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Dissertations / Theses on the topic 'MiR-17(similar to)92'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Chen, Tianji, Qiyuan Zhou, Haiyang Tang, et al. "miR‐17/20 Controls Prolyl Hydroxylase 2 (PHD2)/Hypoxia‐Inducible Factor 1 (HIF1) to Regulate Pulmonary Artery Smooth Muscle Cell Proliferation." WILEY-BLACKWELL, 2016. http://hdl.handle.net/10150/622697.

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Background-Previously we found that smooth muscle cell (SMC)-specific knockout of miR-17 similar to 92 attenuates hypoxia-induced pulmonary hypertension. However, the mechanism underlying miR-17 similar to 92-mediated pulmonary artery SMC (PASMC) proliferation remains unclear. We sought to investigate whether miR-17 similar to 92 regulates hypoxia-inducible factor (HIF) activity and PASMC proliferation via prolyl hydroxylases (PHDs). Methods and Results-We show that hypoxic sm-17 similar to 92(-/-) mice have decreased hematocrit, red blood cell counts, and hemoglobin contents. The sm-17 simila

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2

Fuziwara, Cesar Seigi. "Influência do MicroRNA let-7 e miR-17-92 como oncomiRs no câncer." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-27092010-152352/.

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No câncer, alterações em microRNAs (miRNAs), pequenos RNAs que regulam a tradução protéica, exerce efeito oncogênico (oncomiR). Os oncomiRs regulam genes chave para a proliferação celular e apoptose, sendo importantes para a biologia do câncer. O carcinoma papilífero de tiróide apresenta alterações genéticas alinhadas na via MAPK (RET>RAS>BRAF>ERK). Observamos que a indução do oncogene RET/PTC diminui a expressão de let-7 em células foliculares tiroidianas. Na linhagem TPC-1 (com RET/PTC-1), a introdução de let-7 diminui a proliferação celular e a fosforilaçãode ERK, indicando papel de gene su

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3

Prakash, Meeta B. "Deletion of Cardiac miR-17-92 Cluster Increases Ischemia/ Reperfusion Injury via PTEN Upregulation." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4956.

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The miR-17- 92 cluster is necessary for cell proliferation and development of the cardiovascular system. Deletion of this cluster leads to death in neonatal mice. The role of this cluster still needs to be defined following ischemia and reperfusion. Methods and Results: Adult male mice were injected with Tamoxifen- was to induce inducible cardiac-specific miR-17- 92-deficient (miR-17- 92-def: MCM:TG:miR-17- 92 flox/flox ) and wild type (WT: MCM:NTG:miR-17-92 flox/flox ) mice were subjected to 30 minutes of myocardial ischemia via left anterior descending coronary artery ligation followed by re

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4

Kayali, Samer. "Spi-1,Fli-1et miR-17-92 contribuent au même réseau oncogénique impliqué dans le contrôle de la prolifération dans l’érythroleucémie de Friend." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10100.

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Plus de 90% des érythroleucémies induites par le virus de Friend sont associées à l'activation récurrente de l’un ou l’autre des facteurs de transcription ETS Spi-1 ou Fli-1, ou du cluster miR-17-92. La contribution de ces trois oncogènes à la prolifération des clones érythroleucémiques correspondant a déjà été indépendamment démontrée. De plus, il a été montré dans l’équipe que Spi-1 active de façon directe l’expression de Fli-1 et que les deux facteurs activent des gènes cibles communs. Dans cette thèse, j’ai montré que Spi-1 et Fli-1 activent l’expression du cluster miR-17-92 en se liant su

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5

Stunden, Hilary James [Verfasser]. "The role of the miR-17-92 cluster in macrophage driven innate immunity / Hilary James Stunden." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1173789715/34.

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6

Stunden, H. James [Verfasser]. "The role of the miR-17-92 cluster in macrophage driven innate immunity / Hilary James Stunden." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1173789715/34.

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7

Dakhlallah, Duaa. "Cross-Talk Between Epigenetic Regulation And Mir-17~92 Cluster Expression In Idiopathic Pulmonary Fibrosis (IPF)." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1297960869.

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8

Fuziwara, Cesar Seigi. "O cluster de microRNAs miR-17-92 e seus alvos na oncogênese tiroidiana: influência de BRAFT1799A e de iodo." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-19112014-162309/.

