subject:(Genetic regulation)

1. Guay, Catherine L., 1979-. High-throughput tools for functional genomics.

Degree: PhD, Computational and Integrative Biology, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/57076/

►

Genetic information is stored in DNA sequences, referred to as the genome. Decoding the meaning of these sequences is a critical challenge in biology. The… (more)

▼

Genetic information is stored in DNA sequences, referred to as the genome. Decoding the meaning of these sequences is a critical challenge in biology. The genome contains functional components that modulate information in the genome into cell type specific functions. Of these components, Cis-regulatory modules (CRMs) integrate transcription factor inputs to causally affect gene expression. The genomic locations and sequences of CRMs are useful for resolving interactions within gene regulatory networks, and are therefore useful to address fundamental questions pertaining to development, evolution, cancer, and genetic disease. My work addressed major methodological limitations in CRM analysis. Previously, there was no functional method to identify CRMs at genome-scale. Thus, I developed a Genome-scale Reporter Assay Method for CRMs, or GRAMc, that utilizes random 25bp DNA barcodes (N25s) as reporters to quantitatively and reproducibly identify CRMs across an entire genome. The method was applied in cultured human liver cells and in sea urchin embryos. Due to the limited delivery rate of reporter constructs into embryos, it is often advantageous to test GRAMc libraries containing long (>1kb) genomic inserts. Previously, there was no efficient way to characterize genome-scale reporter libraries containing long inserts. To overcome this limitation, I developed a bi-directional mate-pair library approach to characterize long insert containing libraries of genome-scale magnitude. Although genome-scale identification of CRMs is critical to increase cis-regulatory analysis, in embryos it is also necessary to characterize the spatial activity of CRMs. Available methods to identify the spatial activity of CRMs rely on image analysis. Due to the limited number of optically distinct reporter genes, image-based methods are limited to testing only a few CRMs at a time. To address this challenge, I developed a method for Multiplex and Mosaic Observation of Spatial information encoded In CRMs, or MMOSAIC, that increases throughput of spatial cis-regulatory analysis in embryos by several orders of magnitude over traditional imaging based approaches. Together, these tools for cis-regulatory analysis overcome several major limitations for the study of functional genomics

Advisors/Committee Members: Nam, Jongmin (chair).

Subjects/Keywords: Genetic regulation

13 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Guay, Catherine L., 1. (2018). High-throughput tools for functional genomics. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/57076/

Chicago Manual of Style (16^th Edition):

Guay, Catherine L., 1979-. “High-throughput tools for functional genomics.” 2018. Doctoral Dissertation, Rutgers University. Accessed January 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/57076/.

MLA Handbook (7^th Edition):

Guay, Catherine L., 1979-. “High-throughput tools for functional genomics.” 2018. Web. 17 Jan 2021.

Vancouver:

Guay, Catherine L. 1. High-throughput tools for functional genomics. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Jan 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57076/.

Council of Science Editors:

Guay, Catherine L. 1. High-throughput tools for functional genomics. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57076/

Hong Kong University of Science and Technology

2. Yu, Chuan LIFS. Structure and function study of DISC1.

Degree: 2017, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-103116 ; https://doi.org/10.14711/thesis-991012535960803412 ; http://repository.ust.hk/ir/bitstream/1783.1-103116/1/th_redirect.html

► Since DISC1 (disrupted in schizophrenia 1) has been identified as a risk gene factor of psychiatric disease from a large Scottish family, tons of thousands… (more)

▼ Since DISC1 (disrupted in schizophrenia 1) has been identified as a risk gene factor of psychiatric disease from a large Scottish family, tons of thousands of studies concentrate on this mystery gene. Mutations of DISC1 have been associated with major psychiatric disorders including schizophrenia, bipolar disorder and major recurrent depression. Despite the hundreds of DISC1 binding proteins and various aspects of functions are reported, little is known about how DISC1 interacts with other proteins structurally to impact human brain development. In the first half of this thesis, we focus on the regulation of mitosis and neurogenesis via DISC1/Ndel1 interaction. First, we confirmed the strong direct interaction between DISC1 C-terminal tail and Ndel1 C-terminal coiled-coil region using ITC, FPLC and other biochemical approaches. Then we solved the high resolution structure of DISC1 C-terminal tail in complex with its binding domain of Ndel1 with the help of NMR spectrometry. Surprisingly, we found that DISC1 C-terminal peptide can significantly elongate the mitosis time length and interfere with cell cycle progression. Mechanistically, DISC1 regulates Ndel1’s kinetochore localization but not its centrosome localization during mitosis. Further study uncovers DISC1 can regulate the interaction between Ndel1 and CENPF, one of major outer kinetochore protein. Our study uncovers a new possible mechanism of DISC1-mediated mitosis and neurogenesis regulation and has implications for how risk gene factors may contribute to psychiatric disorders. In the second half of this thesis, we focus on the regulation of gene transcription via DISC1/ATF4 interaction. Similar to the DISC1/Ndel1 project, we also confirmed the strong direct interaction between DISC1 C-terminal tail and ATF4 C-terminal helix region using similar biochemical approaches. Then we solved the high resolution structure of ATF4 C-terminal coiled-coil in complex with DISC1 C-terminal tail. Moreover, we showed that DISC1 can totally disrupt the dimerization of ATF4 which is also mediated by DISC1 binding site. Consistently, we use ITC and NMR spectra method to clearly demonstrate DISC1 can release ATF4 from DNA via strong interaction with ATF4 and disruption the dimerization of ATF4. Our study uncovers another possible mechanism of DISC1-mediated transcriptional regulation.

Subjects/Keywords: Schizophrenia ; Genetic aspects ; Mitosis ; Regulation ; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Yu, C. L. (2017). Structure and function study of DISC1. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-103116 ; https://doi.org/10.14711/thesis-991012535960803412 ; http://repository.ust.hk/ir/bitstream/1783.1-103116/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yu, Chuan LIFS. “Structure and function study of DISC1.” 2017. Thesis, Hong Kong University of Science and Technology. Accessed January 17, 2021. http://repository.ust.hk/ir/Record/1783.1-103116 ; https://doi.org/10.14711/thesis-991012535960803412 ; http://repository.ust.hk/ir/bitstream/1783.1-103116/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yu, Chuan LIFS. “Structure and function study of DISC1.” 2017. Web. 17 Jan 2021.

Vancouver:

Yu CL. Structure and function study of DISC1. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2017. [cited 2021 Jan 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-103116 ; https://doi.org/10.14711/thesis-991012535960803412 ; http://repository.ust.hk/ir/bitstream/1783.1-103116/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yu CL. Structure and function study of DISC1. [Thesis]. Hong Kong University of Science and Technology; 2017. Available from: http://repository.ust.hk/ir/Record/1783.1-103116 ; https://doi.org/10.14711/thesis-991012535960803412 ; http://repository.ust.hk/ir/bitstream/1783.1-103116/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Columbia University

3. Seeley, John. microRNA Regulation of Endotoxin Tolerance.

Degree: 2014, Columbia University

URL: https://doi.org/10.7916/D8HX19V9

► Sepsis affects hundreds of thousands each year in the United States alone, with an estimated 20-30% mortality rate in spite of current treatment regimens. Sepsis… (more)

▼ Sepsis affects hundreds of thousands each year in the United States alone, with an estimated 20-30% mortality rate in spite of current treatment regimens. Sepsis mortality was originally understood to be the caused by overproduction of inflammatory cytokines in response to pathogen detection by the host. However, recent studies suggest that with modern treatments, secondary infection, rather than inflammatory shock, may be of greater concern. In either case, the failure of a large number of anti-inflammatory agents to produce beneficial outcomes in sepsis treatment during clinical trial suggests that the development of a new class of immunomodulatory agents may be required for effective treatment. In experimental models, pre-treatment with sub-lethal doses of lipopolysaccharide (LPS, previously referred to as endotoxin) induces a state of "LPS tolerance" that reduces septic shock lethality. Paradoxically, LPS tolerance also results in increased antimicrobial gene expression and resistance to secondary infection in some models. Further exploration of this process may provide drug targets capable of limiting inflammation without dampening antimicrobial immunity, which could be of great benefit in the treatment of sepsis and chronic inflammatory disease. Many groups have studied signaling changes that occur during LPS tolerance. However, mediators of tolerance that can account for the changes in LPS-induced gene expression that result in increased microbial resistance are not well described. This has prevented proper testing of the physiological effects of tolerance on disease, and it remains unclear if this process could be artificially induced or is of any benefit to sepsis patients. Recent in vitro work suggests that tolerant gene expression patterns are the result of large scale changes in chromatin organization that occur in macrophages after prolonged LPS stimulation. Because microRNAs (miRNAs), a new class of gene regulator, have been found to regulate chromatin modifying complexes in other systems, LPS-induced miRNAs were screened to identify potential mediators of tolerance that could cause changes in gene expression patterns without necessarily impacting LPS signaling itself. Several tolerance-associated miRNAs were identified. One miRNA in particular, miR-222, was found to repress tumor necrosis factor (Tnf) and Brahma-related gene one (Brg1) expression. This attenuates expression of genes dependent on nucleosome remodeling, primarily affecting inflammatory genes. Consequently, miR-222 expression effectively limits septic shock lethality. However, low-level responses, as well as NF-κB signaling and the expression of a subset of antimicrobial and antiviral genes, are left intact. Thus, although miR-222 does not entirely recapitulate the tolerance response, by directing the LPS response into a less damaging expression profile, miR-222 may accelerate the onset of tolerance and be a promising target for therapeutics aiming to treat inflammatory disease without compromising…

Subjects/Keywords: Endotoxins; Septicemia; Genetic regulation; Immunology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Seeley, J. (2014). microRNA Regulation of Endotoxin Tolerance. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8HX19V9

Chicago Manual of Style (16^th Edition):

Seeley, John. “microRNA Regulation of Endotoxin Tolerance.” 2014. Doctoral Dissertation, Columbia University. Accessed January 17, 2021. https://doi.org/10.7916/D8HX19V9.

