Haben die unterschiedlichen Antidepressiva unterschiedliche Wirkmechanismen?" Nervenheilkunde 24, no. 05 (2005): 361–68. http://dx.doi.org/10.1055/s-0038-1629976.

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ZusammenfassungUnsere Kenntnisse über pathophysiologische Mechanismen der Depression oder die Wirkmechanismen der Antidepressiva haben sich in den letzten Jahren erheblich erweitert. Dabei wurde deutlich, dass die Erhöhung der Konzentrationen der Neurotransmitter im synaptischen Spalt oder die Interaktionen mit den entsprechenden Rezeptoren vor allem als initialer Schritt zu betrachten sind, durch den es über zahlreiche Aktivierungsschritte in der Synapse letztendlich zu substantiellen Veränderungen der Proteinexpression und damit der neuronalen Funktion kommt. Auch wenn wir heute zunehmend davon ausgehen, dass diese langfristigen Veränderungen der neuronalen Funktion als sogenannte gemeinsame Endstrecke der Antidepressiva- Wirkung angesehen werden kann, ist der Einfluss der unterschiedlichen initialen Wirkmechanismen sowie deren Interaktion mit den verschiedenen Kompartimenten der Signaltransduktion nicht zu vernachlässigen. Besonders die pharmakogenetischen Studien haben gezeigt, dass die Schnelligkeit des Ansprechens auf die Behandlung doch im erheblichem Maße von diesen Mechanismen beeinflusst wird.

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Patz, Michaela, Nina-Felizitas Linde, Lukas P. Frenzel, Christian P. Pallasch, Reinhild Brinker, Julia Claasen, Michael Hallek, and Clemens Wendtner. "B Cell Receptor Stimulation of CLL Cells Leads to Upregulation of IRF4 Proteinexpression Influenced by SNP Expression,." Blood 118, no. 21 (November 18, 2011): 3886. http://dx.doi.org/10.1182/blood.v118.21.3886.3886.

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Abstract Abstract 3886 Introduction: As previously published by Di Bernado et al. (2008) the single nucleotide polymorphism (SNP) RS872071 located in the 3'UTR of IRF4 (Interleukin Regulatory Factor 4) has influence on the risk for developing chronic lymphocytic leukemia (CLL). IRF4 is a key player in the development of B lymphocytes and multiple myelomas. The SNP is either expressed as Adenine (A) or Guanine (G). Expression of G/G increases the risk to develop CLL. MicroRNAs (miRNAs) adhere posttranscriptional to the 3'untranslated region (UTR) of mRNAs and can influence the expression of mRNA and proteins. The SNP lies within the 3'UTR of IRF4 and offers some putative binding sites for miRNAs. The aim of this project is to proof that this SNP has influence on the binding behavior of miRNAs, which are influencing the IRF4 expression. Methods and results: To identify miRNAs binding to this region we cloned the neighboring region of the SNP into a luciferase expressing vector and generated the SNP by mutagenesis. In luciferase assays 15 miRNAs were checked for differences in binding affinity dependent on SNP expression. Three of them showed significant SNP dependent binding behavior. In all cases expression of SNP G leads to reduced luciferase expression, indicating suppression of IRF4. To elucidate the consequences on SNP expression on cellular level in CLL we collected DNA derived from B cells of CLL patients (n=104) and sequenced the SNP region. All together our pool of patients expressed 25% A/A, 31% A/G and 44% G/G. MRNA and protein expression of IRF4 was considered SNP-dependently and compared to healthy B cells. On mRNA and protein level CLL cells have a significant higher IRF4 expression compared to healthy B cells. SNP-dependent comparison between CLL cells on mRNA-level shows a tendency of less IRF4 expression in B cells of patients expressing the G/G SNP compared to patients expressing A/A SNP. However on protein level this tendency was not detected. As IRF4 is known as a key regulator for extracellular stimuli, we focused on SNP dependent IRF4 regulation after different stimuli. Whereas CD40 and IL-4 stimulation did not show SNP dependent regulation, stimulation of the B cell receptor (BCR) leads to a higher IRF4 induction in patients carrying A/A (n=6) compared to patients carrying G/G (n=5) and A/G (n=8) (p<0.05). Conclusion: For the first time connections between the SNP RS872071 and molecular mechanisms explaining his influence on the pathogenesis on CLL were drawn. Dependent on expressed SNP miRNAs bind with different affinities to the 3'UTR. In further experiments the connection between IgM stimulation and miRNA expression has to be tightened. Disclosures: No relevant conflicts of interest to declare.

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Uchida, Akiko, Yasushi Isobe, Junko Asano, Yu Uemura, Masahiro Hoshikawa, Masayuki Takagi, and Ikuo Miura. "Targeting BCL2 with venetoclax is a promising therapeutic strategy for “double-proteinexpression” lymphoma with MYC and BCL2 rearrangements." Haematologica 104, no. 7 (December 6, 2018): 1417–21. http://dx.doi.org/10.3324/haematol.2018.204958.