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O excesso de iodo inibe a proliferação celular e secreção hormonal, enquanto retarda os efeitos oncogênicos da ativação de RET/PTC3 na célula folicular tiroidiana. A mutação BRAF (T1799A) é a mais prevalente no câncer de tiroide, e modelo transgênico desenvolve câncer que progride para histotipo agressivo. Altos níveis de microRNAs (miRNAs) do cluster miR-17-92 estão associados a histotipos agressivos de câncer de tiroide e modulam a tradução de mRNAs alvo componentes de vias de sinalização oncogênicas. Neste estudo, avaliamos a influência da alta dose de iodo sobre miRNAs frente ativação do o

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9

Paiva, Marcelo Machado. "Identificação de proteínas reguladoras do splicing associadas à microRNAs." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-10112016-101050/.

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Splicing é o processo de remoção de introns e ligação de exons em eucariotos. É realizado pelo spliceossomo, um complexo macromolecular composto por RNAs e mais de cem proteínas. Alguns introns possuem microRNAs, os quais devem ser processados para gerar moléculas maduras. O cluster intrônico miR-17-92 é composto por sete miRNAs que têm sido associados ao desenvolvimento de diferentes tumores em vários tecidos. Neste trabalho o splicing de dois miRNAs deste cluster foi analisado em células HeLa, BCPAP e TPC-I. Os resultados mostraram que introns com miR19a tem o splicing mais eficiente do que

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10

Meyer, Annekarin [Verfasser], and Jörn [Akademischer Betreuer] Lausen. "TAL1 und miR-17-92 bilden eine regulatorische Schleife in der Hämatopoese / Annekarin Meyer ; Betreuer: Jörn Lausen." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2020. http://d-nb.info/1218078847/34.

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11

Souza, Felipe Canto de. "Envolvimento das Aurora-quinases e DIDO na instabilidade cromossômica na leucemia linfoide crônica." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-30032017-112908/.

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Durante a divisão celular as Aurora-quinases (AURKA e AURKB) participam da formação e controle das fibras do fuso mitótico enquanto as isoformas proteicas (DIDO1, DIDO2 e DIDO3), originadas do splicing alternativo do gene DIDO, auxiliam na junção dos microtúbulos aos cinetócoros. Portanto, ambas são relevantes na regulação do ciclo celular. Interessantemente, a superexpressão (ou o ganho de função) das AURKs ou a baixa expressão (ou perda de função) das isoformas de DIDO estão ambos associados com amplificação dos centrossomos e à instabilidade cromossômica (CIN), com consequente aneuploidia.

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12

Jacob, Jimmy. "Post-transcriptional regulation of estrogen receptor-α by miR-17-92 interaction and LMTK3 phosphorylation in breast cancer". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24819.

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Estrogen receptor-α (ERα) is expressed in two-thirds of BCs and is a well-known prognostic and predictive marker. For this reason it is one of the most studied proteins in BC. To understand how ERα positive BC develops, it is crucial to investigate both how this protein is regulated and which genes are modulated by it. MicroRNAs (miRNAs) control gene expression post-transcriptionally by interacting through sequence complementarity to their target transcripts. Through a microarray approach, we identified the subset of miRNAs modulated by ERα, that include up-regulation of miRNAs derived from th

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13

Philippe, Lucas. "Le Cluster Mir-17-92, rôle dans la régulation de la réponse inflammatoire au cours de la polyarthrite rhumatoïde." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00759550.

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La polyarthrite rhumatoïde (PR) est la maladie auto-immune la plus fréquente d'une prévalence de 1%. Les cellules résidentes de la cavité synoviale, les fibroblast-like synoviocytes (FLS), sont des acteurs majeurs de la PR. Leur activation par des récepteurs de l'immunité innée participe à l'acquisition d'un phénotype agressif menant à la destruction ostéo-articulaire. Dans cette étude, nous avons évalué le rôle régulateur de miARN sur les voies de signalisation des Toll-like receptors (TLR). L'activation de TLR2 et de TLR4 dans les FLS induit la diminution de l'expression de plusieurs miARN,

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14

Molitoris, Jason K. "Mechanistic Insights into Glucocorticoid-induced Apoptosis and Autophagy in Lymphoid Malignancies." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1307646327.

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15

Gapihan, Guillaume. "Etude du cluster oncogénique miR17-92 dans les lymphomes B agressifs humains." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC321.