MLA Handbook (7^th Edition):

Seeley, John. “microRNA Regulation of Endotoxin Tolerance.” 2014. Web. 17 Jan 2021.

Vancouver:

Seeley J. microRNA Regulation of Endotoxin Tolerance. [Internet] [Doctoral dissertation]. Columbia University; 2014. [cited 2021 Jan 17]. Available from: https://doi.org/10.7916/D8HX19V9.

Council of Science Editors:

Seeley J. microRNA Regulation of Endotoxin Tolerance. [Doctoral Dissertation]. Columbia University; 2014. Available from: https://doi.org/10.7916/D8HX19V9

Columbia University

4. Lee, Andreia H. Regulation of Proviral Expression and Post-Translational Modifications in Embryonic Cells.

Degree: 2017, Columbia University

URL: https://doi.org/10.7916/D8S46ZCB

► Moloney Murine Leukemia Virus (M-MLV) proviral DNA is transcriptionally silenced in mouse embryonic cells by a repressor complex containing tripartite-motif-containing 28 (Trim28). Trim28 depends on… (more)

▼ Moloney Murine Leukemia Virus (M-MLV) proviral DNA is transcriptionally silenced in mouse embryonic cells by a repressor complex containing tripartite-motif-containing 28 (Trim28). Trim28 depends on post-translational modifications, such as sumoylation and phosphorylation, and its interactions with several co-repressor proteins to regulate its repressive activity. YY1 is one such Trim28 co-repressor protein, recently found to tether the Trim28 silencing complex to the M-MLV promoter. Here, we investigated the biochemical interaction of Trim28 and YY1, and the role of sumoylation and phosphorylation of Trim28 in mediating M-MLV silencing. Experiments probing the binding of YY1 and Trim28 in vitro suggested that their interaction occurs indirectly. Mutational studies demonstrated that the RBCC domain of Trim28 is sufficient for interaction with YY1 while the acidic region 1 and zinc fingers of YY1 were necessary and sufficient for its interaction with Trim28. Additionally, we found that the K779 residue was critical for Trim28-mediated silencing of M-MLV in embryonic cells. The repressor complex that silences M-MLV is very large and likely consists of many protein subunits. A few proteins contained in the repressor complex have been identified, including Trim28, but the identity of most of the components forming the repressor complex are unknown. We detected a new form of the complex that is of even high molecular weight and likely contains additional associated cofactors. We reported an approach for purifying this larger repressor complex and identified new candidates for cofactors that may potentially function in the silencing of M-MLV. We also examined the regulation of sumoylation in embryonic cells. Sumoylation conjugation is a post-translational modification that affects a diverse range of processes and is important for embryo survival. Overall inhibition of the SUMO pathways results in embryonic lethality demonstrating the importance of the SUMO pathways for embryonic viability; however, our understanding of SUMO function in embryos at the cellular and molecular level is still greatly lacking. We demonstrated that SUMO1 cannot be overexpressed in embryonic carcinoma and embryonic stem cells and that SUMO1 overexpression is prevented at a post-transcriptional level. This occurred specifically for SUMO1 and not for SUMO2 overexpression. Furthermore, blocking conjugation or increasing the deconjugation of SUMO1 to substrates significantly improved SUMO1 overexpression. The results indicate that the overexpression of SUMO1 protein, in itself, is tolerated in embryonic cells, but the accumulation of substrate(s) modified by SUMO1 appears to be strongly prevented by an embryonic-specific post-transcriptional mechanism.

Subjects/Keywords: Biology; Virology; Cytology; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lee, A. H. (2017). Regulation of Proviral Expression and Post-Translational Modifications in Embryonic Cells. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8S46ZCB

Chicago Manual of Style (16^th Edition):

Lee, Andreia H. “Regulation of Proviral Expression and Post-Translational Modifications in Embryonic Cells.” 2017. Doctoral Dissertation, Columbia University. Accessed January 17, 2021. https://doi.org/10.7916/D8S46ZCB.

MLA Handbook (7^th Edition):

Lee, Andreia H. “Regulation of Proviral Expression and Post-Translational Modifications in Embryonic Cells.” 2017. Web. 17 Jan 2021.

Vancouver:

Lee AH. Regulation of Proviral Expression and Post-Translational Modifications in Embryonic Cells. [Internet] [Doctoral dissertation]. Columbia University; 2017. [cited 2021 Jan 17]. Available from: https://doi.org/10.7916/D8S46ZCB.

Council of Science Editors:

Lee AH. Regulation of Proviral Expression and Post-Translational Modifications in Embryonic Cells. [Doctoral Dissertation]. Columbia University; 2017. Available from: https://doi.org/10.7916/D8S46ZCB

Hong Kong University of Science and Technology

5. Min, Lan. The functional roles of α2-chimaerin in the development of hippocampus.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-70593 ; https://doi.org/10.14711/thesis-b1240164 ; http://repository.ust.hk/ir/bitstream/1783.1-70593/1/th_redirect.html

► Adult neurogenesis, generation of mammalian new neurons throughout adulthood, occurs in two restricted regions in the brain- the subventricular zone of lateral ventricle and the… (more)

Subjects/Keywords: Sea horses ; Development ; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Min, L. (2013). The functional roles of α2-chimaerin in the development of hippocampus. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-70593 ; https://doi.org/10.14711/thesis-b1240164 ; http://repository.ust.hk/ir/bitstream/1783.1-70593/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Min, Lan. “The functional roles of α2-chimaerin in the development of hippocampus.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed January 17, 2021. http://repository.ust.hk/ir/Record/1783.1-70593 ; https://doi.org/10.14711/thesis-b1240164 ; http://repository.ust.hk/ir/bitstream/1783.1-70593/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Min, Lan. “The functional roles of α2-chimaerin in the development of hippocampus.” 2013. Web. 17 Jan 2021.

Vancouver:

Min L. The functional roles of α2-chimaerin in the development of hippocampus. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Jan 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-70593 ; https://doi.org/10.14711/thesis-b1240164 ; http://repository.ust.hk/ir/bitstream/1783.1-70593/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Min L. The functional roles of α2-chimaerin in the development of hippocampus. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-70593 ; https://doi.org/10.14711/thesis-b1240164 ; http://repository.ust.hk/ir/bitstream/1783.1-70593/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

6. Lau, Kei Man. DNA methylation regulates the transcriptional activity of acetylcholinesterase gene during C2C12 myogenesis.

Degree: 2015, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-74370 ; https://doi.org/10.14711/thesis-b1448956 ; http://repository.ust.hk/ir/bitstream/1783.1-74370/1/th_redirect.html

► In vertebrates, acetylcholinesterase (AChE) is well-known for its role in hydrolyzing neurotransmitter acetylcholine at the neuromuscular junction (nmj), which is critical for proper function of… (more)

▼ In vertebrates, acetylcholinesterase (AChE) is well-known for its role in hydrolyzing neurotransmitter acetylcholine at the neuromuscular junction (nmj), which is critical for proper function of our motor system. Previous studies evidenced that the expression of AChE was developmentally regulated during myogenesis, indicating the significance of intrinsic factors in regulating gene expression. However, these factors involved in the AChE regulation remained unclear. During myogenesis, DNA methylation is essential for temporal control of myogenic gene expression. Vertebrate AChE gene carries highly conserved CG-rich regions in its promoters, implying its likeliness to be methylated. Here, we aimed to investigate the regulation of AChE during myogenesis by DNA methylation. Myogenic differentiation of mouse C2C12 myoblast cells was triggered by serum reduction; the mRNA level, promoter activity, enzymatic activity and protein expression of AChE were up-regulated along with the myotube formation. To investigate the role of DNA methylation in AChE regulation, a DNA methyltransferase inhibitor, 5-Azacytidine (5-Aza), was applied throughout myogenesis. When DNA methylation was inhibited, the promoter activity, transcript expression and enzymatic activity of AChE were markedly increased after day 3 of differentiation, which indicated the putative role of DNA methylation. The effect of 5-Aza led to further investigation on the potential methylated sites on AChE promoter during myogenesis. By bisulfite pyrosequencing, the overall methylation rate was found to peak at day 3 during C2C12 differentiation; a SP1 site on AChE promoter was revealed to be heavily methylated. Additionally, the SP1-driven transcriptional activity was increased in 5-Aza-treated C2C12 culture. By gel mobility shift assay, the DNA methylation on the SP1 site, derived from AChE promoter, totally blocked the binding of SP1. The findings suggest the role of DNA methylation on AChE transcriptional regulation and provide insight for elucidating the DNA methylation-mediated regulatory mechanism on AChE expression during myogenic differentiation.