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Kahle, B., M. Idzko, J. Norgauer, E. Rabe, L. Bruckner-Tuderman, M. Jünger, and Y. Herouy. "Wirkung der Kompressionstherapie auf die parazelluläre Barrierefunktion." Phlebologie 33, no. 04 (2004): 115–19. http://dx.doi.org/10.1055/s-0037-1617284.

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ZusammenfassungTight junctions (TJs) bilden semipermeable interzelluläre Diffusionsbarrieren, die den parazellulären Transport kontrollieren. Als apikale Strukturen des Schlussleistenkomplexes sind TJs selektiv permeabel und somit an der Abdichtung des Interzellularspaltes beteiligt. Ziel: Bestimmung der Expression der TJ-Moleküle Occludin (OCLN), Claudin-1 (CLDN-1), -3 (CLDN-3) und -5 (CLDN-5) auf mRNA- und Proteinebene bei Patienten mit CVI-bedingten Beinödemen und mit venösen Beinulzerationen im Vergleich zu gesunder Haut. Material, Methoden: Gewebeproben von der unteren Extremität aus läsionaler und gesunder Haut wurden mit RT-PCR und Westernblot im Hinblick auf die Expression der genannten TJ-Moleküle untersucht und densitometrisch analysiert. Ergebnisse: CVI-Patienten hatten im Vergleich zu gesunder Haut in allen Proben eine erniedrigte mRNA- und Proteinexpression von CLDN-1 und CLDN-5. Kein statistischer Unterschied wurde für die OCLN- und CLDN-3-Expression festgestellt. Densitometrisch wurde eine signifikant erhöhte Expression von CLDN-1 und CLDN-5 nach einer vierwöchigen Kompressionsstrumpftherapie im Vergleich zum Expressionsmuster vor Therapiebeginn nachgewiesen. Schlussfolgerung: Diese Daten weisen daraufhin, dass spezifische TJ-Moleküle bei Patienten mit CVI in läsionaler Haut vermindert exprimiert werden und dass der antiödematöse Effekt der Kompressionsstrumpftherapie möglicherweise zusätzlich über eine Stärkung der parazellulären Barrierefunktion vermittelt wird.

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Nurulita, Nunuk Aries, Edy Meiyanto, Eishou Matsuda, and Masashi Kawaichi. "Gynura procumbens Prevents Chemoresistance through Inhibition MDR1 Expression on MCF-7 Breast Cancer Cell Line and Sensitizes the Cells to Doxorubicin." Indonesian Journal of Biotechnology 17, no. 1 (November 9, 2015): 51. http://dx.doi.org/10.22146/ijbiotech.15998.

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The long-term exposure of doxorubicin (Dox) causes enhancement in MDR1 expression that leads tobreast cancer cell resistance. This protein become a serious problem in cancer treatment and also well-knownas negative prognostic factor in breast cancer malignancies. The new approach using natural chemopreventivesubstance was developed to inhibit this resistance progress. This study was aimed to investigate whether ethylacetate fraction of Gynura procumnens (FEG) can prevent chemoresistance through suppressing the MDR1 proteinexpression. MCF-7 cell was used as chemoresistance cell model. The MCF-7 cells were maintained with 100nM Dox-contained medium for five weeks. The chemoprevention effect of FEG was investigated by treatedMCF-7/Dox with sub-toxic concentration of FEG. The cytotoxic properties of MCF-7 cells were determinedusing MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay. Immunofluorescenceand western blotting analysis was performed to detect the MDR1 expression. MCF-7/Dox cells need higherconcentration for inhibiting cell growth, were compared with MCF-7, shown by IC50value. The MDR1 proteinlevel elevated after Dox exposure in time dependent manner. The FEG treatment decreased MDR-1 proteinlevel with dose dependent manner. FEG in combination with DOX potentiates the DOX effect on breast cancercell growth inhibition. The FEG prevents the chemoresistance development in breast cancer cell line, MCF-7induced by Dox through inhibiting MDR1 expression. The additional of FEG enhances Dox effect on cell deathinduction. Thus, FEG could be developed as co-chemotherapy agent for reverse multidrug resistance

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Weigand, Annika, Kereshmeh Tasbihi, Pamela Strissel, Reiner Strick, Raymund Horch, and Anja Boos. "Entwicklung eines neuen Zellisolationsverfahrens zur Erforschung der Mammakarzinompathogenese und -angiogenese für experimentelle in vitro und in vivo Assays." Handchirurgie · Mikrochirurgie · Plastische Chirurgie 49, no. 02 (April 2017): 111–22. http://dx.doi.org/10.1055/s-0042-123706.

