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Добірка наукової літератури з теми "Cox-2 expression"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Cox-2 expression"

Laino, Charlene. "COX-2 Inhibitorsʼ Effect Dependent on COX-2 Tumor Expression". Oncology Times 26, № 11 (червень 2004): 24. http://dx.doi.org/10.1097/01.cot.0000292129.98424.b1.

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Laino, Charlene. "COX-2 inhibitorsʼ effect dependent on COX-2 tumour expression". Oncology Times 1, № 6 (липень 2004): 13. http://dx.doi.org/10.1097/01434893-200407000-00007.

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Karim, Mohammed Mohibul, Yoshitake Hayashi, Masanori Inoue, Yukihiro Imai, Hiroshi Ito, and Misao Yamamoto. "Cox-2 expression in retinoblastoma." American Journal of Ophthalmology 129, no. 3 (March 2000): 398–401. http://dx.doi.org/10.1016/s0002-9394(99)00355-4.

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Telliez, Aurelie, Christophe Furman, Nicole Pommery, and Jean-Pierre Henichart. "Mechanisms Leading to COX-2 Expression and COX-2 Induced Tumorigenesis: Topical Therapeutic Strategies Targeting COX-2 Expression and Activity." Anti-Cancer Agents in Medicinal Chemistry 6, no. 3 (May 1, 2006): 187–208. http://dx.doi.org/10.2174/187152006776930891.

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Hazar, Burhan, Melek Ergin, Ertuğrul Seyrek, Şeyda Erdoğan, ılhan Tuncer, and Sibel Hakverdi. "Cyclooxygenase-2 (Cox-2) Expression in Lymphomas." Leukemia & Lymphoma 45, no. 7 (July 2004): 1395–99. http://dx.doi.org/10.1080/10428190310001654032.

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Mungo, David V., Xinping Zhang, Regis J. O'Keefe, Randy N. Rosier, J. Edward Puzas, and Edward M. Schwarz. "COX-1 and COX-2 expression in osteoid osteomas." Journal of Orthopaedic Research 20, no. 1 (January 2002): 159–62. http://dx.doi.org/10.1016/s0736-0266(01)00065-1.

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Menczer, Joseph, Letizia Schreiber, Oleg Sukmanov, Vladimir Kravtsov, Esther Berger, Abraham Golan, and Tally Levy. "COX-2 expression in uterine carcinosarcoma." Acta Obstetricia et Gynecologica Scandinavica 89, no. 1 (January 2010): 120–25. http://dx.doi.org/10.3109/00016340903342006.

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Gatalica, Zoran, and Brian Loggie. "COX-2 expression in pseudomyxoma peritonei." Cancer Letters 244, no. 1 (November 2006): 86–90. http://dx.doi.org/10.1016/j.canlet.2005.12.013.

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Menczer, Joseph. "Cox-2 expression in ovarian malignancies." European Journal of Obstetrics & Gynecology and Reproductive Biology 146, no. 2 (October 2009): 129–32. http://dx.doi.org/10.1016/j.ejogrb.2009.05.030.

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Kawamoto, Toru, Tohru Asano, Junichi Shoda, Mira Datta, Takeshi Todoroki, Naomi Tanaka, Takashi Fukao, and Masanao Miwa. "Immunohistochemical expression of cyclooxygenase-2 (COX-2) in gallbladder carcinoma — Association of enhanced COX-2 expression with tumor progression." Gastroenterology 118, no. 4 (April 2000): A189. http://dx.doi.org/10.1016/s0016-5085(00)82830-9.

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Дисертації з теми "Cox-2 expression"

Sun, Haipeng. "Regulation of Cyclooxygenase Gene Expression by Glucocorticoids in Cardiomyocytes." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/194896.

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Glucocorticoids (GCs) are endogenous steroid hormones that regulate a number of critical physiological processes. Psychological stress increases the level of GCs in the circulating system. The biological effect of elevated GCs on the heart is not well understood. We found that GCs induced Cyclooxygenase-1 (COX-1) and COX-2 gene expression in cardiomyocytes. COX-1 or COX-2 encodes the rate-limiting enzyme in the biosynthesis of prostanoids, which modulate crucial physiological and pathophysiological responses. The present studies aim to elucidate the signaling transduction pathway and the mechanism underlying GC induced COX expression.Our data demonstrate that GCs activate COX-1 gene expression through transcriptional regulation. COX-1 gene promoter studies support a role of Sp binding site in CT induced COX-1 gene expression. The nuclear protein binding to this site appears to be Sp3 transcription factor. Co-immunoprecipitation assays indicated a physical interaction between GR and Sp3 protein. Silencing of Sp3 transcription factor with small interfering RNA suppressed CT-induced COX-1 promoter activation. These data suggest that the activated GR interacts with Sp3 transcription factor that binds to COX-1 promoter to up-regulate COX-1 gene expression in cardiomyocytes.We also found that administration of GC in adult mice increased the level of COX-2 in the ventricles. With isolated neonatal cardiomyocytes, corticosterone (CT) induces the transcription of COX-2 gene. This response appears to be cardiomyocyte cell type specific and GC receptor (GR)-dependent. CT causes activation of p38 MAPK and subsequently CREB phosphorylation that mediates COX-2 gene expression. Mifepristone, a GR antagonist, failed to inhibit p38 and CREB activation and p38 inhibition failed to prevent activation of GR. These data suggest that two parallel signaling pathways, GR and p38 MAPK, act in concert to regulate the expression of COX-2 gene in cardiomyocytes.In addition to the investigation of mechanism and signaling transduction pathway, I have explored pharmacological agents that modulate COX expression. LY294002, a commonly used PI3K inhibitor, inhibited COX-2 gene expression via a PI3K-independent mechanism. Whereas GSK-3 inhibitors, such as lithium chloride, upregulated COX-2 gene expression, but suppressed GC-induced COX-1 expression. These data have paved the foundation for pharmacological manipulation of COX-1 and COX-2 gene expression in the heart.

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Fritzsche, Julia. "Expression von EGFR, HER-2 und COX-2 beim Zervixkarzinom: Vergleich von Primärtumoren und Rezidiven." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-119352.