Subjects/Keywords: Acetylcholinesterase ; Regulation ; Genetic transcription ; Myogenesis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lau, K. M. (2015). DNA methylation regulates the transcriptional activity of acetylcholinesterase gene during C2C12 myogenesis. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-74370 ; https://doi.org/10.14711/thesis-b1448956 ; http://repository.ust.hk/ir/bitstream/1783.1-74370/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lau, Kei Man. “DNA methylation regulates the transcriptional activity of acetylcholinesterase gene during C2C12 myogenesis.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed January 17, 2021. http://repository.ust.hk/ir/Record/1783.1-74370 ; https://doi.org/10.14711/thesis-b1448956 ; http://repository.ust.hk/ir/bitstream/1783.1-74370/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lau, Kei Man. “DNA methylation regulates the transcriptional activity of acetylcholinesterase gene during C2C12 myogenesis.” 2015. Web. 17 Jan 2021.

Vancouver:

Lau KM. DNA methylation regulates the transcriptional activity of acetylcholinesterase gene during C2C12 myogenesis. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2021 Jan 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-74370 ; https://doi.org/10.14711/thesis-b1448956 ; http://repository.ust.hk/ir/bitstream/1783.1-74370/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lau KM. DNA methylation regulates the transcriptional activity of acetylcholinesterase gene during C2C12 myogenesis. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: http://repository.ust.hk/ir/Record/1783.1-74370 ; https://doi.org/10.14711/thesis-b1448956 ; http://repository.ust.hk/ir/bitstream/1783.1-74370/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

East Carolina University

7. Vick, Stephen. VALIDATION OF CANDIDATE GENES IN RESPONSE TO VERSICAN MANIPULATION IN DEVELOPING SYNOVIAL JOINTS.

Degree: 2012, East Carolina University

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14830

► Little is understood about the complex process of synovial joint formation in early limb development. It has been shown that versican is highly expressed in… (more)

Subjects/Keywords: Genetic regulation; Joints; Chondroitin sulfates

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Vick, S. (2012). VALIDATION OF CANDIDATE GENES IN RESPONSE TO VERSICAN MANIPULATION IN DEVELOPING SYNOVIAL JOINTS. (Masters Thesis). East Carolina University. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14830

Chicago Manual of Style (16^th Edition):

Vick, Stephen. “VALIDATION OF CANDIDATE GENES IN RESPONSE TO VERSICAN MANIPULATION IN DEVELOPING SYNOVIAL JOINTS.” 2012. Masters Thesis, East Carolina University. Accessed January 17, 2021. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14830.

MLA Handbook (7^th Edition):

Vick, Stephen. “VALIDATION OF CANDIDATE GENES IN RESPONSE TO VERSICAN MANIPULATION IN DEVELOPING SYNOVIAL JOINTS.” 2012. Web. 17 Jan 2021.

Vancouver:

Vick S. VALIDATION OF CANDIDATE GENES IN RESPONSE TO VERSICAN MANIPULATION IN DEVELOPING SYNOVIAL JOINTS. [Internet] [Masters thesis]. East Carolina University; 2012. [cited 2021 Jan 17]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14830.

Council of Science Editors:

Vick S. VALIDATION OF CANDIDATE GENES IN RESPONSE TO VERSICAN MANIPULATION IN DEVELOPING SYNOVIAL JOINTS. [Masters Thesis]. East Carolina University; 2012. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=14830

University of Aberdeen

8. Hay, Elizabeth A. The effects of genetic and epigenetic variation on the control of the cannabinoid-1 receptor gene and their role in disease and drug efficacy.

Degree: PhD, 2019, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152970690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774032

► Gene regulatory DNA regions are essential for controlling gene expression and they contain a significant proportion of disease-associated variants. Understanding variation within gene regulatory regions… (more)

▼ Gene regulatory DNA regions are essential for controlling gene expression and they contain a significant proportion of disease-associated variants. Understanding variation within gene regulatory regions may facilitate understanding of disease progression or the development of stratified medicines. The CB1 receptor is involved in controlling many physiological processes such as appetite and reward signalling and has been investigated as a drug target. Differences in response and side effects, however, may indicate that genetic variation within the CB1 receptor gene (CNR1), may need to be investigated to better predict disease and drug efficacy. As disease-associated polymorphisms have been identified in non-coding sequences of CNR1, the aim was to investigate the role of CNR1 regulatory elements and how genetic and epigenetic variation influence their activity. This study identified that the CNR1 promoter is active in primary cell cultures generated from the hypothalamus and dorsal root ganglia (DRGs) of rats and is highly susceptible to CpG methylation in DRGs. Additionally, a highly conserved intronic sequence, ECR1, was disrupted in mice using the CRISPR/Cas9 system. Disruption of ECR1 led to reduced CNR1 expression in the hippocampus but not in the hypothalamus as well as reduced CB1 agonistinduced hypothermia, a reduction in ethanol intake and altered anxiety-like behaviour. The major allele of a SNP within ECR1, permitted CNR1 promoter activity and the minor allele significantly repressed CNR1 promoter activity in hypothalamic and DRG cell cultures. In DRGs, allelic variation within ECR1 altered the response of the CNR1 promoter to the CB1 receptor antagonist/inverse agonist, rimonabant. In conclusion, this study indicates that ECR1 is a tissue specific enhancer and may be involved in regulating physiological processes, and, genetic variation in ECR1 can alter its control of the CNR1 promoter. Overall, this study elucidates possible CNR1 gene regulatory mechanisms, and how genetic and epigenetic variation influences gene regulation.

Subjects/Keywords: Genetic regulation; Cannabinoids; Drug receptors

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hay, E. A. (2019). The effects of genetic and epigenetic variation on the control of the cannabinoid-1 receptor gene and their role in disease and drug efficacy. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152970690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774032

Chicago Manual of Style (16^th Edition):

Hay, Elizabeth A. “The effects of genetic and epigenetic variation on the control of the cannabinoid-1 receptor gene and their role in disease and drug efficacy.” 2019. Doctoral Dissertation, University of Aberdeen. Accessed January 17, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152970690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774032.

MLA Handbook (7^th Edition):

Hay, Elizabeth A. “The effects of genetic and epigenetic variation on the control of the cannabinoid-1 receptor gene and their role in disease and drug efficacy.” 2019. Web. 17 Jan 2021.

Vancouver:

Hay EA. The effects of genetic and epigenetic variation on the control of the cannabinoid-1 receptor gene and their role in disease and drug efficacy. [Internet] [Doctoral dissertation]. University of Aberdeen; 2019. [cited 2021 Jan 17]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152970690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774032.

Council of Science Editors:

Hay EA. The effects of genetic and epigenetic variation on the control of the cannabinoid-1 receptor gene and their role in disease and drug efficacy. [Doctoral Dissertation]. University of Aberdeen; 2019. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152970690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.774032

Montana State University

9. Saley, Tara Carolyne. Introducing the ArsR regulated arsenic stimulon.

Degree: MS, College of Agriculture, 2017, Montana State University

URL: https://scholarworks.montana.edu/xmlui/handle/1/13486

► The United States EPA ranks arsenic as the number one environmental toxin. Since microorganisms are significant drivers of arsenic toxicity and mobility in nature, it… (more)

Subjects/Keywords: Genetic regulation.; Arsenic.; Toxicology.; Bacteria.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Saley, T. C. (2017). Introducing the ArsR regulated arsenic stimulon. (Masters Thesis). Montana State University. Retrieved from https://scholarworks.montana.edu/xmlui/handle/1/13486

Chicago Manual of Style (16^th Edition):

Saley, Tara Carolyne. “Introducing the ArsR regulated arsenic stimulon.” 2017. Masters Thesis, Montana State University. Accessed January 17, 2021. https://scholarworks.montana.edu/xmlui/handle/1/13486.

MLA Handbook (7^th Edition):

Saley, Tara Carolyne. “Introducing the ArsR regulated arsenic stimulon.” 2017. Web. 17 Jan 2021.

Vancouver:

Saley TC. Introducing the ArsR regulated arsenic stimulon. [Internet] [Masters thesis]. Montana State University; 2017. [cited 2021 Jan 17]. Available from: https://scholarworks.montana.edu/xmlui/handle/1/13486.