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Zusammenfassung Hintergrund Brustkrebs gilt als die weltweit häufigste Krebserkrankung bei Frauen. Zunehmend wird autologer Lipotransfer zum Wiederaufbau der Brust nach Tumorresektion angewandt. Im zellunterstützenden Lipotransfer wird das Transplantat mit Stammzellen aus dem Fettgewebe (ADSC) angereichert. Trotz der positiven klinischen Ergebnisse gibt es aufgrund des Stammzellanteils Bedenken hinsichtlich der onkologischen Sicherheit. Bislang gibt es nur wenige Studien mit primären Zellen aus derselben Patientin, durch die es möglich werden könnte die Komplexität der Zell-Zell-Interaktionen im Mamma(karzinom)gewebe besser in experimentellen Settings darzustellen. Material und Methoden Es wurde eine Literaturrecherche zum Thema autologer Lipotransfer durchgeführt. Aus Mamma(karzinom)gewebe, bzw. Blut wurden 5 unterschiedliche Zelltypen (epitheliale, mesenchymale Zellen, ADSC, Endothelzellen, endotheliale Progenitorzellen) isoliert und nachfolgend hinsichtlich ihrer Gen- und Proteinexpression sowie funktioneller Eigenschaften charakterisiert. Das arteriovenöse (AV) loop Modell in der Ratte wurde als mögliches in vivo Modell für die Mammakarzinompathogenese und -angiogenese im Rahmen dieser Studie evaluiert. Ergebnisse In der Literatur konnten Hinweise auf eine in vitro Interaktion zwischen ADSC und Zellen des Mamma(karzinom)gewebes gefunden werden. In einigen klinischen Studien erschienen bestimmte Patientensubgruppen einem erhöhten Tumorrezidivrisiko nach Lipotransfer ausgesetzt zu sein, jedoch konnte in der Mehrzahl der Studien kein Zusammenhang zwischen Lipotransfer und Rezidivrate festgestellt werden. Aus Gewebe derselben Patientin konnten unterschiedliche Zellpopulationen isoliert werden, die sich hinsichtlich ihrer Oberflächenmarker, der Genexpression sowie funktioneller Eigenschaften deutlich voneinander differenzieren lassen. Im AV loop Modell konnte erfolgreich axial vaskularisiertes Gewebe gezüchtet werden. Schlussfolgerung Anhand dieser Studie können wir erstmalig zeigen, dass aus derselben Gewebeprobe unterschiedliche Zellpopulationen isoliert werden können, die die Heterogenität im Tumorgewebe widerspiegeln. Dadurch werden exakte Analysen der Zell-Zell-Interaktionen und ihre Auswirkungen auf die Tumorangiogenese und -pathogenese im Mammakarzinom möglich. In Kombination mit dem AV loop Modell könnten neue Wege eröffnet werden vaskularisiertes Mammakarzinom- sowie gesundes Mammagewebe in vivo als optimales Modell für das klinische Setting zu generieren.

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Yahya, Yulia Farida, Radema Maradom, Hari Darmawan, Theresia L. Toruan, and Ika Kartika. "The Role Protein Sonic Hedgehog in Carcinoma Basal Cell." Bioscientia Medicina : Journal of Biomedicine and Translational Research 5, no. 1 (December 25, 2020): 212–18. http://dx.doi.org/10.32539/bsm.v5i1.210.

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A B S T R A C TIntroduction: Basal cell carcinoma (KSB) is a non-melanoma skin cancer (KKNM),which is most commonly found compared to other skin cancers. KSB originates fromstem cells in the bulk of hair follicles or inter-follicular epidermis, through the Sonichadgehog (SHH) activation pathway, an increase in Sonic hadgehog (SHH) proteinexpression, involving Patches protein (PTCH), smothened protein (SMO), in the formof increased protein transcription activation Glia (GLI) in the nucleus, binds to DNAto initiate tumor-aggressive growth and tissue. Objective: to determine therelationship between Sonic hadgehog (SHH) expression and non-aggressive andaggressive basal cell carcinoma. Methods: The study was carried out in anobservational laboratory with 35 primary KSB patients, the tissue was taken usingelliptic biopsy technique, made paraffin block specimens for histopathologicalexamination of the subtype of KSB consisting of 20 non-aggressive KSB patients,namely nodular and superficial KSB; 15 patients with aggressive KSB werepigmented KSB; Infiltrates KSB, micronodular KSB, metypical KSB (basosquamousKSB) and SHH immunohistochemical (CPI) examination using SHH antibodies, inthe Anatomy Pathology section, FK Unsri / RSMH Palembang. The characteristics ofKSB patients were recorded, namely sex, age, occupation based on the length ofexposure to BC, namely exposure <3 hours / day, exposure 3-6 hours / day,exposure ≥ 6 hours / day. The data were processed using the Statistical AnalysisSoftware Package (SPSS) version 20.0 (IBM Corporation), tested with Pearsoncorrelation test and chi square test and presented in the form of diagrams, andnarrative tables. Results: Pearson's test showed a significant correlation betweenthe clinical features of KSB and the histopathologic features of non-aggressive andaggressive types of KSB (p 0.020), there was a significant relationship between thesubtypes of histopathologic features of KSB with non-aggressive and aggressivetypes of KSB (p 0.000), there was a significant relationship between strong SHHexpression and BCC aggressive compared to non-aggressive KSB, p 0.000 (p <05α),and r = 732 Conclusion: There is a relationship between SHH expression and KSBaggressiveness. The increase in strong SHH expression shows the aggressiveness ofKSB, SHH expression can be used as a biological gene target both as a prognosticindicator and can be used as a target for treatment of aggressive KSB, especially inthe elderly.