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Ziel dieser Studie war es, die Häufigkeit der Expression von EGFR, HER-2 sowie COX-2 im Zervixkarzinom zu eruieren. Dabei galt es herauszufinden, ob Unterschiede hinsichtlich des Nachweises dieser drei, möglicherweise therapeutisch relevanten Moleküle zwischen den primären, nicht vortherapierten und operierten Karzinomen und den multimodal vorbehandelten Rezidiven gab. In der vorliegenden retrospektiven Arbeit wurden 45 TMMR-operierte Primärtumoren und 28 LEER-operierte Rezidivtumoren der Universitätsfrauenklinik Leipzig (Triersches Institut) einbezogen und zusätzlich hinsichtlich der prognostischen Überlebensanalyse durch das Tumorstadium, Lymphknotenmetastasen und Rezidivauftreten sowie histologischer Charakteristika untersucht. Dazu wurden Tissue - Microarrays angefertigt mit anschließender immunhistochemischer Untersuchung dieser. Die Ergebnisse zeigten, dass die TMMR-Operation die Überlebensprognose signifikant verbessert, denn lediglich bei den LEER-therapierten Rezidivtumoren erlitten die Patientinnen sowohl Fernmetastasen als auch erneute Rezidive. Weder die Expression der drei untersuchten Moleküle noch die histopathologischen Parameter haben eine prognostische Relevanz. Es gibt keine signifikanten Zusammenhänge zwischen der Häufigkeit der Expression von EGFR, HER-2 sowie COX-2 und Primär-, bzw. Rezidivtumoren, sodass diese Moleküle keine Targets für eine individualisierte, zielgerichtete Therapie beim Zervixkarzinom darstellen.

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Kim, Janet Heejung. "Cyclooxygenase-2 Expression in Post-Mastectomy Chest Wall Relapse." Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06282006-104942/.

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The purpose of this study was to assess the prognostic significance and clinical correlations of cyclooxgenase-2 expression (COX) in a cohort of patients treated with radiation (RT) for post-mastectomy chest wall relapse (PMCWR). Between 1975 and 1999, 113 patients were treated for isolated PMCWR. All patients were treated with biopsy and/or excision of the CWR followed by RT. Median follow-up was 10 years. All clinical data including demographics, pathology, staging, receptor status, HER-2/neu status, and adjuvant therapy were entered into a computerized database. Paraffin-embedded CWR specimens were retrieved from 42 patients, of which 38 were evaluated, created into a tissue microarray, stained by immunohistochemical methods for COX, and graded 0-3+. A score of 2-3+ was considered positive. Overall survival from original diagnosis for the entire cohort was 44% at 10 years. Survival rate after chest wall recurrence was 28% at 10 years. The distant metastasis-free survival rate after CWR was 40% at 10 years. Local-regional control of disease was achieved in 79% at 10 years after CWR. COX was considered positive in 13 of 38 cases. COX was inversely correlated with ER (p= .045) and PR (p = .028), and positively correlated with HER-2/neu (p =.003). COX was also associated with a shorter time to PMCWR. The distant metastasis-free rate for COX negative patients was 70% at 10 years, compared with 31% at 10 years for COX-2 positive patients (p = 0.029). COX positive had a poorer local-regional progression-free rate of 19% at 10 years, compared with 81% at 10 years for COX negative (p = 0.003). Outcome following RT for PMCWR is relatively poor. Positive COX correlated with other markers of poor outcome including a shorter time to local relapse, negative ER/PR and positive Her-2/neu status. Positive COX correlated with higher distant metastasis and lower local-regional control of disease. If confirmed with larger studies, these data have implications with respect to the concurrent use of COX-2 inhibitors and radiation for PMCWR.

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Kim, Youngsoo. "Molecular characterization of cyclooxygenase-2 (COX-2) expression in murine skin carcinoma cells /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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Rowe, Kherie Sheheda Janelle. "Cox-2 expression : interaction of Neisseria meningitidis with human cells." Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.519420.

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Abdalla, Salem Ishtiwi. "Cyclooxygenase-2 (cox-2) expression in Barrett's oesphageal epithelium : relationship to inflammation and cancer." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418127.

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Lysitsa, Stella. "Evolution du lichen plan buccal et expression de la COX-2 /." Genève : [s.n.], 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253996.

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Huppes, Rafael Ricardo [UNESP]. "Expressão gênica de MMP-2 e 9, TIMP-1 e 2, ATM, TP53, VEGF, COX-2 e CDH-1 no TVT canino." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/122030.