Council of Science Editors:

Saley TC. Introducing the ArsR regulated arsenic stimulon. [Masters Thesis]. Montana State University; 2017. Available from: https://scholarworks.montana.edu/xmlui/handle/1/13486

Rutgers University

10. Caratozzolo, Rose Marie, 1978-. Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP.

Degree: PhD, Biochemistry, 2011, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530

►

The 3’-end processing of nearly all eukaryotic pre-mRNAs comprises multiple steps which culminate in the addition of a poly(A) tail, which is essential for mRNA… (more)

▼

The 3’-end processing of nearly all eukaryotic pre-mRNAs comprises multiple steps which culminate in the addition of a poly(A) tail, which is essential for mRNA stability, translation, and export. Consequently, polyadenylation regulation is an important component of gene expression. One way to regulate polyadenylation is to inhibit the activity of a single poly(A) site, as exemplified by the U1A protein that negatively autoregulates itself by binding to a Polyadenylation Inhibitory Element (PIE) site within the 3’ UTR of its own pre-mRNA. U1 snRNP, which is primarily involved in splice site recognition, inhibits poly(A) site activity in papillomaviruses by binding to 5’ splice site-like sequences, which have recently been named “U1-sites”. Here, a recently identified U1-site in the human U1A 3'UTR is examined and shown to synergize with the adjacent PIE site to inhibit polyadenylation. However, unlike the sites found in papillomaviruses, the U1A U1-site has no inhibitory activity on its own and is dependent on a wild-type PIE. This lack of activity is due to the site being masked within a phylogenetically conserved stem structure (U1-STEM). The secondary RNA structure of this region was confirmed by RNase digestion analysis. Mutation of the U1-STEM, thereby opening up the U1-site, greatly increases U1-site mediated inhibition. The region between the U1-STEM and PIE (referred to as Region C) was also revealed to be required for synergy. Since biotin pulldown assays indicated that U1 snRNP binding to the U1-site was not affected by the presence of the U1-STEM, a model was proposed suggesting that U1 snRNP binds to the U1-STEM, but remains trapped in an inactive conformation until PIE is bound by two U1A molecules. However, further experiments showed that U1 snRNP binding did actually increase when the U1-STEM was mutated, but no corresponding change to the U1-STEM structure was detected. The discrepancies within these data suggest there is still much to be determined regarding the binding of U1 snRNP to the U1-Site. A more refined model is then presented which involves remodeling of Region C and part of the U1-STEM.

Advisors/Committee Members: Caratozzolo, Rose Marie, 1978- (author), GUNDERSON, SAMUEL I (chair), Brewer, Gary (internal member), Covey, Lori (internal member), Tian, Bin (outside member).

Subjects/Keywords: Gene expression; Genetic regulation; RNA

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Caratozzolo, Rose Marie, 1. (2011). Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP. (Doctoral Dissertation). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530

Chicago Manual of Style (16^th Edition):

Caratozzolo, Rose Marie, 1978-. “Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP.” 2011. Doctoral Dissertation, Rutgers University. Accessed January 17, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530.

MLA Handbook (7^th Edition):

Caratozzolo, Rose Marie, 1978-. “Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP.” 2011. Web. 17 Jan 2021.

Vancouver:

Caratozzolo, Rose Marie 1. Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP. [Internet] [Doctoral dissertation]. Rutgers University; 2011. [cited 2021 Jan 17]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530.

Council of Science Editors:

Caratozzolo, Rose Marie 1. Studies of polyadenylation regulation of U1A mRNA by an RNP complex containing U1A and U1 snRNP. [Doctoral Dissertation]. Rutgers University; 2011. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000057530

Rutgers University

11. Dirschbacher, Nina, 1991-. Topology of contacts in interacting polymers.

Degree: MS, Physics and Astronomy, 2014, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/45235/

► Recent developments in the study of chromatin loop domains and gene regulation motivates us to investigate the topology of contacts in interacting polymers. To describe… (more)

Subjects/Keywords: Genetic regulation; Chromatin – genetics

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Dirschbacher, Nina, 1. (2014). Topology of contacts in interacting polymers. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/45235/

Chicago Manual of Style (16^th Edition):

Dirschbacher, Nina, 1991-. “Topology of contacts in interacting polymers.” 2014. Masters Thesis, Rutgers University. Accessed January 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/45235/.

MLA Handbook (7^th Edition):

Dirschbacher, Nina, 1991-. “Topology of contacts in interacting polymers.” 2014. Web. 17 Jan 2021.

Vancouver:

Dirschbacher, Nina 1. Topology of contacts in interacting polymers. [Internet] [Masters thesis]. Rutgers University; 2014. [cited 2021 Jan 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/45235/.

Council of Science Editors:

Dirschbacher, Nina 1. Topology of contacts in interacting polymers. [Masters Thesis]. Rutgers University; 2014. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/45235/

Rutgers University

12. Li, Ying, 1987-. Gene regulation during central nervous system development and post-injury regeneration.

Degree: PhD, Biomedical Engineering, 2016, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/49255/

►

Central nervous system (CNS) development and post-injury neurogenesis require accurate coordination of neural stem cell proliferation, progenitor cell differentiation, neuron, glia migration and maturation, and… (more)

▼

Central nervous system (CNS) development and post-injury neurogenesis require accurate coordination of neural stem cell proliferation, progenitor cell differentiation, neuron, glia migration and maturation, and synapse formation between axons and dendrites. Such systems with high complexity require strict temporal and spatial control via several levels of regulation, in which the transcription regulation is one of the most critical steps. The developmental and injury-repair process involves over 18,000 genes, for majority of which the molecular mechanism governing their transcription remains largely unknown. In an attempt to address this question, four projects were conducted focusing on two levels of transcription regulation: i.e., chromatin modification, and the interaction of cis-acting regulatory sequences with trans-acting protein factors. Computational methods were adopted to analyze the sequences of the cis-elements and iii make predictions for their interacting transcription factors (TFs). The functional roles of these cis- and trans-elements were further determined in vivo and in vitro. The following findings are presented: 1) the function of DNA topoisomerase II beta (Top2b) in proper laminar formation and cell survival during retinal development; 2) the development of computational method for identifying gene regulatory networks involving enhancers and master TFs that are important in retinal cell differentiation; 3) the mechanism of Notch1 regulation in neural stem/progenitor cells via the interaction between Nkx6.1 and a CNS specific enhancer CR2 during the development of the spinal cord interneurons; and 4) the role of CR2 in aNSC activation after injury. Findings from this dissertation provide new insights into the molecular mechanisms underlying transcription regulation during CNS development and post-injury neurogenesis. They can also serve as a basis for future development of gene therapies and regenerative medicine for neurological disorders including spinal cord injury.

Advisors/Committee Members: Cai, Li (chair), Firestein, Bonnie (internal member), Grumet, Martin (internal member), Kwan, Kelvin (outside member), Rasin, Mladen-Roko (outside member).

Subjects/Keywords: Genetic regulation; Developmental neurobiology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Li, Ying, 1. (2016). Gene regulation during central nervous system development and post-injury regeneration. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/49255/

Chicago Manual of Style (16^th Edition):

Li, Ying, 1987-. “Gene regulation during central nervous system development and post-injury regeneration.” 2016. Doctoral Dissertation, Rutgers University. Accessed January 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/49255/.

MLA Handbook (7^th Edition):

Li, Ying, 1987-. “Gene regulation during central nervous system development and post-injury regeneration.” 2016. Web. 17 Jan 2021.

Vancouver:

Li, Ying 1. Gene regulation during central nervous system development and post-injury regeneration. [Internet] [Doctoral dissertation]. Rutgers University; 2016. [cited 2021 Jan 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/49255/.

Council of Science Editors:

Li, Ying 1. Gene regulation during central nervous system development and post-injury regeneration. [Doctoral Dissertation]. Rutgers University; 2016. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/49255/

Columbia University

13. Rajbhandari, Presha. Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma.

Degree: 2016, Columbia University

URL: https://doi.org/10.7916/D8J67H0X

► Neuroblastoma is a heterogeneous pediatric malignancy originating from the developing sympathetic nervous system, with poor long-term survival for high-risk patients (~40%). About half of advanced… (more)

▼ Neuroblastoma is a heterogeneous pediatric malignancy originating from the developing sympathetic nervous system, with poor long-term survival for high-risk patients (~40%). About half of advanced neuroblastomas harbor high-level amplification of the MYCN gene, and these tumors show few, if any, additional driver lesions. Despite significant increase in the body of knowledge of genetics in neuroblastoma, all the high-risk patients follow similar therapeutic procedures and little advancement has been made on molecular target based therapies. The major challenge is to dissect the complexity and heterogeneity of these tumors to find driver genes and activated pathways that are essential for the survival of these cancer cells. We used an integrated systems biology approach to define the core regulatory machinery responsible for maintenance of an aggressive neuroblastoma phenotypic state. In the first part of the thesis, I will discuss our computational approach to decipher the tumor heterogeneity by subtype classification, followed by identification of master regulator protein modules for three distinct molecular subtypes of high-risk neuroblastomas, which were validated in a large independent cohort of cases. We propose that such modules are responsible for integrating the effect of mutations in upstream pathways and for regulating the genetic programs and pathways necessary for tumor state implementation and maintenance. The second part of the thesis is focused on experimental validation of putative master regulators in the subtype of neuroblastomas associated with MYCN amplification. By using RNAi screening followed by experimental and computational analyses to elucidate the interdependencies between the top master regulators, we identified TEAD4-MYCN positive feedback loop as a major tumor maintenance mechanism in this subtype. While MYCN regulates TEAD4 transcriptionally, TEAD4 regulates MYCN through transcriptional and post-translational mechanisms. Jointly, MYCN and TEAD4 regulate 90% of inferred MR proteins and causally orchestrate 70% of the subtype-specific gene expression signature. TEAD4 gene expression was associated with neuroblastoma patient survival independently of age, tumor stage and MYCN status (P=2.1e-02). In cellular assays, MYCN promoted growth and repressed differentiation, while TEAD4 activated proliferation and DNA damage repair programs, the signature hallmarks of MYCN-amplified neuroblastoma cells. Specifically, TEAD4 was shown to induce MYCN-independent proliferation by transactivating key genes implicated in high-risk neuroblastoma pathogenesis, including cyclin-dependent kinases, cyclins, E2Fs, DNA replication factors, checkpoint kinases and ubiquitin ligases. The critical role of the core master regulator module in controlling tumor cell viability, both in vitro and in vivo, and its clinical relevance as a prognostic factor highlights TEAD4 as a novel and highly effective candidate target for therapeutic intervention. In this thesis, we demonstrate that interrogation of…