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Hutter, Grit, Yvonne Zimmermann, Malte Rieken, Elena Hartmann, Vindi Jurinovic, Andreas Rosenwald, Marc Weinkauf, Wolfgang Hiddemann, and Martin H. Dreyling. "Synergistic Antilymphoma Effect of Protein Kinase C Beta (PKCβ) and mTOR Inhibition in Mantle Cell Lymphoma." Blood 114, no. 22 (November 20, 2009): 4780. http://dx.doi.org/10.1182/blood.v114.22.4780.4780.

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Abstract Abstract 4780 Introduction The protein kinase C (PKC) family of enzymes are serine/threonine kinases essential to the cell signal cascades effecting cellular growth, proliferation and apoptosis. Accordingly PKCβ overexpression correlates with poor clinical prognosis in diffuse large cell lymphoma. The pivotal role of PKCb in neoplastic transformation renders it a potential therapeutic target in the therapy of hematologic malignancies. Aim To determine drugs which are efficiently inhibiting cell proliferation in combination with enzastaurin in MCL. Methods Five MCL cell lines (HBL-2, GRANTA 519, Jeko-1, Z138, Rec-1) and patient samples were cultured in the presence of LY317615 (PKCb inhibitor), rapamycin (mTOR inhibitor) and LY294002 (PI3K inhibitor). Cell proliferation and viability was assessed by cell count and WST-1 proliferation assay. Analysis of cell cycle profile and apoptosis was performed by flow cytometry (PI and Annexin V FITC staining). mRNA expression was measured before and after treatment (8h) by microarray and real time PCR in cell lines. Protein expression was analysed by Western blot. Results In a panel of mantle cell lymphoma cell lines, with IC50 values ranging from 2 to 5 microM for enzastaurin treatment, a refractory to enzastaurin cell line (Rec-1) was characterized. Treatment of the cell lines with enzastaurin induced apoptosis and lead to accumulation of cells in the G2, M phase in susceptible cell lines (Hbl-2, Jeko-1), whereas cell cycle profile remained unaltered in the refractory cell line (Rec-1). While enzastaurin induced increased phosphorylation of mTOR and MEK and decrease of p90RSK phosphorylation in all MCL cell lines, mTOR phosphorylation was twice as high in the refractory cell line (Rec-1). In line with this observation the combination of enzastaurin with rapamycin lead to a synergistic effect on the inhibition of cell proliferation in the Rec-1 cell line as well as in an additional MCLpatient sample. Protein expression levels (low CCND1, phAkt, php90RSK, phPDK) achieved in Rec-1 after treatment with enzastaurin were also characteristic for the cell lines more sensitive to rapamycin. In contrast in some cell lines combination of enzastaurin and the PI3K inhibitor (LY294002) displayed antagonism. Further mRNAand proteinexpression analysis of patient samples are ongoing to determine molecular predictors of drug sensitivity. Conclusion In our study a combination of rapamycin and enzastaurin acted synergistically in MCL cell lines and a patient samples whereas the combination with a PI3K inhibitor displayed partial antagonism. Based on this results we have identified the underlying signal pathways to develop new synergistic molecular combinations in MCL. Disclosures: Hutter: Lilly Deutschland GmbH: Research Funding. Zimmermann:Lilly Deutschland GmbH: Research Funding. Rieken:Lilly Deutschland GmbH: Research Funding. Weinkauf:Lilly Deutschland GmbH: Research Funding. Dreyling:Lilly Deutschland GmbH: Research Funding.

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Hutter, Grit, Yvonne Zimmermann, Marc Weinkauf, Alina Postnikova, Tobias Weiglein, Wolfgang Hiddemann, and Martin Dreyling. "The Functional Impact of PKCβ/PI3K/AKT Signalling on Translational Initiation in MCL." Blood 112, no. 11 (November 16, 2008): 2624. http://dx.doi.org/10.1182/blood.v112.11.2624.2624.