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Les lymphomes à grandes cellules B primitifs du médiastin (PMBL) partagent des caractéristiques pathologiques avec les lymphomes diffus à grandes cellules B (DLBCL), et des caractéristiques moléculaires communes aux lymphomes de Hodgkin classiques (cHL). Le cluster oncogénique miR-17-92, localisé au niveau du chromosome 13q31, est un gène amplifié dans les DLBCL. Dans notre étude, nous avons comparé le niveau d’expression de chaque membre du clustermiR-17-92 dans une série de prélèvements de patients de 40 PMBL, 20 DLBCL et 20 cHL, et étudié les gènes cibles liés aux microARN dérégulés dans le

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16

Culpin, Rachel Emily. "Expression of the MiR-17-92 cluster in DLBCL and B-CLL and its relationship with disease outcome and established prognostic factors." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.582656.

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Diffuse large B-cell lymphoma is an aggressive malignancy of large transformed B- lymphocytes. The disease is biologically and clinically highly heterogeneous and this nature has impacted on patients response to treatment. Gene profiling studies have identified two biologically diverse sub-groups, that exhibit different prognoses, namely; the germinal centre (GC)- and activated B-cell (ABC)- like DLBCL. B-cell chronic lymphocytic leukemia is also a heterogeneous disease. Patients may follow an indolent clinical course and survive for >20 years, but others have a rapidly progressive disease req

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17

Busch, Martin [Verfasser], and Alma [Akademischer Betreuer] Zernecke. "Aortic Dendritic Cell Subsets in Healthy and Atherosclerotic Mice and The Role of the miR-17~92 Cluster in Dendritic Cells / Martin Busch. Betreuer: Alma Zernecke." Würzburg : Universität Würzburg, 2013. http://d-nb.info/1111124612/34.

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18

Pospíšil, Vít. "Role onkogenních mikroRNA miR-17-92 a miR-155 v krvetorbě a leukémii." Doctoral thesis, 2011. http://www.nusl.cz/ntk/nusl-312159.

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(English version): Hematopoietic differentiation is highly ordered multistep process, where generation of terminal blood cells is dependent upon coordinated regulation of gene expression by key regulators: transcription factors and mikroRNAs. PU.1 (Sfpi1) is a versatile hematopoetic transcription factor required for the proper generation of both myeloid and lymphoid lineages. MikroRNAs represent a novel class of ~22 nucleotide long non-coding posttranscriptional regulators that inhibit expression of genes by blocking protein translation or by mRNA degradation. In this PhD thesis I present rese

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19

Rybářová, Jana. "Regulace transkripce mikroRNA klastru miR-17-92 v průběhu diferenciace makrofágů." Master's thesis, 2010. http://www.nusl.cz/ntk/nusl-296232.

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miR-17-92 cluster (Oncomir1) encodes seven microRNAs (miRNA, miR) regulating many biological processes including proliferation, differentiation or apoptosis. Overexpression of microRNAs encoded by miR-17-92 cluster is found in a number of tumors including acute and chronic myeloid leukemias (Dixon-McIver et al., 2008; Li et al., 2008; Venturini et al., 2007). Myeloid progenitors express miR-17-92 cluster at a high level, while macrophage differentiation associates with its downregulation. Our laboratory found, that miR-17-92 cluster is repressed by transcription factor Early growth response 2

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20

Li, Shao Yun, and 李劭筠. "LSD1 control bladder cancer cell growth through c-Myc regulated miR-17-92 cluster." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/78736065063054161947.

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碩士<br>長庚大學<br>生物醫學研究所<br>100<br>Lysine-specific histone demethylase 1 (LSD1) is the first histone demethylase discovered. The enzyme catalyzes demethylation of histone H3-lysine-4 and H3 lysine-9 and modulates the expression levels of a subset of protein-coding genes. LSD1 plays an essential role in mammalian development and is involved in many biological processes. Dysergulation of LSD1 has also been reported in several types of solid tumor, including bladder cancer. However, the effect of LSD1 on miRNA expressions and their roles in bladder cancer progression has not been explored. In our pr

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21

Yang, Yu-Jen, and 楊宇仁. "The Effect of miR-17-92 cluster on Tumor Migration in Human Oral Squamous Cell Carcinoma." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/73524972999371689998.