Subjects/Keywords: Genetic regulation; Carcinogenesis; Neuroblastoma – Genetic aspects; Oncology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Rajbhandari, P. (2016). Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8J67H0X

Chicago Manual of Style (16^th Edition):

Rajbhandari, Presha. “Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma.” 2016. Doctoral Dissertation, Columbia University. Accessed January 17, 2021. https://doi.org/10.7916/D8J67H0X.

MLA Handbook (7^th Edition):

Rajbhandari, Presha. “Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma.” 2016. Web. 17 Jan 2021.

Vancouver:

Rajbhandari P. Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma. [Internet] [Doctoral dissertation]. Columbia University; 2016. [cited 2021 Jan 17]. Available from: https://doi.org/10.7916/D8J67H0X.

Council of Science Editors:

Rajbhandari P. Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma. [Doctoral Dissertation]. Columbia University; 2016. Available from: https://doi.org/10.7916/D8J67H0X

University of Aberdeen

14. McFarland, Matthew R. Transfer RNAs as regulatory agents in the translational control of gene expression.

Degree: PhD, 2016, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152811310005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715449

► Translational efficiency is dictated in part by the availability of charged transfer RNA. Depletion of aminoacylated tRNAs (e.g. during recombinant protein expression) can increase translational… (more)

▼ Translational efficiency is dictated in part by the availability of charged transfer RNA. Depletion of aminoacylated tRNAs (e.g. during recombinant protein expression) can increase translational errors and associated stress responses. Here, the role of tRNAs as regulators of gene expression was explored through development of synthetic, tRNA-regulated gene circuits, and through an investigation of the impact of tRNA aminoacylation on endogenous gene expression. Synthetic gene circuits initially explored the use of dominant negative alleles of the release factor eRF1 to modulate stop codon readthrough and translationally regulate gene expression. Mutant eRF1 proteins exhibited only a six-fold stimulatory effect on stop codon readthrough. The dominant negative phenotype was rescued partially by overexpression of eRF1, but not eRF3. Ultimately the severity of growth inhibition by these eRF1 alleles limited their utility in synthetic gene circuit design. A novel synthetic circuit was then implemented that utilised TetR interaction with a TetR-inducing peptide in order to control the expression of a suppressor tRNA, and thus a luciferase reporter gene. Using a parameterised mathematical model, the promoter configuration of the circuit was successfully optimised, allowing suppressor tRNAs to regulate the production of luciferase in both feedforward and positive feedback modes of operation. The effects of charged tRNA levels on the global translation network were dissected by regulating the S.cerevisiae glutamine tRNA synthetase gene GLN4 using a tet-off doxycyclineregulated promoter. tRNA synthetase depletion caused the activation of the Gcn4 amino acid starvation response due to accumulation of uncharged glutamine tRNAs. Doxycycline GLN4 shut-off caused increased amino acid production, and decreased ribosome biosynthesis at the transcriptomic and proteomic level, and further physiological changes proposed to result from compromised translation of glutamine-rich regulatory proteins. tRNA overexpression in the GLN4 depletion strain successfully caused altered competition between different isoacceptor tRNA types for their cognate synthetase resource. Together, these results support a growing understanding of tRNA as a key modulator of translation and gene expression in synthetic and natural systems.

Subjects/Keywords: 572.8; Genetic translation; Genetic regulation; Transfer RNA

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

McFarland, M. R. (2016). Transfer RNAs as regulatory agents in the translational control of gene expression. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152811310005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715449

Chicago Manual of Style (16^th Edition):

McFarland, Matthew R. “Transfer RNAs as regulatory agents in the translational control of gene expression.” 2016. Doctoral Dissertation, University of Aberdeen. Accessed January 17, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152811310005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715449.

MLA Handbook (7^th Edition):

McFarland, Matthew R. “Transfer RNAs as regulatory agents in the translational control of gene expression.” 2016. Web. 17 Jan 2021.

Vancouver:

McFarland MR. Transfer RNAs as regulatory agents in the translational control of gene expression. [Internet] [Doctoral dissertation]. University of Aberdeen; 2016. [cited 2021 Jan 17]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152811310005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715449.

Council of Science Editors:

McFarland MR. Transfer RNAs as regulatory agents in the translational control of gene expression. [Doctoral Dissertation]. University of Aberdeen; 2016. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152811310005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715449

Washington University in St. Louis

15. Hoynes-O'Connor, Allison. Development and Characterization of Genetic Sensors and Regulators for the Construction of Environmentally-Responsive Genetic Circuits.

Degree: PhD, Energy, Environmental & Chemical Engineering, 2016, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/eng_etds/202

► Genetic circuits enable engineers to program complex logical behaviors into living organisms. Organisms can be programmed to optimize the production of fuels and chemicals,… (more)

Subjects/Keywords: Genetic circuit; Genetic engineering; Genetic regulator; Genetic sensor; RNA regulation; Synthetic biology; Engineering

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hoynes-O'Connor, A. (2016). Development and Characterization of Genetic Sensors and Regulators for the Construction of Environmentally-Responsive Genetic Circuits. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/eng_etds/202

Chicago Manual of Style (16^th Edition):

Hoynes-O'Connor, Allison. “Development and Characterization of Genetic Sensors and Regulators for the Construction of Environmentally-Responsive Genetic Circuits.” 2016. Doctoral Dissertation, Washington University in St. Louis. Accessed January 17, 2021. https://openscholarship.wustl.edu/eng_etds/202.

MLA Handbook (7^th Edition):

Hoynes-O'Connor, Allison. “Development and Characterization of Genetic Sensors and Regulators for the Construction of Environmentally-Responsive Genetic Circuits.” 2016. Web. 17 Jan 2021.

Vancouver:

Hoynes-O'Connor A. Development and Characterization of Genetic Sensors and Regulators for the Construction of Environmentally-Responsive Genetic Circuits. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2016. [cited 2021 Jan 17]. Available from: https://openscholarship.wustl.edu/eng_etds/202.

Council of Science Editors:

Hoynes-O'Connor A. Development and Characterization of Genetic Sensors and Regulators for the Construction of Environmentally-Responsive Genetic Circuits. [Doctoral Dissertation]. Washington University in St. Louis; 2016. Available from: https://openscholarship.wustl.edu/eng_etds/202

University of Utah

16. Updike, Dustin L. An analysis of PHA-4 and its cofactors during pharynx development in C; elegans;.

Degree: PhD, Oncological Sciences;, 2006, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/436/rec/25

► As development progresses, cells become specialized and adopt a regional, cellular, tissue, or organ specific fate. This fate is directed by a specialized group of… (more)

▼ As development progresses, cells become specialized and adopt a regional, cellular, tissue, or organ specific fate. This fate is directed by a specialized group of transcription factors called selector genes. Selector genes act at the top of a hierarchy and orchestrate expression of multiple target genes, thereby enacting developmental differentiation programs. One of these selector genes is the winged helix transcription factor FoxA. FoxA is essential for digestive tract development in all animals that it has been studied. For example, in the nematode Caenorhabditis elegans the FoxA homolog, pha-4, specifies pharyngeal, or foregut, cells. When it is disrupted, cells that would have become the pharynx develop as ectoderm. Despite the importance of FoxA proteins during foregut development, little is known about FoxA regulators and cofactors. To identify cofactors of FoxA, we performed a mutagenesis in C. elegans to screen for loci that interact genetically with pha-4. From this screen, 2 recessive and 11 dominant regulators of PHA-4 expression or activity were identified that suppress lethality associated with a partial loss of pha-4 function. Single nucleotide polymorphisms were used to map the 13 pha-4 suppressors, which showed that at least 9 genes were obtained from the screen. One of the dominant suppressors was identified as an allele of pha-4 itself, which demonstrated the effectiveness of the screen. Next, we looked in depth at a second pha-4 suppressor that was identified as a loss-of-function in the predicted DNA helicase ruvb-1. ruvb-1 is a known component of the Esa1/TIP60 and Swr1/p400 chromatin modifying and remodeling complex in eukaryotes. We investigated the role of chromatin remodeling during pharyngeal development and discovered that homologous components of the Esa1/TIP60 and Swr1/p400 remodeling complex act synergistically with pha-4 by associating the H2A histone variant, HTZ-1/H2AZ, to pharyngeal promoters. These findings are the first to demonstrate an in vivo requirement for chromatin remodeling during foregut development. Finally, we investigated additional phenotypes associated with the ruvb-1 mutant, which resemble mutations in the TOR kinase nutrient sensing pathway in C. elegans. The roles of ruvb-1 and pha-4 in nutrient sensing and metabolism during postembryonic development were examined.

