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You searched for +publisher:"Temple University" +contributor:("Biemar, Frederic"). Showing records 1 – 2 of 2 total matches.

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Temple University

1. Faggins, Athenesia. Elucidation of the Role of miR-184 in the Development and Maintenance of the Drosophila Melanogaster Nervous System.

Degree: PhD, 2013, Temple University

Biology

MicroRNAs (miRNAs) are short, non-coding RNA sequences that are generated from longer primary transcripts (pri-miRNA). These pri-miRNAs are processed by the endonuclease Drosha into a hairpin secondary structure (pre-miRNA), exported from the nucleus and cleaved by the enzyme Dicer to form a duplex RNA molecule. This miRNA:miRNA* duplex is subsequently further processed to form a single-stranded, mature miRNA. miRNAs have been extensively characterized and are known to play important roles in various physiologic and pathologic pathways. One hallmark of miRNAs function is their ability to modulate the downstream activities of protein-coding genes, as well as various other aspects of gene expression, by acting as post-transcriptional repressors of their messengerRNA (mRNA) targets. miR-184 is a highly conserved miRNA gene expressed in the Drosophila nervous system throughout development; and has been shown to target key regulators of differentiation, proliferation and apoptosis. Here we identify a novel role for miR-184 in regulating the development and maintenance of the Drosophila melanogaster post-embryonic nervous system. We present evidence which suggest miR-184 targets (i) paralytic (para), a voltage-gated sodium channel, shown to control neuronal excitability; and (ii) tramtrack69 (ttk69), a transcription factor known to regulate glial cell number and fate determination during embryonic development. In the absence of miR-184, homozygous loss-of-function mutant adult flies demonstrate hyperactive episodes in response to mechanical shock, indicative of increased susceptibility to seizures. Homozygous loss-of-function mutants also exhibit shortened lifespan, as well as reduced group longevity. Additionally, miR-184 deficient mutant larvae exhibit abnormal development of glia and glial progenitors; while expression of miR-184 exclusively in glia - reversed polarity- (repo) expressing cells - up-regulates development of glial cells. Phenotypes of the adult loss-of-function mutant are suppressed by genetic loss of para function; while larval phenotypes are rescued by reducing the genetic dosage of ttk69. These data imply that miR-184 functions to control post-embryonic gliogenesis, as well as in maintaining neuronal excitability and integrity of the Drosophila aging brain.

Temple University – Theses

Advisors/Committee Members: Biemar, Frederic;, Habas, Raymond, Balciunas, Darius, Kramer, Sunita;.

Subjects/Keywords: Developmental biology; Animal behavior; Genetics;

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Faggins, A. (2013). Elucidation of the Role of miR-184 in the Development and Maintenance of the Drosophila Melanogaster Nervous System. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,233416

Chicago Manual of Style (16th Edition):

Faggins, Athenesia. “Elucidation of the Role of miR-184 in the Development and Maintenance of the Drosophila Melanogaster Nervous System.” 2013. Doctoral Dissertation, Temple University. Accessed November 26, 2020. http://digital.library.temple.edu/u?/p245801coll10,233416.

MLA Handbook (7th Edition):

Faggins, Athenesia. “Elucidation of the Role of miR-184 in the Development and Maintenance of the Drosophila Melanogaster Nervous System.” 2013. Web. 26 Nov 2020.

Vancouver:

Faggins A. Elucidation of the Role of miR-184 in the Development and Maintenance of the Drosophila Melanogaster Nervous System. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Nov 26]. Available from: http://digital.library.temple.edu/u?/p245801coll10,233416.

Council of Science Editors:

Faggins A. Elucidation of the Role of miR-184 in the Development and Maintenance of the Drosophila Melanogaster Nervous System. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,233416


Temple University

2. Yuan, Ke. THE CHARACTERIZATION OF HSA-MIR148A IN HEPATOCARCINOGENESIS.

Degree: PhD, 2011, Temple University

Biology

Chronic Hepatitis B Virus (HBV) infection is a global health problem because of its connection to acute and chronic liver diseases as well as hepatocellular carcinoma (HCC). There is increasing evidence showing that HBV contributes to HCC due to persistently high levels of trans-activating protein – hepatitis B encoded x antigen (HBxAg). Studies have shown that the HBxAg affects and alters the activity of many different transcription factors and plays an essential role in several cytoplasmic signaling transduction pathways, such as Wnt signaling pathways. One of the upregulated genes, designated URG11, was found transactivated by HBxAg. URG11 could stimulate the ß-catenin promoter and hepatocellular growth and survival which suggest that URG11 may be a regulatory element in the ß-catenin signaling pathways. microRNA148a (miR148a) was identified from two miRNA microarrays as one of the up-regulated miRNAs in cells stably expressing HBxAg or over-expressing URG11. Moreover, the expression of miR148a was also elevated in HBV-mediated HCC patient tissue samples. To study the function of miR148a, HepG2 (hepatoblastoma) and Hep3B (hepatoma) cells stably expressing HBxAg or over-expressing URG11 were transduced by recombinant lentiviruses encoding anti-miR148a. anti-miR148a suppressed cell proliferation, cell cycle progression, cell migration, anchorage independent growth in soft agar and subcutaneous tumor formation in SCID mice. Further, introduction of anti-miR148a increased PTEN protein and mRNA expression, suggesting that PTEN was suppressed by miR148a. In addition, anti-miR148a blocked the stimulation of Akt signaling, resulting in decreased expression of ß-catenin. Thus, miR148a may play a central role in HBxAg/URG11 mediated HCC, and may be an early diagnostic marker and/or therapeutic target associated with this tumor type.

Temple University – Theses

Advisors/Committee Members: Feitelson, Mark, Waring, Richard B., Biemar, Frederic, Ramirez, Servio.

Subjects/Keywords: Virology; Biochemistry; Cellular Biology; AKT; hepatitis B x antigen; hepatocellular carcinoma; miR148a; PTEN; URG11

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Yuan, K. (2011). THE CHARACTERIZATION OF HSA-MIR148A IN HEPATOCARCINOGENESIS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,154268

Chicago Manual of Style (16th Edition):

Yuan, Ke. “THE CHARACTERIZATION OF HSA-MIR148A IN HEPATOCARCINOGENESIS.” 2011. Doctoral Dissertation, Temple University. Accessed November 26, 2020. http://digital.library.temple.edu/u?/p245801coll10,154268.

MLA Handbook (7th Edition):

Yuan, Ke. “THE CHARACTERIZATION OF HSA-MIR148A IN HEPATOCARCINOGENESIS.” 2011. Web. 26 Nov 2020.

Vancouver:

Yuan K. THE CHARACTERIZATION OF HSA-MIR148A IN HEPATOCARCINOGENESIS. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Nov 26]. Available from: http://digital.library.temple.edu/u?/p245801coll10,154268.

Council of Science Editors:

Yuan K. THE CHARACTERIZATION OF HSA-MIR148A IN HEPATOCARCINOGENESIS. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,154268

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