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Abstract Introduction: Mantle cell lymphoma (MCL) is an aggressive form of B-cell non-Hodgkin’s lymphoma (NHL). It is characterized by the t(11;14)(q13;q32) translocation, which results in the overexpression of cyclinD1, a cyclin regulated by the PI3K/AKT pathway. Activation of the PI3K/AKT pathway has been shown to be involved in the pathogenesis of MCL. In addition overexpression of the protein kinase C beta (PKCβ) has been described for most cases of MCL, inhibited by enzastaurin which in turn induces apoptosis and reduces proliferation through the PKCβ/PI3K/AKT pathways. 4EBP1 is described as one of the downstream targets of PI3K/mTOR pathway linking translation initiation with PI3K/mTOR signalling as a EIF4E binding protein and playing therefore critical role in the control of protein synthesis, survival and cell growth. Targeting 4EBP1 and/or EIF4E via the PI3K/AKt/mTOR signalling or directly will affect tumor tissue. Aim of the study: The aim of the study was to determine the functional impact of PKCβ/PI3K/AKt/mTOR signaling on the translation initiation factor EIF4E, its binding protein and regulated proteins in MCL cell lines. Methods: MCL cell lines were treated with inhibitors of the PKCβ/PI3K/AKt/mTOR pathways (enzastaurin, LY294002, rapamycin) for up to 48h.The impact of the drugs on the proliferation rate of the cells was accessed after 48h by WST-assay and/or cell count. mRNA expression levels were determined using Taqmanassays. Protein phosphorylation status and protein expression were identified by westernblot. For downregulation of EIF4E in the cells sodium arsenite was used. Specific silencing of EIF4E was achieved by transfection of cells with siRNA against EIF4E. Results: The MCL celllines (5) responded to the treatment with the inhibitors of the PI3K/AKt/mTOR pathway at a IC50 for rapamycin between 5nM-50nM and for the PI3Kinhibitor between 0,31μM-5μM. Treatment of the cells with the PI3K/AKt/mTOR inhibitors induced dephosphorylation of 4EBP1 in a time-and dosedependent manner while a potential effect of the PI3K and mTOR inhibitors on the EIF4E expression and its target genes (cyclinD1, BCL2) could not be shown consistently. 4 out of 5 MCL cell lines were susceptible to enzastaurin with an IC50 between 2μM-5μM. In the not responding to enzastaurin and most resistant to rapamycin cell line (Rec-1) no 4EBP1 proteinexpression was detectable. Dephosphorylation of 4EBP1 achieved by treatment of the cells with sodium arsenit was accompanied by downregulation of EIF4E, cyclinD1 and BCL2 proteins but also stop of proliferation. The potential involvement of eIF4E gene expression in the NaAsO2-induced cytotoxicity and cell death in MCL cell lines was shown by silencing the expression of the eIF4E gene by transfection with siRNA specifically targeting the eIF4E gene expression leading to downregulation of cyclinD1, 4EBP1 proteins and cell proliferation. Conclusion: Eventhough treatment of the cells with the PI3K/AKt/mTOR inhibitors induced dephosphorylation of 4EBP1 a potential effect of the PI3K and mTOR inhibitors on the EIF4E expression and its target genes (cyclinD1, BCL2) could not be shown consistently. Instead dephosphorylation of 4EBP1 accomponied by downregulation of EIF4E or targeted downregulation of eIF4E gene expression lead to downregulation of cyclinD1 and BCL2 proteins as well as cell death in MCL. Therefore targeting the downstream targets of the PI3K/AKt/mTOR signalling 4EBP1 and/or EIF4E directly seems to be a promising anticancer strategy.

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Kornblau, Steven M., Chenyue W. Hu, Yihua Qiu, Suk Young Yoo, Kavita Chauhan, Elias Jabbour, Farhad Ravandi, Kevin Coombes, and Amina A. Qutub. "CREB/ATF Family Protein Expression States in AML: Active CREB1, but Not ATF Is an Adverse Prognostic Factor." Blood 124, no. 21 (December 6, 2014): 2344. http://dx.doi.org/10.1182/blood.v124.21.2344.2344.