Subjects/Keywords: Genetics; Genetic Regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Updike, D. L. (2006). An analysis of PHA-4 and its cofactors during pharynx development in C; elegans;. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/436/rec/25

Chicago Manual of Style (16^th Edition):

Updike, Dustin L. “An analysis of PHA-4 and its cofactors during pharynx development in C; elegans;.” 2006. Doctoral Dissertation, University of Utah. Accessed January 17, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/436/rec/25.

MLA Handbook (7^th Edition):

Updike, Dustin L. “An analysis of PHA-4 and its cofactors during pharynx development in C; elegans;.” 2006. Web. 17 Jan 2021.

Vancouver:

Updike DL. An analysis of PHA-4 and its cofactors during pharynx development in C; elegans;. [Internet] [Doctoral dissertation]. University of Utah; 2006. [cited 2021 Jan 17]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/436/rec/25.

Council of Science Editors:

Updike DL. An analysis of PHA-4 and its cofactors during pharynx development in C; elegans;. [Doctoral Dissertation]. University of Utah; 2006. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/436/rec/25

University of Alberta

17. Macaulay, Colin G. Regulation of gene expression in Shope fibroma virus.

Degree: PhD, Department of Biochemistry, 1990, University of Alberta

URL: https://era.library.ualberta.ca/files/p2676x290

Subjects/Keywords: Genetic regulation.; Viruses.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Macaulay, C. G. (1990). Regulation of gene expression in Shope fibroma virus. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/p2676x290

Chicago Manual of Style (16^th Edition):

Macaulay, Colin G. “Regulation of gene expression in Shope fibroma virus.” 1990. Doctoral Dissertation, University of Alberta. Accessed January 17, 2021. https://era.library.ualberta.ca/files/p2676x290.

MLA Handbook (7^th Edition):

Macaulay, Colin G. “Regulation of gene expression in Shope fibroma virus.” 1990. Web. 17 Jan 2021.

Vancouver:

Macaulay CG. Regulation of gene expression in Shope fibroma virus. [Internet] [Doctoral dissertation]. University of Alberta; 1990. [cited 2021 Jan 17]. Available from: https://era.library.ualberta.ca/files/p2676x290.

Council of Science Editors:

Macaulay CG. Regulation of gene expression in Shope fibroma virus. [Doctoral Dissertation]. University of Alberta; 1990. Available from: https://era.library.ualberta.ca/files/p2676x290

University of Delaware

18. Shuman, Kevin E. Metabolic and regulatory properties of sulfide oxidation in Chlorobaculum tepidum.

Degree: PhD, University of Delaware, School of Marine Science and Policy, 2016, University of Delaware

URL: http://udspace.udel.edu/handle/19716/17755

► Hydrogen sulfide has a multifaceted way of interacting with life. To humans and some aerobic organisms, sulfide is toxic at low concentrations, but it also… (more)

▼ Hydrogen sulfide has a multifaceted way of interacting with life. To humans and some aerobic organisms, sulfide is toxic at low concentrations, but it also serves as the primary energy source for chemolithoautotrophic based ecosystems like those found at hydrothermal vents, hot springs, and sulfidic caves. Sulfide is produced from the anaerobic degradation of organic matter and is a byproduct of, or waste material from, various industrial operations. Therefore, the development of methods for removing hydrogen sulfide from waste streams is important. Microorganisms that oxidize sulfide, such as the Chlorobi, provide insights into understanding how sulfide can fuel microbial growth in various environments, which could help develop efficient methods for treating sulfide containing waste streams. Chlorobaculum (Cba.) tepidum, an anaerobic photoautotroph preferentially uses sulfide as an electron donor in anoxygenic photosynthesis to fix carbon dioxide into biomass. Three homologs of sulfide:quinone oxidoreductase (SQR), the key sulfide oxidizing enzyme, are encoded by the genome of Cba. tepidum: CT0117, CT0876, and CT1087. SQR can be divided into six types. Each SQR homolog from Cba. tepidum is affiliated with a phylogenetically distinct type of SQR: type IV, type V, and type VI, respectively. Of the three homologs, CT1087 appears to be adapted to high sulfide concentrations since it is required for growth at high sulfide concentrations and is expressed in a sulfide-dependent manner. This dissertation investigates what the physiological roles of each SQR homolog are, and how Cba. tepidum may regulate the sulfide oxidation system. Here I will describe the purification and characterization of a high sulfide adapted SQR homolog encoded by CT1087. Unlike other characterized SQRs, CT1087 has a low affinity for sulfide and high turnover rate. I will also describe a phenotype of a Cba. tepidum strain in which the non-functioning homolog of SQR, encoded by CT0876, was mutagenized. Without CT0876, the sulfide uptake rate of Cba. tepidum is significantly reduced at micromolar sulfide concentrations. The growth of the CT0876 mutant lagged behind the wild type, suggesting it plays a role in increasing the efficiency of sulfide oxidation. Finally, I will describe the role of the putative transcription regulator, encoded by CT1277, in regulating the expression of CT1087. A CT1277 mutant strain of Cba. tepidum expressed CT1087 at significantly higher levels than observed in the wild type indicating that CT1277 functioned as a repressor of CT1087. However, CT1087 expression was still increased in the CT1277 mutant strain after sulfide exposure. These results expand on our understanding of SQR functional diversity by characterizing the first type VI SQR, CT1087, as well as describe a phenotype that suggests a potential functional for a non-sulfide-oxidizing type V SQR, CT0876. These results also identify one of the first transcription regulators involved in sulfide-dependent gene regulation. Advisors/Committee Members: Hanson, Thomas E..

Subjects/Keywords: Chlorobaculum tepidum.; Sulfides – Oxidation.; Genetic regulation.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Shuman, K. E. (2016). Metabolic and regulatory properties of sulfide oxidation in Chlorobaculum tepidum. (Doctoral Dissertation). University of Delaware. Retrieved from http://udspace.udel.edu/handle/19716/17755

Chicago Manual of Style (16^th Edition):

Shuman, Kevin E. “Metabolic and regulatory properties of sulfide oxidation in Chlorobaculum tepidum.” 2016. Doctoral Dissertation, University of Delaware. Accessed January 17, 2021. http://udspace.udel.edu/handle/19716/17755.

MLA Handbook (7^th Edition):

Shuman, Kevin E. “Metabolic and regulatory properties of sulfide oxidation in Chlorobaculum tepidum.” 2016. Web. 17 Jan 2021.

Vancouver:

Shuman KE. Metabolic and regulatory properties of sulfide oxidation in Chlorobaculum tepidum. [Internet] [Doctoral dissertation]. University of Delaware; 2016. [cited 2021 Jan 17]. Available from: http://udspace.udel.edu/handle/19716/17755.

Council of Science Editors:

Shuman KE. Metabolic and regulatory properties of sulfide oxidation in Chlorobaculum tepidum. [Doctoral Dissertation]. University of Delaware; 2016. Available from: http://udspace.udel.edu/handle/19716/17755

University of Houston

19. Davis, Joshua Tyler 1985-. Genetic Regulation of Retinal Cells by Variation of Underlying Elastic Modulus.

Degree: PhD, Physics, 2013, University of Houston

URL: http://hdl.handle.net/10657/951

► A major breakthrough in the development of engineering hydrogels for regenerative medicine occurred when it was noticed that when cells are plated on substrates of… (more)

▼ A major breakthrough in the development of engineering hydrogels for regenerative medicine occurred when it was noticed that when cells are plated on substrates of different stiffnesses undergo certain conformational changes in their cytoskeleton. Specifically, the tension in cytoskeleton of the cells on the substrates increased with stiffness. Many different cell types were noted to have a larger spread area and the presence of stress fibers. This was called, by Donald Ingber and Buckminster Fuller, tensegrity and is likened to a tent erected in different soils. The tent poles act as the skeleton with the outer covering as the membrane, the poles create tension on the pegs and, if they are not planted in firm ground, the tent snaps back. It has also been shown that pluripotent cells will develop into different specialized cells purely under the influence of substrate stiffness. This finding implies an alteration of the genetic regulation arising from the tension in the cytoskeleton. Hence, a structure that does not exist inside the nucleus is changing the transcription of DNA. How this non-chemical signaling occurs, as well as which genes are affected in which cells and what stiffness levels trigger these changes, is now what needs to be investigated. We began working with a retinal cell line to see if these unique cells change genetic expression in the same way, which might help to explain the buildup of scar tissue in the retina after reattachment surgery. This scar tissue (proliferative vitreoretiopathy), in many cases, leads to secondary retinal detachments. We discovered that there were many changes, both physically and genetically, that Müller cells undergo when exposed to varying levels of substrate stiffness. Changes found include varying expression of different extracellular matrix genes, an inverse relationship between the amount of phagocytosis and substrate stiffness, and determining that not only is protein expression of the cells different across substrates, the time of peak expression varies. Advisors/Committee Members: Foster, William J. (advisor), Pinsky, Lawrence S. (committee member), Miller, John H. (committee member), Otteson, Deborah C. (committee member).