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A literatura cita que 1 a 5% dos casos de tumor venéreo transmissível (TVT) primário são metastáticos. Sendo assim, é importante estudar os mecanismos que colaborem para a invasão metastática assim como para sua implantação. Dentre estes mecanismos as metaloproteinases (MMP-2 e MMP-9) e seus inibidores (TIMP-1 e TIMP-2), assim como o ATM, COX-2, VEGF e CDH-1 podem explicar a implantação tumoral no sítio primário e a ocorrência da invasão metastática do TVT no cão. O objetivo do presente trabalho é avaliar a expressão gênica dos marcadores acima e correlacionar a sua expressão com o poder de implantação e invasão metastática no TVT. Para este estudo foram avaliadas 32 amostras tumorais, que foram congeladas e delas extraídos RNAm. Utilizou-se o método de qRT-PCR para todos os transcritos. Os resultados foram comparados com sangue periférico de 10 cães saudáveis (grupo controle) com o teste de Mann Whitney. A expressão gênica de MMP-2 e TIMP-1 foi significativamente maior do que o grupo controle (p < 0,001; p = 0,037; respetivamente). A expressão dos transcritos dos genes MMP-9 e TIMP-2 não apresentou diferença estatística entre o TVT e grupo controle (p = 0,535; p = 0, 906; respetivamente). A avaliação de expressão de transcritos do ATMapresentou aumento significativo (p < 0,0001) de sua expressão no tecido tumoral (TVT) quando comparado com o grupo controle, enquanto a expressão dos transcritos do gene TP53 não apresentou diferença estatística entre os grupos (p = 0,26). Na avaliação da COX-2, VEGF, CDH-1 foi verificado aumento significativo (p < 0,0001; p < 0,0001; p = 0,04, respectivamente) da expressão de transcritos dos genes no tecido tumoral (TVT) em relação ao grupo controle. A super-expressão de MMP-2 e o TIMP-1 pode explicar a capacidade de implantação das células tumorais assim como a maior expressão de VEGF e COX-2 pode explicar o crescimento rápido local do tumor e ...
The literature reports that 1-5% of cases of primary trasmissible venereal tumor (TVT) are metastatic. Thus, it is interesting to study the mechanisms that collaborate to the metastatic invasion and implantation of TVT. Among these mechanisms, the metalloproetinases (MMP-2 and MMP-9) and their inhibitors (TIMP-1 and TIMP-2), as well as ATM, COX-2, VEGF and CDH-1 may explain the tumoral implantation in the primary site and metastatic invasion of TVT in dogs. The objectives of this study are to evaluate the gene expression of these markers and to correlate their expression with the high ability of deployment and metastatic invasion of TVT. For this study, 32 tumor samples were frozen and their mRNA were extract using the qRT-PCR method for all transcripts. The results were compared with peripheral blood of 10 healthy dogs (control group) using the Mann Whitney test. The expression of MMP-2 and TIMP-1 were significantly higher than the control group (p <0.001, p = 0.037, respectively). The expression of MMP-9 and TIMP-2 showed no statistical difference between the TVT and the control group (p = 0.535, p = 0, 906, respectively). The expression of ATM was increased in tumor tissue (TVT) when compared with the control group, while the expression of TP53 had no statistical difference between groups (p = 0.26). The evaluation of COX-2, VEGF and CDH-1 were increas in tumor tissue when compared with control group. The over expression of MMP-2 and TIMP-1 may explain the implantation ability of the tumor cells, as well as the increase of VEGF and COX-2 may explain the rapid tumor growth and the rich vasculatization. While the over expression of ATM, TP53 and CDH-1 may contribute to the low metastatic capacity of the TVT tumor

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Huppes, Rafael Ricardo. "Expressão gênica de MMP-2 e 9, TIMP-1 e 2, ATM, TP53, VEGF, COX-2 e CDH-1 no TVT canino /." Jaboticabal, 2014. http://hdl.handle.net/11449/122030.

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Orientador: Renée Laufer Amorim
Coorientador: Andrigo Barboza De Nardi
Coorientador: Mirela Tinucci Costa
Banca: Rosemere de Oliveira Vasconcelos
Banca: Geórgia Mode Magalhães
Banca: Rafael Torres Neto
Banca: Bruno Watanabe Minto
Resumo: A literatura cita que 1 a 5% dos casos de tumor venéreo transmissível (TVT) primário são metastáticos. Sendo assim, é importante estudar os mecanismos que colaborem para a invasão metastática assim como para sua implantação. Dentre estes mecanismos as metaloproteinases (MMP-2 e MMP-9) e seus inibidores (TIMP-1 e TIMP-2), assim como o ATM, COX-2, VEGF e CDH-1 podem explicar a implantação tumoral no sítio primário e a ocorrência da invasão metastática do TVT no cão. O objetivo do presente trabalho é avaliar a expressão gênica dos marcadores acima e correlacionar a sua expressão com o poder de implantação e invasão metastática no TVT. Para este estudo foram avaliadas 32 amostras tumorais, que foram congeladas e delas extraídos RNAm. Utilizou-se o método de qRT-PCR para todos os transcritos. Os resultados foram comparados com sangue periférico de 10 cães saudáveis (grupo controle) com o teste de Mann Whitney. A expressão gênica de MMP-2 e TIMP-1 foi significativamente maior do que o grupo controle (p < 0,001; p = 0,037; respetivamente). A expressão dos transcritos dos genes MMP-9 e TIMP-2 não apresentou diferença estatística entre o TVT e grupo controle (p = 0,535; p = 0, 906; respetivamente). A avaliação de expressão de transcritos do ATMapresentou aumento significativo (p < 0,0001) de sua expressão no tecido tumoral (TVT) quando comparado com o grupo controle, enquanto a expressão dos transcritos do gene TP53 não apresentou diferença estatística entre os grupos (p = 0,26). Na avaliação da COX-2, VEGF, CDH-1 foi verificado aumento significativo (p < 0,0001; p < 0,0001; p = 0,04, respectivamente) da expressão de transcritos dos genes no tecido tumoral (TVT) em relação ao grupo controle. A super-expressão de MMP-2 e o TIMP-1 pode explicar a capacidade de implantação das células tumorais assim como a maior expressão de VEGF e COX-2 pode explicar o crescimento rápido local do tumor e ...
Abstract: The literature reports that 1-5% of cases of primary trasmissible venereal tumor (TVT) are metastatic. Thus, it is interesting to study the mechanisms that collaborate to the metastatic invasion and implantation of TVT. Among these mechanisms, the metalloproetinases (MMP-2 and MMP-9) and their inhibitors (TIMP-1 and TIMP-2), as well as ATM, COX-2, VEGF and CDH-1 may explain the tumoral implantation in the primary site and metastatic invasion of TVT in dogs. The objectives of this study are to evaluate the gene expression of these markers and to correlate their expression with the high ability of deployment and metastatic invasion of TVT. For this study, 32 tumor samples were frozen and their mRNA were extract using the qRT-PCR method for all transcripts. The results were compared with peripheral blood of 10 healthy dogs (control group) using the Mann Whitney test. The expression of MMP-2 and TIMP-1 were significantly higher than the control group (p <0.001, p = 0.037, respectively). The expression of MMP-9 and TIMP-2 showed no statistical difference between the TVT and the control group (p = 0.535, p = 0, 906, respectively). The expression of ATM was increased in tumor tissue (TVT) when compared with the control group, while the expression of TP53 had no statistical difference between groups (p = 0.26). The evaluation of COX-2, VEGF and CDH-1 were increas in tumor tissue when compared with control group. The over expression of MMP-2 and TIMP-1 may explain the implantation ability of the tumor cells, as well as the increase of VEGF and COX-2 may explain the rapid tumor growth and the rich vasculatization. While the over expression of ATM, TP53 and CDH-1 may contribute to the low metastatic capacity of the TVT tumor
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Laube, Markus. "Synthese von Cyclooxygenase-2-Inhibitoren als Grundlage für die funktionelle Charakterisierung der COX-2-Expression mittels PET." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-160091.