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Abstract Background. The cAMP responsive element-binding (CREB) and Activating transcription factor (ATF) family of transcription factors regulates many cellular stress responses including proliferation, differentiation and survival, possibly through chromatin modification. CREB is a critical regulator of normal myelopoiesis and is over-expressed in AML, with knockdown inhibiting proliferation, suggesting a proto-oncogene role. CREB/ATF proteins have typically been studied individually , and in small series. Interactions with multiple signaling and functional pathways are suspected, but the actual relationship in primary AML samples is unknown. We therefore assessed the protein expression of two CREB/ATF family members; CREB binding protein 1 (CREB1) a leucine zipper transcription factor, active when phosphorylated on serine 133 (CREB1.pS133) and ATF 3 (ATF3), in a series of 511 newly diagnosed AML patients and compared expression to 228 simultaneously measured proteins Methods. A reverse phase protein array (RPPA) using leukemia enriched cells from 511 AML patients. Both bone marrow (BM, n=387) and peripheral blood (PB, n=283) samples were used, with 140 cases having both. The RPPA was probed with 231 strictly validated antibodies, including antibodies against CREB1, phopsho CREB1 CREB1.pS133 and ATF3. Expression was compared to that of normal BM derived CD34+ cells. Interaction networks with the other 228 proteins were generated using glasso, supplemented by the literature of known interactions. Results. A heatmap of CREB1,CREB1.pS133 and ATF expression was generated and k-means clustering performed (Figure A). Most cases of AML demonstrated high expression of CREB or ATF, but not both, although ATF levels were modest with high CREB1 expression, Using the Prototype Clusteringmethod an optimal division into three clusters C1) Pan Low expression C2) High CREB and C3) High ATF3 with 26%, 55% and 19% of patients in each respectively was selected. Consistent with the literature, expression of CREB1 & CREB1pS133 were strongly positively (Figure B) correlated with several histone modification proteins including Histone3, H3K4Me2, H3K4Me3, ASH2L, proliferation associated proteins RB1 and ELK1.pS383, and transcription factors including DLX1, Fli1, GATA3, Smad4, SPI1, TAZ.pS89 and Trim24. They were inversely correlated with histone demethylase KDR, protein kinase A and prostaglandin synthetase 2. ATF3 expression was positively correlated with histone modifier JMJD6, proliferation proteins EIF2AK2.pT451, CCND1 , and transcription factors JUNB, Smads 3 and 4, ZNF296, ZNF346. ATF levels were negatively correlated with Signal transduction via including STAT1, MAPK1, and PA2G4.pT37. While directionality cannot be inferred these proteins showed clear changes in expression of either ATF3 or CREB1/CREB1.pS133 between the pan off and the individual on states. WBC (14, 33, 30K respectively for C1,C2 and C3, p = 0.01) and %PB blasts (20, 34, 32%, p = 0.001) were significantly lower in C1, but most other clinical features including cytogenetics, and FLT3-ITD status did not differ between the clusters. Cluster membership was not associated with complete remission or primary resistance rates. Overall survival (OS) for all patients did not differ by cluster (p=0.45), but those with intermediate cytogenetics (IntCyto) and high CREB fared worse (median survival of 58 weeks vs. 66 and 87 for C3 and C1 (p=0.036) and this effect was more prominent in FLT3 mutant (p =0.05) than wildtype cases (p=0.34). Remission duration (RemDur) was similarly inferior in IntCyto C2 patients (median 39 vs. 76vs 89 weeks for C3 and C 1, p= 0.007) Conclusions. Over expression of a CREB family member was very common in AML (74%) but was exclusive foreither ATF3 or CREB1, but not both. Overexpression was independent of clinical features, excluding higher WBC and %PBblast % with high CREB1. In those with IntCyto high CREB1 expression was adverse for OS and RemDur. High CREB1 or ATF expression correlated with histone modification, proliferation and transcription factor proteinexpression, but with different members of these protein functional classes. These results imply a central role for CREB/ATF family in deregulation of many pathways, but suggests that therapy directed towards interfering with CREB/ATF family must be selective to which side of the family is overexpressed to be effective. Figure 1 Figure 1. Disclosures Ravandi: Cellerant Therapeutics: Research Funding.

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"Pulmonale Sarkoidose - Proteinexpression offenbar stadien- und phänotypspezifisch." Pneumologie 61, no. 3 (March 2007): 144. http://dx.doi.org/10.1055/s-2007-973915.

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Mees, S., J. Schwarze, M. Starke, N. Senninger, and M. Stölting. "Inhibition von miR-200c im Pankreaskarzinom führt zu veränderter Proteinexpression und Zellfunktion." Zeitschrift für Gastroenterologie 53, no. 08 (August 18, 2015). http://dx.doi.org/10.1055/s-0035-1559516.

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Dietrich, CG, A. Geier, F. Lammert, S. Matern, and C. Gartung. "Regulation der Mrp4/Abcc4-Proteinexpression in der Rattenleber während Cholestase und Regeneration." Zeitschrift für Gastroenterologie 42, no. 08 (August 18, 2004). http://dx.doi.org/10.1055/s-2004-831788.

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Schechinger, W., K. Hojlund, K. Levin, H. Beck-Nielsen, and HH Klein. "Die Prohibitin-1-Proteinexpression im humanen Skelettmuskel ist mit der Insulinempfindlichkeit korreliert." Diabetologie und Stoffwechsel 3, S 1 (2008). http://dx.doi.org/10.1055/s-2008-1076266.

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Nehls, O., T. Okech, C.-J. Hsieh, M. Sarbia, F. Borchard, HH Gruenagel, V. Gaco, R. Porschen, M. Gregor, and B. Klump. "Eine niedrige BAX-Proteinexpression korreliert mit der Rezidivhäufigkeit beim präoperativ bestrahlten Rektumkarzinom." Zeitschrift für Gastroenterologie 41, no. 08 (May 28, 2015). http://dx.doi.org/10.1055/s-0035-1555495.