Subjects/Keywords: Biophysics; Material Science; Genetic Regulation; Retina; Physics

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Davis, J. T. 1. (2013). Genetic Regulation of Retinal Cells by Variation of Underlying Elastic Modulus. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/951

Chicago Manual of Style (16^th Edition):

Davis, Joshua Tyler 1985-. “Genetic Regulation of Retinal Cells by Variation of Underlying Elastic Modulus.” 2013. Doctoral Dissertation, University of Houston. Accessed January 17, 2021. http://hdl.handle.net/10657/951.

MLA Handbook (7^th Edition):

Davis, Joshua Tyler 1985-. “Genetic Regulation of Retinal Cells by Variation of Underlying Elastic Modulus.” 2013. Web. 17 Jan 2021.

Vancouver:

Davis JT1. Genetic Regulation of Retinal Cells by Variation of Underlying Elastic Modulus. [Internet] [Doctoral dissertation]. University of Houston; 2013. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/10657/951.

Council of Science Editors:

Davis JT1. Genetic Regulation of Retinal Cells by Variation of Underlying Elastic Modulus. [Doctoral Dissertation]. University of Houston; 2013. Available from: http://hdl.handle.net/10657/951

Columbia University

20. Corrigan, David Joseph. Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis.

Degree: 2018, Columbia University

URL: https://doi.org/10.7916/D8S19K1D

► PRDM16 is a transcriptional co-regulator that is highly expressed in HSCs and required for their maintenance. It is also involved in translocations in acute myeloid… (more)

▼ PRDM16 is a transcriptional co-regulator that is highly expressed in HSCs and required for their maintenance. It is also involved in translocations in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS) and T-cell acute lymphoblastic leukemia. Prdm16 is expressed as both full-length (f Prdm16) and short-length (s-Prdm16) isoforms, the latter lacking an N-terminal PR domain homologous to SET methyltransferase domains. The roles of both isoforms in normal and malignant hematopoiesis are unclear. In chromosomal rearrangements involving PRDM16, the PR domain is deleted. Furthermore, overexpression of s-Prdm16, but not f-Prdm16, can cause leukemia in a p53-/- background predisposed to malignancy. Based on this, s-Prdm16 has been proposed as an oncogene whereas f-Prdm16 has been suggested to possess tumor suppressor activity. The aim of this thesis was to more clearly elucidate the role of each Prdm16 isoform in normal and malignant hematopoiesis. We first showed that Prdm16 is essential for adult HSC maintenance using a conditional deletion mouse model specific for hematopoietic cells, as previous findings using an embryonic-lethal global Prdm16-/- mouse demonstrated this only in fetal liver. We then found, using a specific f-Prdm16-/- mouse model, that full-length Prdm16 is essential for HSC maintenance and induces multiple genes involved in GTPase signaling and represses inflammation. Based on a comparison of Prdm16-/- HSCs lacking both isoforms, and f-Prdm16-/- HSCs which express s-Prdm16, we were able to infer some hematopoietic properties of s-Prdm16 – namely that this isoform induces inflammatory gene expression and supports development of a Lineage-Sca1+cKit- lymphoid progenitor distinct from CLPs which predominantly differentiates into marginal zone B cells. s-Prdm16 expression alone, however, was not sufficient to maintain HSCs. We used a mouse model of human MLL-AF9 leukemia and found that leukemia derived from Prdm16-deficient HSCs had extended latency, although expression of Prdm16 decreases during MLL-AF9 transformation and is undetectable in ex vivo leukemic cells. Forced expression of f-Prdm16 in these cells further extended leukemic latency, while forced expression of s-Prdm16 shortened latency. Gene expression profiling using RNAseq indicated that forced expression of f-Prdm16 resulted in altered respiratory metabolism of MLL-AF9 cells, whereas expression of s-Prdm16 induced a strong inflammatory gene signature, comparable to that seen in HSCs expressing only s-Prdm16. Several inflammatory cytokines and chemokines induced by s-Prdm16 are associated with MDS and with a worse prognosis in human AML. Furthermore, leukemia expressing s-Prdm16 had an elevated number of cells with abnormal nuclei, characteristic of dysplasia. Finally, we performed an analysis of PRDM16 in human AML from the publically-available Cancer Genome Atlas dataset, containing clinical and gene expression data for 179 cases of AML. PRDM16 expression negatively correlated with overall survival, both in the…

Subjects/Keywords: Immunology; Microbiology; Hematopoiesis; Genetic transcription – Regulation; Proteins

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Corrigan, D. J. (2018). Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8S19K1D

Chicago Manual of Style (16^th Edition):

Corrigan, David Joseph. “Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis.” 2018. Doctoral Dissertation, Columbia University. Accessed January 17, 2021. https://doi.org/10.7916/D8S19K1D.

MLA Handbook (7^th Edition):

Corrigan, David Joseph. “Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis.” 2018. Web. 17 Jan 2021.

Vancouver:

Corrigan DJ. Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis. [Internet] [Doctoral dissertation]. Columbia University; 2018. [cited 2021 Jan 17]. Available from: https://doi.org/10.7916/D8S19K1D.

Council of Science Editors:

Corrigan DJ. Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis. [Doctoral Dissertation]. Columbia University; 2018. Available from: https://doi.org/10.7916/D8S19K1D

Columbia University

21. Chen, Yaqiong. Studies on RNA Regulation: From Enhancer RNAs to RBBP6 Isoform3.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-e3p7-st32

► This dissertation contains two separate yet interconnected pieces of work, which shed light on the complicated RNA regulatory mechanism. The first part, as the main… (more)

▼ This dissertation contains two separate yet interconnected pieces of work, which shed light on the complicated RNA regulatory mechanism. The first part, as the main focus of the thesis, characterizes a large pool of human polyadenylated enhancer RNA under deficient nuclear surveillance conditions, and investigates their metabolism mechanisms. The second part elucidates the dynamic localization mechanism of RBBP6 isoform3, which inhibits pre-mRNA 3’ processing by completing with RBBP6 isoform1. Despite being composed of approximately 3 billion base pairs, only 1 to 2% of the human genome codes for proteins. The non-coding DNA regions can however function as transcription units and generate non-coding RNAs such as enhancer-derived RNAs, or eRNAs, that play crucial roles in gene expression regulation, cell differentiation, development, and diseases. Previous studies have suggested that most eRNAs are transcribed by RNA polymerase II (RNAP II), but not polyadenylated. In Chapter 3, I identify a large fraction of polyadenylated enhancer RNAs under deficient nuclear surveillance conditions via genome-wide analyses, and explore their biogenesis and degradation mechanisms. I find that the Integrator complex plays an important role in polyadenylated eRNA biogenesis, and that their exosome-dependent degradation requires two cofactor complexes containing the RNA helicase Mtr4: the PAXT/PPC complex and the NEXT complex. Additionally, the canonical poly(A) polymerases PAP-α and PAP-γ play a major role in the 3’ end processing of pA+ eRNA. Finally, I show that under deficient nuclear surveillance conditions, pA+ eRNAs accumulate in the cytoplasm and associate with polysomes, suggesting that at least some might have translation potential. I also contributed to the discovery of two novel complexes both containing the RNA helicase Mtr4, which is a master player of the nuclear surveillance system. Mtr4 and ZFC3H1 form the PAXT/PPC complex, which facilitates the turnover of polyadenylated nuclear RNAs, including prematurely terminated RNAs (ptRNAs), upstream antisense RNAs (uaRNAs), and eRNAs (see the paper in Appendix II). Mtr4 also associates with NRDE2 to form a complex, functioning in the DNA damage response pathway (see the paper in Appendix III). These works provide additional insights into the complexity and significance of the RNA helicase Mtr4. In the second part of the thesis, presented in Chapter 4, I studied a polyadenylation factor known as Retinoblastoma-binding protein 6 (RBBP6). RBBP6 was initially identified as a large multidomain protein, interacting with tumor suppressors p53 and Rb. Later, its diverse roles were uncovered in cell cycle progression, apoptosis, nucleic acid metabolism, differentiation, and mRNA processing. RBBP6 protein has four isoforms, among which the shortest isoform, iso3, has only one domain: the DWNN (Domain With No Name) domain. The DWNN domain displays high similarities with ubiquitin, implying its function as a novel ubiquitin-like modifier. However, I show that the DWNN…

Subjects/Keywords: Molecular biology; RNA; Genetic regulation; Biology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chen, Y. (2019). Studies on RNA Regulation: From Enhancer RNAs to RBBP6 Isoform3. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-e3p7-st32

Chicago Manual of Style (16^th Edition):

Chen, Yaqiong. “Studies on RNA Regulation: From Enhancer RNAs to RBBP6 Isoform3.” 2019. Doctoral Dissertation, Columbia University. Accessed January 17, 2021. https://doi.org/10.7916/d8-e3p7-st32.