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碩士<br>國立臺灣大學<br>口腔生物科學研究所<br>99<br>Metastasis is always an important concern in oral squamous cell carcinoma (OSCC) treatment, and migration is the first and crucial step in this process. To investigate this issue, we established a more aggressive cell line-TW2.6 MS-10 by transwell selection from low-migration ability oral cancer cell line: TW2.6. To better understand the effect of microRNAs (miRNA) profile in OSCC metastasis, the miRNA microarray analysis between TW2.6 and TW2.6 MS-10 was performed. According to the array data, a miRNA cluster miR-17-92, including miR-17, miR19b, miR-20a, miR

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22

"The Functions And Molecular Mechanisms Of Microrna-17-92 Cluster In Primary Liver Cancer." Tulane University, 2014.

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MiR-17-92 is an oncogenic miRNA cluster implicated in the development of several human cancers; however, it remains unknown whether miR-17-92 cluster is able to regulate hepatobiliary carcinogenesis. This study was designed to investigate the biological functions and molecular mechanisms of miR-17-92 cluster in primary liver cancer.<br>In-situ hybridization and qRT-PCR analysis showed that miR-17-92 cluster is highly expressed in human cholangiocarcinoma cells compared to the non-neoplastic biliary epithelial cells. Forced overexpression of the miR-17-92 cluster or its members, miR-92a and miR

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23

He, Yi Tian, and 何宜恬. "Investigation of the Role of Epstein-Barr Nuclear Antigen 1 in the Expression of myc and miR-17-92 cluster." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/88633106835180884293.

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碩士<br>長庚大學<br>生物醫學研究所<br>98<br>Epstein-Barr nuclear antigen 1 (EBNA1) is the only viral protein expressed in all EBV-associated tumors. It has been have demonstrated in the lab that various EBNA1 clones isolated from the nasopharyngeal carcinoma (N-EBNA1), prototype B95.8 (B-EBNA1), and the peripheral blood lymphocyte (PBL) of healthy individuals (P-EBNA1), exhibited distinct effect on cell proliferate, survival and migration/invasion. I hypothesize that EBNA1 regulates the expression of cellular genes including protein-coding genes and miRNA genes, which in turn promote the tumor formation. T

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24

Sylvestre, Yannick. "Étude du mécanisme d'autorégulation entre les facteurs de transcription E2F et le microARN miR-20a." Thèse, 2007. http://hdl.handle.net/1866/15252.

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25

Busch, Martin. "Aortic Dendritic Cell Subsets in Healthy and Atherosclerotic Mice and The Role of the miR-17~92 Cluster in Dendritic Cells." Doctoral thesis, 2013. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-71683.

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Atherosclerosis is accepted to be a chronic inflammatory disease of the arterial vessel wall. Several cellular subsets of the immune system are involved in its initiation and progression, such as monocytes, macrophages, T and B cells. Recent research has demonstrated that dendritic cells (DCs) contribute to atherosclerosis, too. DCs are defined by their ability to sense and phagocyte antigens, to migrate and to prime other immune cells, such as T cells. Although all DCs share these functional characteristics, they are heterogeneous with respect to phenotype and origin. Several markers have bee

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26

Prinz, Robert [Verfasser]. "Regulation of proto-oncogenic Pim-1 kinase and miR-17-92 microRNA cluster in the human leukemia cell line K562 / vorgelegt von Robert Prinz." 2009. http://d-nb.info/1003961835/34.

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27

De, Guire Vincent. "Conception de miARN artificiels basée sur la caractérisation de la boucle de régulation miR-20/E2F." Thèse, 2009. http://hdl.handle.net/1866/4141.

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La biologie moléculaire et, plus spécifiquement, la régulation de l’expression génique ont été révolutionnées par la découverte des microARN (miARN). Ces petits ARN d’une vingtaine de nucléotides sont impliqués dans la majorité des processus cellulaires et leur expression est dérégulée dans plusieurs maladies, comme le cancer. Un miARN reconnaît ses cibles principalement par son noyau, ce qui lui permet de réguler simultanément la traduction de centaines d’ARN messagers. Nos travaux ont montré l’existence d’une boucle de rétro-activation négative, entre deux miARN du polycistron miR-17-92 et t

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28

Pantazi, Angeliki. "microRNA expression profile of undifferentiated and differentiating pluripotent cells." Doctoral thesis, 2009. http://hdl.handle.net/11858/00-1735-0000-0006-AF62-2.

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29

Budde, Holger. "Role of miRNAs in Oligodendrocyte Development." Doctoral thesis, 2010. http://hdl.handle.net/11858/00-1735-0000-0006-ADBB-A.

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