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Reiter, R., H. Riechelmann, and T. Deutschle. "Gentranskription und Proteinexpression von Epithelzellen, T-Zellen und Makrophagen nach Stimulation mit Hausstaub." HNO-Informationen (Kongressabstracts) 84, no. 01 (April 26, 2005). http://dx.doi.org/10.1055/s-2005-868762.

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Csepregi, A., C. Röcken, J. Hoffmann, P. Malfertheiner, C. Lofton-Day, and M. Ebert. "Der Einfluss der Promotermethylierung auf die APC-Proteinexpression in nicht-virusinduziertem hepatozellulärem Karzinom." Zeitschrift für Gastroenterologie 44, no. 01 (January 16, 2006). http://dx.doi.org/10.1055/s-2006-931673.

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Rau, SJ, E. Hildt, HE Blum, and R. Fischer. "CD40 Ligand vermindert Hepatitis C Proteinexpression und Virusreplikation in JFH1 infizierten primären humanen Hepatozyten." Zeitschrift für Gastroenterologie 47, no. 09 (September 2009). http://dx.doi.org/10.1055/s-0029-1241341.

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Rau, SJ, E. Hildt, HE Blum, and R. Fischer. "CD40 Ligand vermindert Hepatitis C Proteinexpression und Virusreplikation in JFH1 infizierten primären humanen Hepatozyten." Zeitschrift für Gastroenterologie 47, no. 06 (June 2009). http://dx.doi.org/10.1055/s-0029-1225681.

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Wirz, C., A. Dietz, R. Dollner, C. Wittekind, A. Tannapfel, and A. Weber. "Erlaubt die Proteinexpression in Zusammenschau mit der Bildmorphologie von zervikalen Lymphknotenmetastasen Rückschlüsse auf die Primärtumorlokalisation?" HNO-Informationen (Kongressabstracts) 84, no. 01 (April 26, 2005). http://dx.doi.org/10.1055/s-2005-869188.

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Ling, FC, N. Leimbach, SE Baldus, J. Brabender, U. Drebber, HP Dienes, AH Hölscher, and PM Schneider. "Neoadjuvante Radio-/Chemotherapie beim Ösophaguscarcinom: Einfluss der HIF-1α mRNA und Proteinexpression auf den histomorphologischen Response." Zeitschrift für Gastroenterologie 44, no. 08 (September 19, 2006). http://dx.doi.org/10.1055/s-2006-950940.

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Neumeier, M., G. Wehrwein, A. Schäffler, J. Schölmerich, and C. Buechler. "Die Lipopolysaccharid-vermittelte Proteinexpression ist in Monozyten von Patientinnen mit Typ 1 Diabetes nur partiell verändert." Diabetologie und Stoffwechsel 1, S 1 (2006). http://dx.doi.org/10.1055/s-2006-944181.

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Giehl, KA, U. Nägele, M. Volkenandt, and C. Berking. "Proteinexpression von Wachstumsfaktoren (bFGF, SCF) und deren Rezeptoren (FGFR-1 und c-kit) in Nävuszellnävi und Melanomen." Aktuelle Dermatologie 30, no. 08/09 (August 24, 2004). http://dx.doi.org/10.1055/s-2004-832582.

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Opitz, D., E. Lenzen, T. Kreutz, C. Brinkmann, A. Wacker, M. Redmann, T. Schiffer, K. Brixius, W. Bloch, and C. Capin. "Ausdauertraining beeinflusst die MCT1- und MCT4- Proteinexpression in der Skelettmuskulatur bei männlichen nicht-insulinpflichtigen Typ 2 Diabetikern." Diabetologie und Stoffwechsel 6, S 01 (May 2011). http://dx.doi.org/10.1055/s-0031-1277544.

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Luca, AC, C. Driemel, JM Pietsch, S. Mersch, R. Deenen, WT Knoefel, and NH Stoecklein. "Der Einfluss der extrazellulären Matrix auf den Phänotyp, die Gen- und Proteinexpression und die EGFR Inhibition bei CRC Zelllinien." Zentralblatt für Chirurgie 136, no. 05 (October 2011). http://dx.doi.org/10.1055/s-0031-1289093.

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Opitz, D., E. Lenzen, T. Kreutz, A. Wacker, M. Redmann, S. Romberg, G. Montiel, K. Brixius, W. Bloch, and C. Capin. "Ausdauertraining verbessert die MCT1-Proteinexpression und die belastungsabhängige Verteilung des MCT1-Transporters in Erythrozyten von männlichen nicht-insulinpflichtigen Typ 2 Diabetikern." Diabetologie und Stoffwechsel 6, S 01 (May 2011). http://dx.doi.org/10.1055/s-0031-1277308.