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Eine erhöhte COX-2-Expression wird bei Krankheiten wie rheumatoider Arthritis aber auch Parkinson, Alzheimer und Krebs beobachtet. Die nichtinvasive Visualisierung und Quantifizierung der COX 2-Expression in vivo mittels Positronen-Emissions-Tomographie (PET) könnte wertvolle Beiträge zur Diagnose dieser Krankheiten liefern. Zur Nutzung der PET-Technik werden geeignete COX-2-adressierende Radiotracer benötigt, deren Entwicklung auch die Identifizierung neuer, der Radiomarkierung zugänglicher COX-2-Inhibitoren als Leitstrukturen voraussetzt. Ziel dieser Arbeit war die Synthese von selektiven, der Radiomarkierung zugänglichen COX 2-Inhibitoren und deren In-vitro-Evaluierung, um Verbindungen zu identifizieren, die für eine weitere Entwicklung zu COX-2-adressierenden Radiotracern geeignet sind. Im Rahmen dieser Arbeit wurden ausgehend von literaturbekannten COX-2-Inhibitoren zwei grundlegende Strategien verfolgt: die Derivatisierung an der Peripherie sowie der Austausch von Strukturelementen im Grundgerüst der COX-2-selektiven Inhibitoren. In dieser Arbeit wird zum einen die Synthese der Zielverbindungen (Diphenyl-substituierte Indol-, Pyrazolo[1,5-b]pyridazin-, 1,2-Dihydropyrrolo[3,2,1-hi]indol- und Pyrrolo[3,2,1-hi]indol-Derivate sowie 2-Carbaboranyl-substituierte Indol-Derivate) und deren strukturanalytische Charakterisierung vorgestellt. Es konnte die McMurry-Cyclisierung als neuer Zugang für die Synthese von Carbaboranyl-substituierten Verbindungen und 1,2-Dihydropyrrolo[3,2,1-hi]indol-Derivaten sowie die Dehydrogenierung mittels DDQ als neue Variante zur Synthese von Pyrrolo[3,2,1-hi]indol-Derivaten etabliert werden. Durch Röntgeneinkristallstrukturanalyse wurde die Molekülstruktur von sechs Zwischenverbindungen und neun Zielverbindungen aufgeklärt. Zum anderen erfolgte die Charakterisierung der Verbindungen in vitro, wobei die COX-inhibitorischen Eigenschaften mit einem Fluoreszenz-basierten, einem Enzymimmunoassay (EIA)-basierten und einem [14C]Arachidonsäure-basierten COX-Assay bestimmt und zudem viele Verbindungen hinsichtlich ihrer Redoxeigenschaften untersucht wurden. Im Besonderen die hergestellten Indol-Derivate besitzen antioxidative Eigenschaften, die bei der Untersuchung der COX inhibitorischen Eigenschaften beachtet werden müssen. Die Derivatisierung an der Peripherie der bekannten Inhibitoren führte zur Identifizierung von zwei Aminosulfonyl-substituierten Indol-Derivaten und einem Fluorethoxy-substituierten Pyrazolo[1,5 b]pyridazin-Derivat, die grundsätzlich geeignete Kandidaten für eine weitere Entwicklung zum Radiotracer darstellen. Das Fluorethoxy-substituierte Pyrazolo[1,5 b]pyridazin-Derivat wurde im Rahmen dieser Arbeit mit Fluor-18 markiert und die initiale Charakterisierung des Radiotracers in vitro durchgeführt. Der Austausch von Strukturelementen im Grundgerüst der literaturbekannten COX-2-Inhibitoren mit voluminöseren Gruppen führte zum einen bei Austausch eines Phenylrings gegen einen Carbaboranyl-Cluster zum Verlust der COX-inhibitorischen Eigenschaften, was eine weitere Entwicklung dieser Verbindungen zum Radiotracer ausschließt. Zum anderen wurde ausgehend von 2,3-Diphenyl-1H-indol-Derivaten die bicyclische auf eine tricyclische Kernstruktur vergrößert. Dies lieferte hoch affine und selektive COX-2-Inhibitoren. Unter den hergestellten Verbindungen wurden ein 1,2-Dihydropyrrolo[3,2,1-hi]indol- und drei Pyrrolo[3,2,1-hi]indol-Derivate als vielversprechende Kandidaten für die weitere Entwicklung zum Radiotracer identifiziert.

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Книги з теми "Cox-2 expression"

United States. Congress. House. Committee on International Relations, ed. 106-2 MARKUP: Markup Of H. CON. RES. 232, Expressing The Sense Of Congress Concerning The Safety And Well-Being Of United States Citizens Injured While Travelling In Mexico, June 14, 2000. [S.l: s.n., 2000.

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United States. Congress. House. Committee on International Relations., ed. 106-2 MARKUP: Markup Of H. CON. RES. 232, Expressing The Sense Of Congress Concerning The Safety And Well-Being Of United States Citizens Injured While Travelling In Mexico, June 14, 2000. [S.l: s.n., 2000.

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United States. Congress. House. Committee on International Relations. Subcommittee on the Middle East and Central Asia. Expressing the grave concern of Congress regarding the continuing gross violations of human rights and civil liberties of the Syrian and Lebanese people by the government of the Syrian Arab republic; and expressing the grave concern of Congress regarding the occupation of the Republic of Lebanon by the Syrian Arab Republic: Markup before the Subcommittee on the Middle East and Central Asia of the Committee on International Relations, House of Representatives, One Hundred Ninth Congress, first session, on H. Con. Res. 18 and H. Con. Res. 32, March 2, 2005. Washington: U.S. G.P.O., 2005.

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Rights, United States Congress House Committee on International Relations Subcommittee on International Operations and Human. H. Con. Res. 28, expressing the sense of Congress that the United States should introduce and make all efforts necessary to pass a resolution criticizing the People's Republic of China for its human rights abuses in China and Tibet at the annual meeting of the United Nations Commission on Human Rights: Markup before the Subcommittee on International Operations and Human Rights of the Committee on International Relations, House of Representatives, One Hundred Sixth Congress, first session, March 2, 1999. Washington: U.S. G.P.O., 1999.