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SURYADARMA, SANI, KAMIZAR ., ENDANG SUPRASTIWI, RATNA MEIDYAWATI, and MAIDA FITRI. "DIFFERENCES IN THE POTENTIAL MUTAGENICITY OF RESIN-, SILICONE-, AND BIOCERAMIC-BASED SEALERS ON LYMPHOCYTES: A PROTEIN EXPRESSION ANALYSIS." International Journal of Applied Pharmaceutics, April 4, 2019, 153–56. http://dx.doi.org/10.22159/ijap.2019.v11s1.16021.

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Objective: The objective of this study was to compare the potential mutagenicity of resin-, silicone-, and bioceramic-based sealers on proteinexpression in human lymphocytes. There has been limited research on resin-, silicone-, and bioceramic-based sealers effects on protein expressionin lymphocytes.Methods: Nine samples of each sealer were incubated in 2 mL human blood for 1, 3, and 7 days. Then, the isolated lymphocytes are observed forprotein separation by electrophoresis method. Profile of protein bands observed and data were analyzed statistically by Kruskal–Wallis and post hocMann–Whitney.Results: Although no statistically significant differences in protein bands were observed among the resin-, silicone-, and bioceramic-based sealers(p=0.111), there was a statistically significant difference between the resin- and silicone-based sealers on the 1st day (p=0.046) and 3rd day (p=0.046)and between the silicone- and bioceramic-based sealers on the 1st day (p=0.046). Thus, the present study shows that there were differences in thepotential mutagenicity on the 1st day; resin was potentially more mutagenic followed by bioceramic and silicone. On the 3rd and 7th days, bioceramicwas potentially more mutagenic followed by resin and silicone.Conclusion: The manuscript describes the study in detail and concludes that resin was potentially more mutagenic followed by bioceramic- andsilicone-based sealers.

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Dietrich, CG, A. Geier, HE Wasmuth, F. Lammert, DR de Waart, RPJ Oude Elferink, S. Matern, and C. Gartung. "Abnahme der Proteinexpression der Transporter Mrp2/Abcc2 und Bcrp/Abcg2 im Rahmen einer biliären Fibrose führt zu einer Reduktion der hepatischen Metabolisierungskapazität." Zeitschrift für Gastroenterologie 42, no. 08 (August 18, 2004). http://dx.doi.org/10.1055/s-2004-831799.

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Opitz, D., T. Kreutz, E. Lenzen, S. Voss, P. Wahl, W. Bloch, and K. Brixius. "Krafttraining verbessert die MCT1-Proteinexpression und die trainingsinduzierte Translokation des MCT1-Transporters in den Erythrozyten bei männlichen nicht-insulinpflichtigen Typ 2 Diabetikern." Diabetologie und Stoffwechsel 4, S 01 (April 2009). http://dx.doi.org/10.1055/s-0029-1221987.

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Bo, Shumin. "OR-054 A Comparative Study of Different Intervention Methods on Protein Expression of ERα in Uterus of Ovariectomized Osteoporosis Rats." Exercise Biochemistry Review 1, no. 2 (October 4, 2018). http://dx.doi.org/10.14428/ebr.v1i2.9843.

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Objective The aim of this study was to compare the effects of different intervention methods on the protein expression of estrogen receptor alpha (ERα) in the uterus of ovariectomized osteoporosis rats. Methods Eighty healthy female SD rats, aged 3 months, were randomly divided into the following two groups by body weight: sham-operation (Sham) and ovariectomized (OVX). After ten weeks, the OVX groups were randomly divided into the following six groups by body weight: OVX; 17β-estradiol (E2); Genisteine (G); treadmill exercise (TE); Lithium chloride (Licl); Whole-body vertical vibration (WBVV). Then the rats was began to be treated with different intervention methods. The WBVV group rats were vibrated on a vibration platform twice per day for 7 weeks according to the following schedule: 90 hertz a minute and 15 minutes a time. The TE group rats were running on 5-uphill treadmills 45 minutes per day, 4 times a week, at a speed of 18 meters per minute. The G group rats were lavaged by genistein once per day according to body weight (dose 1mg/kg).The E2 group rats were treated with neck subcutaneous injection with 17β-E2 three times a week according to their body weight (dose 25ug/kg). At the end of 8 weeks intervention, during 36-48 hours, took blood from the abdominal aorta, and extracted the protein. The proteinexpression of ERα in uterus was detected by western blot. Results After OVX, the uterus weight index and serum E2 was significantly decreased. Both the uterus weight index and the serum E2 level were significantly increased after treatment with E2. However, no significant differences were seen after treatment with the other four methods. As revealed by the western blot results, the protein expression of ERα in the OVX groups was significantly higher than that of in the Sham group. After treatment with E2, treadmill exercise, whole-body vertical vibration, and lithium chloride, the protein expression of ERα was significantly lower than that of in OVX group. However, the genistein treatment had no significant difference. Conclusions Apart from genistein treatment, the other four interventions had inhibitive effects on the protein expression of ERα in uterus of OVX osteoporosis rats.

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Journal articles on the topic 'Proteinexpression'

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