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United States. Congress. House. Committee on International Relations. Subcommittee on International Operations and Human Rights. H. Con. Res. 28, expressing the sense of Congress that the United States should introduce and make all efforts necessary to pass a resolution criticizing the People's Republic of China for its human rights abuses in China and Tibet at the annual meeting of the United Nations Commission on Human Rights: Markup before the Subcommittee on International Operations and Human Rights of the Committee on International Relations, House of Representatives, One Hundred Sixth Congress, first session, March 2, 1999. Washington: U.S. G.P.O., 1999.

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Частини книг з теми "Cox-2 expression"

Dixon, D. A. "Regulation of COX-2 Expression in Human Cancers." In COX-2, 52–71. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071363.

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Bennett, P., and D. Slater. "COX-2 expression in labour." In Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors, 167–88. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-010-9029-2_10.

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Patrono, C., P. Patrignani, M. R. Panara, F. Cipollone, G. Santini, M. G. Sciulli, M. T. Rotondo, R. Padovano, and M. Di Giamberardino. "COX-2 expression and inhibition in human monocytes." In Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors, 121–31. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-010-9029-2_7.

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Dixon, Dan A., Fernando F. Blanco, Annalisa Bruno, and Paola Patrignani. "Mechanistic Aspects of COX-2 Expression in Colorectal Neoplasia." In Recent Results in Cancer Research, 7–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30331-9_2.

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Hinz, Burkhard, Robert Ramer, and Kay Brune. "Induction of COX-2 Expression by the Endocannabinoid Derivative R(+)-Methanandamide." In Advances in Experimental Medicine and Biology, 145–52. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9194-2_30.

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Crofford, L. J. "Expression and regulation of COX-2 in synovial tissues of arthritic patients." In Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors, 133–43. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-010-9029-2_8.

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Herschman, Harvey R., David J. Wadleigh, and Srinivasa T. Reddy. "Regulation of COX-2 Expression in Fibroblasts, Osteoblasts, Mast Cells, and Macrophages." In Advances in Prostaglandin and Leukotriene Research, 41–47. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9721-0_8.

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Berg, Jörg, Thomas Christoph, Angelika Bodenteich, and Robertson Towart. "Heterogeneous Distribution of COX-2 Over-Expression in Human Colon Carcinoma Cells." In Advances in Experimental Medicine and Biology, 327–30. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1810-9_70.

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Luna, Marian, Angela Ferrario, Sam Wong, and Charles J. Gomer. "Identification of MAP Kinase Pathways Involved in COX-2 Expression Following Photofrin Photodynamic Therapy." In Methods in Molecular Biology, 47–63. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-697-9_4.

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Bazan, N. G., V. M. Marcheselli, G. Allan, K. Van Meter, and J. P. Moises. "Brain COX-2 in experimental models of epilepsy and stroke: signalling pathways leading to enhanced expression." In New Targets in Inflammation, 47–53. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-5386-7_5.

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Тези доповідей конференцій з теми "Cox-2 expression"

Shao, W., C. Kuhn, D. Mayr, N. Ditsch, S. Mahner, N. Harbeck, V. Cavaillès, U. Jeschke та S. Sixou. "Untersuchungen zur differenzierten Expression von PPARγ, Cox-1 und Cox-2 beim Mammakarzinom". У Abstracts zum Kongress 2019 der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde (BGGF) und der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1693862.

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Russell-Puleri, Sparkle, Eno E. Ebong, and John M. Tarbell. "Mechanisms of flow-dependent endothelial COX-2 and PGI2 expression." In 2014 40th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2014. http://dx.doi.org/10.1109/nebec.2014.6972924.

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Pirker, T., E. Pferschy-Wenzig, and R. Bauer. "Inhibition of COX-2 mRNA expression by damask rose flowers." In GA – 69th Annual Meeting 2021, Virtual conference. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1736970.

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Lin, Shih-Chieh, and Shaw-Jenq Tsai. "Abstract 3083: Dual-specificity phosphatase-2 (DUSP2) negatively control cyclooxygenase-2 (COX-2) expression in cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3083.

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Bu, Rong, Sandeep K. Parvathareddy, Abdul K. Siraj, Padmanaban Annaiyappanaidu, Kaleem Iqbal, Maha Al Rasheed, Wael Haqawi, and Khawla S. Al-Kuraya. "Abstract 729: Prognostic significance of COX-2 over-expression inBRAFmutated Middle Eastern PTC." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-729.

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Yang, Wan-Yu, Chih-Hsin Tang, and Jing-Yuan Chuang. "Abstract 1392: CTGF inhibits cell motility in oral cancer cells through reducing COX-2 expression." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1392.

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Shim, Minsub, Julie Foley, Colleen Anna, Yuji Mishina, and Thomas E. Eling. "Abstract LB-338: Increased apoptosis and p53 expression in sclerotome of COX-2 transgenic embryo." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-338.

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Zago, Michela, Angela Rico de Souza, Simon Rousseau, David H. Eidelman, Qutayba Hamid, and Carolyn J. Baglole. "The Aryl Hydrocarbon Receptor (AhR) Exerts Post-Transcriptional Control Over Cigarette Smoke-Induced Cyclooxygenase-2 (Cox-2) Protein Expression." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2009.

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Killian, Megan L., Barbara Zielinska, and Tammy L. Haut Donahue. "Role of IL-1 on Aggrecanase and COX-2 Gene Expression of Meniscal Explants Following Dynamic Compression." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19110.

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The menisci within the knee likely respond to adverse loading conditions, leading to aggravated cartilage damage and fissuring [1]. Upregulation of catabolic molecules such as interleukin-1α (IL-1α), metalloproteinases (MMPs), aggrecanases (ADAMTS-4 and -5), and cyclooxygenase-2 (COX-2), as well as release of proteoglycans [2], have been shown in vitro for meniscal explants following dynamic loading [3]. A crucial event in matrix degradation is the loss of aggrecan, caused by the ADAMTS family [4]. In osteoarthritic cartilage, IL-1 has been shown to influence COX-2 activity, leading to increased synthesis of prostaglandin E2 and subsequent proteinase activity [5].

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SHIN, JONG WOOK, In Won Park, Jae Chul Choi, Byoung Whui Choi, and Jae Yeol Kim. "Expression Of C-ErbB-2 And COX-2 In Adenocarcinoma And Squamous Cell Carcinoma In The Surgically Removed Lung Cancers." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3500.

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Звіти організацій з теми "Cox-2 expression"

Shapiro, Charles L., William Burak, and Robert Brueggemeier. The Effect of COX-2 Inhibitors on the Aromatase Gene Expression in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada418325.

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Shapiro, Charles L. The Effect of COX-2 Inhibitors on the Aromatase Gene (CYP19) Expression in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada468021.

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Fields, Michael J., Mordechai Shemesh, and Anna-Riitta Fuchs. Significance of Oxytocin and Oxytocin Receptors in Bovine Pregnancy. United States Department of Agriculture, August 1994. http://dx.doi.org/10.32747/1994.7568790.bard.

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Oxytocin has multiple actions in bovine reproductive tract and it was our purpose to determine the nature of these actions and their significance for the physiology of bovine reproduction. The bovine oxytocin receptors (OTR) gene was cloned and its expression studied during the cycle and pregnancy. OTR mRNA changed in parallel with OTR with control occurring mainly at the transcriptional level. However, the endocrine regulation of OTR were found in endometrium and cervical mucosa at estrus and at parturition. In both tissues OTR were suppressed in the luteal phase and early pregnancy. Whereas cervical OTR remained suppressed throughout pregnancy, endometrial OTR began to increase soon after implantation and reached higher concentrations in midpregnancy than at estrus. OTR in caruncles did not increase until third trimester, and OTR in cervical mucosa, cotyledons and fetal membranes increased only at term. Myometrial OTR showed less variation and OTR were present throughout the cycle and pregnancy but increased significantly during mid- and late pregnancy. OTR were localized in endometrial epithelial cells and lumina epithelial cells of cervical mucosa as determined by immunohistochemistry. Endometrial OTR were functional throughout pregnancy and mediated PGF release from day 50 onwards in a receptor density related manner. OTR in cervical mucosa mediated PGE release both in vivo and in vitro, as shown in cyclic cows. The ontogeny of uterine OTR was studied from third trimester fetal stage until puberty. OTR were present in endometrium and cervical mucosa in high concentrations throughout this period; myometrial OTR began to increase somewhat later but also reached adult values by 6-mo of age. In the prepuberal heifers OT injections failed to initiate PGF2a, release. The influence of steroids on the effect of OT was examined. Ovariectomy and E2 were without effect, but P4 with or without E2 induced a massive PGF2a release in response to OT in spite of reduced OTR. Bovine cyclooxygenases (COX-1 and COX-2) were cloned and their expression studied in the endometrium of prepuberal heifers and pregnant cows. Untreated and E2 treated prepuberal heifers did not express COX-2 but P4 treated heifers did express the mRNA for COX-2, albeit weakly. During the second half of pregnancy COX-2 mRNA was strongly expressed in cotyledons and somewhat less in caruncles, whereas endometrium, myometrium and cervical mucosa showed only weak, if any, COX-2 mRNA under basal conditions. However, 2 h after OT injection significant increases in COX-2 mRNA were found in endometrial RNA. Thus OT is capable of inducing the expression of the inducible COX-2 gene, and hence the conversion of arachidonic acid to prostanoids. The results indicate that the functions of OT are numerous and probably essential for successful pregnancy and parturition.

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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.

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Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.

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Dudareva, Natalia, Alexander Vainstein, Eran Pichersky, and David Weiss. Integrating biochemical and genomic approaches to elucidate C6-C2 volatile production: improvement of floral scent and fruit aroma. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7696514.bard.

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The specific objectives of approved proposal include to: 1. Elucidate the C6-C2 biochemical pathways leading to the biosynthesis of phenylacetaldehyde, phenylethyl alcohol and phenylethyl acetate in floral tissues of ornamentally important plants, pefunia and roses. 2. Isolate and characterrze genes responsible for the production of these C6-C2 compounds and those involved in the regulation of the pathway using genomic and transcriptomic tools. 3. Determine whether altering the expression of key genes of this pathway can result in changing the aroma characteristics of flowers. Aldehydes are intermediates in a variety of biochemical pathways including those involved in the metabolism of carbohydrates, vitamins, steroids, amino acids, benzylisoquinoline alkaloids, hormones, and lipids. In plants they are also synthesized in response to environmental stresses such as salinity, cold, and heat shock or as flavors and aromas in fruits and flowers. Phenylacetaldehyde along with 2-phenylethanol and its acetate ester, are important scent compounds in numerous flowers, including petunias and roses. However, little is known about the biosynthesis of these volatile compounds in plants. We have shown that the formation PHA and 2-phenylethanol from Phe does not occur via trans-cinnamic acid and instead competes with the key enzyme of phenypropanoid metabolism Pheammonia-lyase (PAL) for Phe utilization. Using functional genomic approach and comparative gene expression profiling, we have isolated and characterized a novel enzyme from petunia and rose flowers that catalyzes the formation of the Ca-Czcompound phenylacetaldehyde (PHA) from L-phenylalanine (Phe) by the removal of both the carboxyl and amino groups. This enzyme, designated as phenylacetaldehyde synthases (PAAS), is a bifunctional enzyme that catalyzes the unprecedented efficient coupling of phenylalanine decarboxylation to oxidation, generating phenylacetaldehyde, CO2, ammonia, and hydrogen peroxide in stoichiometric amounts. Down-regulation of PAAS expression via RNA interference-based (RNAi) technology in petunia resulted in no PHA emission when compared with controls. These plants also produced no 2-phenylethanol, supporting our conclusion that PHA is a precursor of 2-phenylethanol. To understand the regulation of scent formation in plants we have also generated transgenic petunia and tobacco plants expressing the rose alcohol acetyltransferase (RhAAT) gene under the control of a CaMV-35S promoter. Although the preferred substrate of RhAAT in vitro is geraniol, in transgenic petunia flowers, it used phenylethyl alcohol and benzyl alcohol to produce the corresponding acetate esters, not generated by control flowers. These results strongly point to the dependence of volatile production on substrate availability. Analysis of the diurnal regulation of scent production in rose flowers revealed that although the daily emission of most scent compounds is synchronized, various independently evolved mechanisms control the production, accumulation and release of different volatiles. This research resulted in a fundamental discovery of biochemical pathway, enzymes and genes involved in biosynthesis of C6-C2s compounds, and provided the knowledge for future engineering plants for improved scent quality.

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Grumet, Rebecca, Rafael Perl-Treves, and Jack Staub. Ethylene Mediated Regulation of Cucumis Reproduction - from Sex Expression to Fruit Set. United States Department of Agriculture, February 2010. http://dx.doi.org/10.32747/2010.7696533.bard.

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Reproductive development is a critical determinant of agricultural yield. For species with unisexual flowers, floral secualdifferentation adds additional complexity, that can influenec productivity. The hormone ethylene has long, been known to play a primary role in sex determination in the Cucumis species cucumber (C. sativus) and melon (C. melo). Our objectives were to: (1) Determine critical sites of ethylene production and perception for sex determination; (2) Identify additional ethylene related genes associated with sex expression; and (3) Examine the role of environment ami prior fruit set on sex expression, pistillate flower maturation, and fruit set. We made progress in each of these areas. (1) Transgenic melon produced with the Arabidopsis dominant negative ethylene perception mutant gene, etrl-1, under the control of floral primordia targeted promoters [AP3 (petal and stamen) and CRC (carpel and nectary)], showed that ethylene perception by the stamen primordia, rather than carpel primordia, is critical for carpel development at the time of sex determination. Transgenic melons also were produced with the ethylene production enzyme gene. ACS, encoding l-aminocyclopropane-lcarboylate synthase, fused to the AP3 or CRC promoters. Consistent with the etr1-1 results, CRC::ACS did not increase femaleness; however, AP3::ACS reduced or eliminated male flower production. The effects of AP3:ACS were stronger than those of 35S::ACS plants, demonstratin g the importance of targeted expression, while avoiding disadvantages of constitutive ethylene production. (2) Linkage analysis coupled with SNP discovery was per formed on ethylene and floral development genes in cucumber populations segregating for the three major sex genes. A break-through towards cloning the cucumber M gene occurred when the melon andromonoecious gene (a), an ACS gene, was cloned in 2008. Both cucumber M and melon a suppress stamen development in pistillate flowers. We hypothesized that cucumber M could be orthologous to melon a, and found that mutations in CsACS2 co-segregated perfectly with the M gene. We also sought to identify miRNA molecules associated with sex determination. miRNA159, whose target in Arabidopsis is GAMYB[a transcription factor gene mediating response to10 gibberellin (GA)], was more highly expressed in young female buds than male. Since GA promotes maleness in cucumber, a micro RNA that counteracts GAMYB could promote femaleness. miRNA157, which in other plants targets transcription factors involved in flower development , was expressed in young male buds and mature flower anthers. (3) Gene expression profiling showed that ethylene-, senescence-, stress- and ubiquitin-related genes were up-regulated in senescing and inhibited fruits, while those undergoing successful fruit set up-regulated photosynthesis, respiration and metabolic genes. Melon plants can change sex expression in response to environmental conditions, leading to changes in yield potential. Unique melon lines with varying sex expression were developed and evaluated in the field in Hancock, Wisconsin . Environmental changes during the growing season influenced sex expression in highly inbred melon lines. Collectively these results are of significance for understanding regulation of sex expression. The fact that both cucumber sex loci identified so far (F and M) encode isoforms of the same ethylene synthesis enzyme, underscores the importance of ethylene as the main sex determining hormone in cucumber. The targeting studies give insight into developmental switch points and suggest a means to develop lines with earlier carpel-bearing flower production and fruit set. These results are of significance for understanding regulation of sex expression to facilitate shorter growing seasons and earlier time to market. Field results provide information for development of management strategies for commercial production of melon cultivars with different sex expression characteristics during fruit production.

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Rodriguez, Russell J., and Stanley Freeman. Gene Expression Patterns in Plants Colonized with Pathogenic and Non-pathogenic Gene Disruption Mutants of Colletotrichum. United States Department of Agriculture, February 2009. http://dx.doi.org/10.32747/2009.7592112.bard.

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Fungal plant pathogens are responsible for extensive annual crop and revenue losses throughout the world. To better understand why fungi cause diseases, we performed gene-disruption mutagenesis on several pathogenic Colletotrichum species and demonstrated that pathogenic isolates can be converted to symbionts expressing non-pathogenic lifestyles. One group of nonpathogenic mutants confer disease protection against pathogenic species of Col!etotrichum, Fusarium and Phytophthora; drought tolerance; and growth enhancement to host plants. These mutants have been defined as mutualists and disease resistance correlates to a decrease in the time required for hosts to activate defense systems when exposed to virulent fungi. A second group of non-pathogenic mutants did not confer disease resistance and were classified as commensals. In addition, we have demonstrated that wildtype pathogenic Colletotrichum species can express non-pathogenic lifestyles, including mutualism, on plants they colonize asymptomatically. We have been using wildtype and isogenic gene disruption mutants to characterize gene expression patterns in plants colonized with a pathogen, mutualist or commensal. The US group is contrasting genes expressed during colonization by mutuahstic and commensal mutants of C. magna and a pathogenic wildtype C. coccodes on tomato. The Israeli group is characterizing genes expressed during asymptomatic colonization of tomato by wildtype C. acutatum and a non-pathogenic mutant.To accomplish this we have been utilizing suppressive subtraction hybridization, microarray and sequencing strategies. The expected contribution of this research to agriculture in the US and Israel is: 1) understanding how pathogens colonize certain hosts asymptomatic ally will shed light on the ecology of plant pathogens which has been described as a fundamental deficiency in plant pathology; 2) identifying genes involved in symbiotically conferred disease resistance will help explain why and how pathogens cause disease, and may identify new candidate targets for developing genetically modified disease resistant crop plants.

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Xu, Jin-Rong, and Amir Sharon. Comparative studies of fungal pathogeneses in two hemibiotrophs: Magnaporthe grisea and Colletotrichum gloeosporioides. United States Department of Agriculture, May 2008. http://dx.doi.org/10.32747/2008.7695585.bard.

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Plant pathogenic fungi have various life styles and different plant infection strategies. Hemibiotrophs like Magnaporthe grisea and Colletotrichum species develop specialized structures during plant infection. The goal of this study was to identify, characterize, and compare genes required for plant infection in M. grisea and C. gloeosporioides. Specific objectives are to: 1) further characterize genes identified in the preliminary studies of C. gloeosporioides and M. grisea;2) identify and characterize additional fungal genes tagged by GFP; and 3) identify in planta growth and appressorium-specific genes by subtractive hybridization and transcript profiling by the LongSAGE method. In this study, the PI and Co-PI collaborated closely on studies in M. grisea and C. gloeosporioides. In M. grisea, REMI and ATMT were used to transform the wildtype with promoter-less EGFP constructs. A total of 28 mutants defective in different plant infection processes or expressing EGFP during plant infection were identified. Genes disrupted in five selected mutants have been identified, including MG03295 that encodes a putative Rho GTPase. In transformant L1320, the transforming vector was inserted in the MIRI gene that encodes a nuclear protein. The expression of MIRI was highly induced during infection. Deletion and site-directed mutagenesis analyses were used to identify the promoter regions and elements that were essential for induced in planta expression of MIRI. This was the first detailed characterization of the promoter of an in planta gene in M. grisea and the MIRI promoter can be used to monitor infectious growth. In addition, the Agilent whole-genome array of M. grisea was used for microarray analyses with RNA samples from appressoria formed by the wild-type shain and the pmkl and mstl2 mutants. Over 200 genes were downregulated in the mst I 2 and pmkl mutants. Some of them are putative transcription factors that may regulate appressorium formation and infectious hyphal growth. In C. gloeosporioides, various REMI mutants showing different pathogenic behavior were identified and characterized. Mutants N3736 had a single insertion and was hyper-virulent. The gene disrupted in mutant3736 (named CgFMOI) encodes a FAD-dependent monooxygenase. Expression analyses linked the expression of the CgFMOI gene with the necrotrophic phase of fungal infection, and also suggest that expression of CgFMOl is unnecessary for the first stages of infection and for biotrophy establishment. All CgFMOl-silenced mutants had reduced virulence. In REMI mutant N159, the tagged gene encodes a putative copper transporter that is homologue of S. cerevisiae CTR2. In yeast, Ctr2 is a vacuolar transporter for moving copper from the vacuole to the cytoplasm. The gene was therefore termed CgCTR2. In addition to characterization of CgCTR2, we also conducted comparative analyses in M. grisea. The M. grisea CgCTR-2 homolog was isolated, knockout strains were generated and characterized and the M. grisea was used to complement the Nl 59 C. gloeosporioides mutant. Overall, we have accomplished most of proposed experiments and are in the process of organizing and publishing other data generated in this project. For objective 3, we used the microarray analysis approach. Several genes identified in this study are novel fungal virulence factors. They have the potential to be used as targets for developing more specific or effective fungicides. In the long run, comparative studies of fungal genes, such as our CgCTR2 work, may lead to better disease control strategies.

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Izhar, Shamay, Maureen Hanson, and Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, February 1996. http://dx.doi.org/10.32747/1996.7604933.bard.

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The main goal of the proposed research was to continue the mutual investigations into the molecular basis of CMS and male fertility restoration [MRF], with the ultimate goal of understanding these phenomena in higher plants. The experiments focused on: (1) dissecting apart the complex CMS - specific mitochondrial S-Pcf locus, in order to distinguish its essential parts which cause sterility from other parts and study its molecular evolution. (2) Studying the expression of the various regions of the S-Pcf locus in fertile and sterile lines and comparing the structure and ultrastructure of sterile and fertile tissues. (3) Determine whether alteration in respiration is genetically associated with CMS. Our mutual investigations further substantiated the association between the S-Pcf locus and CMS by the findings that the fertile phenotype of a population of unstable petunia somatic hybrids which contain the S-Pcf locus, is due to the presence of multiple muclear fertility restoration genes in this group of progenies. The information obtained by our studies indicate that homologous recombination played a major role in the molecular evolution of the S-Pcf locus and the CMS trait and in the generation of mitochondrial mutations in general. Our data suggest that the CMS cytoplasm evolved by introduction of a urs-s containing sublimon into the main mitochondrial genome via homologous recombination. We have also found that the first mutation detected so far in S-Pcf is a consequence of a homologous recombination mechanism involving part of the cox2 coding sequence. In all the cases studied by us, at the molecular level, we found that fusion of two different cells caused mitochondrial DNA recombination followed by sorting out of a specific mtDNA population or sequences. This sequence of events suggested as a mechanism for the generation of novel mitochondrial genomes and the creation of new traits. The present research also provides data concerning the expression of the recombined and complex CMS-specific S-Pcf locus as compared with the expression of additional mitochondrial proteins as well as comparative histological and ultrastructural studies of CMS and fertile Petunia. Evidence is provided for differential localization of mitochondrially encoded proteins in situ at the tissue level. The similar localization patterns of Pcf and atpA may indicate that Pcf product could interfere with the functioning of the mitochondrial ATPase in a tissue undergoing meiosis and microsporogenesis. Studies of respiration in CMS and fertile Petunia lines indicate that they differe in the partitioning of electron transport through the cytochrome oxidase and alternative oxidase pathways. The data indicate that the electron flux through the two oxidase pathways differs between mitochondria from fertile and sterile Petunia lines at certain redox states of the ubiquinone pool. In summary, extensive data concerning the CMS-specific S-Pcf locus of Petunia at the DNA and protein levels as well as information concerning different biochemical activity in CMS as compared to male fertile lines have been accumulated during the three years of this project. In addition, the involvement of the homologous recombination mechanism in the evolution of mt encoded traits is emphasized.

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