MLA Handbook (7^th Edition):

Chen, Yaqiong. “Studies on RNA Regulation: From Enhancer RNAs to RBBP6 Isoform3.” 2019. Web. 17 Jan 2021.

Vancouver:

Chen Y. Studies on RNA Regulation: From Enhancer RNAs to RBBP6 Isoform3. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Jan 17]. Available from: https://doi.org/10.7916/d8-e3p7-st32.

Council of Science Editors:

Chen Y. Studies on RNA Regulation: From Enhancer RNAs to RBBP6 Isoform3. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-e3p7-st32

Columbia University

22. Stupnikov, Maria Rose. Genetic regulation of pulmonary progenitor cell differentiation.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-kgxh-ga80

► The respiratory system represents a major interface between the body and the external environment. Its design includes a tree-like network of conducting tubules (airways) that… (more)

▼ The respiratory system represents a major interface between the body and the external environment. Its design includes a tree-like network of conducting tubules (airways) that carries air to millions of alveoli, where gas exchange occurs. The conducting airways are characterized by their great diversity in epithelial cell types with multiple populations of secretory, multiciliated, and neuroendocrine cells. How these different cell types arise and how these populations are balanced are questions still not well understood. Aberrant patterns of airway epithelial differentiation have been described in various human pulmonary diseases, chronic bronchitis, asthma, neuroendocrine hyperplasia of infancy, and others. The goal of this thesis is to investigate mechanisms of regulation of airway epithelial cell fate in the developing lung epithelium. More specifically, these studies focus on Notch signaling and address a long unresolved issue whether the different Notch ligands (Jagged and Delta) have distinct roles in the epithelial differentiation program of the extrapulmonary and intrapulmonary airways. Moreover, these studies investigate the ontogeny of the bHLH transcription factor Ascl1 and identify its targets in the developing airways as potential regulators of neuroepithelial body (NEB) size and maturation. My studies provide evidence that the Notch ligand families Jag and Dll are required for the specification and formation of different cell lineages in the developing airway epithelia. Jag ligands regulate multiciliated versus secretory (club) cell fates but also controls abundance of basal cell progenitors in extrapulmonary airways. Dll ligands regulate pulmonary neuroendocrine versus club cell fates in intrapulmonary airways. Analysis of mouse mutants showed that loss of Jag ligands has minimal impact on the size or abundance of NEBs and their associated secretory cells while loss of Dll ligands results in an expansion of NEB size and associated cells. To gain additional insights into the potential mechanisms of how neuroendocrine cells develop and undergo aberrant hyperplasia, I characterized the global transcriptional profile of embryonic lungs from mice deficient in Ascl1, which lack NEBs and neuroendocrine cells and identified a number of genes associated with neuroendocrine cell development, maturation, and the NEB microenvironment. Among these genes, components of the catecholamine biosynthesis pathway, such as tyrosine hydroxylase (Th), a key enzyme for catecholamine production, were downregulated in Ascl1 null lungs. Subsequent functional analysis using a pharmacological inhibitor of this pathway in lung organ cultures showed expansion of pulmonary neuroendocrine cells and NEB size, an observation of potential relevance in human diseases in which neuroendocrine cells are aberrantly expanded. Together these studies highlight the distinct role of Notch ligands and further implicate Ascl1 targets, as illustrated by catecholamine pathway components, in regulating epithelial cell fate. Further…

Subjects/Keywords: Genetic regulation; Stem cells; Cell differentiation; Lungs

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Stupnikov, M. R. (2019). Genetic regulation of pulmonary progenitor cell differentiation. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-kgxh-ga80

Chicago Manual of Style (16^th Edition):

Stupnikov, Maria Rose. “Genetic regulation of pulmonary progenitor cell differentiation.” 2019. Doctoral Dissertation, Columbia University. Accessed January 17, 2021. https://doi.org/10.7916/d8-kgxh-ga80.

MLA Handbook (7^th Edition):

Stupnikov, Maria Rose. “Genetic regulation of pulmonary progenitor cell differentiation.” 2019. Web. 17 Jan 2021.

Vancouver:

Stupnikov MR. Genetic regulation of pulmonary progenitor cell differentiation. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Jan 17]. Available from: https://doi.org/10.7916/d8-kgxh-ga80.

Council of Science Editors:

Stupnikov MR. Genetic regulation of pulmonary progenitor cell differentiation. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-kgxh-ga80

Hong Kong University of Science and Technology

23. Ip, Pak Kan. Characterizing the functional roles of α2-chimaerin in the development of cerebral cortex.

Degree: 2012, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-65735 ; https://doi.org/10.14711/thesis-b1169572 ; http://repository.ust.hk/ir/bitstream/1783.1-65735/1/th_redirect.html

► Proper functioning of the nervous system depends on the correct positioning of neurons, establishment of axon-dendrite polarity, formation of neural circuits and maintenance of the… (more)

▼ Proper functioning of the nervous system depends on the correct positioning of neurons, establishment of axon-dendrite polarity, formation of neural circuits and maintenance of the wired neural circuits. These steps are critically controlled by various molecular signaling pathways. Defect in any of these processes greatly impair neural functions. In particular, defects in neuronal migration are associated with various neurological disorders in human including lissencephaly (smooth brain), cortical heterotopias (double cortex), microcephaly (small brain) and autism (Gleeson, 2000; Hashimoto-Torii et al., 2008; Manent et al., 2009). These clinical observations highlight the importance of the precise neuronal positioning and organization during the development of the nervous system. Nonetheless, little is known about how neuronal migration is regulated in vivo and the molecular mechanisms underlying the regulation of neuronal polarization during neuronal migration remain to be elucidated. Signaling proteins that regulate cytoskeletal dynamics are suggested to be involved in neuronal polarization and migration. In the present study, I identify α2-chimaerin as an essential regulator in neuronal migration and laminar positioning of the cortex. α2-chimaerin is highly expressed in the intermediate zone (IZ) and cortical plate (CP) of the cerebral cortex during developmental stage. Knockdown of α2-chimaerin in utero arrests neurons in the IZ with abnormal polarity. By live-imaging analysis, I show that α2-chimaerin regulates the multipolar-to-bipolar transition of migrating neurons. α2-chimaerin-depleted neurons show reduced neurite dynamics as well as impaired neuronal migration. Knockdown of α2-chimaerin in utero leads to the formation of a heterotopic band of neurons in the subcortical white matter in postnatal mice. Mice with such migration defects display imbalanced excitation/inhibition of local cortical circuitry, and exhibit increased susceptibility to convulsant-induced seizures. I further demonstrate the functional importance of the SH2 domain-mediated association of α2-chimaerin in neuronal migration. α2-chimaerin binds to Trk receptors and modulates neurotrophin-mediated Trk signaling. Importantly, α2-chimaerin regulates bipolar transition and neuronal migration through modulating the activity of collapsin response mediator protein-2 (CRMP-2), a microtubule-associated protein. These findings establish a new α2-chimaerin-dependent mechanism underlying neuronal migration and proper functioning of the cerebral cortex, and provide significant insights into understanding the pathogenesis of seizure-related neurodevelopmental disorders.

Subjects/Keywords: Cerebral cortex ; Growth ; Genetic regulation ; Proteins ; Analysis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ip, P. K. (2012). Characterizing the functional roles of α2-chimaerin in the development of cerebral cortex. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-65735 ; https://doi.org/10.14711/thesis-b1169572 ; http://repository.ust.hk/ir/bitstream/1783.1-65735/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ip, Pak Kan. “Characterizing the functional roles of α2-chimaerin in the development of cerebral cortex.” 2012. Thesis, Hong Kong University of Science and Technology. Accessed January 17, 2021. http://repository.ust.hk/ir/Record/1783.1-65735 ; https://doi.org/10.14711/thesis-b1169572 ; http://repository.ust.hk/ir/bitstream/1783.1-65735/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ip, Pak Kan. “Characterizing the functional roles of α2-chimaerin in the development of cerebral cortex.” 2012. Web. 17 Jan 2021.

Vancouver:

Ip PK. Characterizing the functional roles of α2-chimaerin in the development of cerebral cortex. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2012. [cited 2021 Jan 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-65735 ; https://doi.org/10.14711/thesis-b1169572 ; http://repository.ust.hk/ir/bitstream/1783.1-65735/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ip PK. Characterizing the functional roles of α2-chimaerin in the development of cerebral cortex. [Thesis]. Hong Kong University of Science and Technology; 2012. Available from: http://repository.ust.hk/ir/Record/1783.1-65735 ; https://doi.org/10.14711/thesis-b1169572 ; http://repository.ust.hk/ir/bitstream/1783.1-65735/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

24. Ip, Kelvin Ka Kay. Systematic analysis of cis-acting element of a transcription factor regulating C. elegans ray assembly - tbx-2.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-62361 ; https://doi.org/10.14711/thesis-b1254481 ; http://repository.ust.hk/ir/bitstream/1783.1-62361/1/th_redirect.html

► C. elegans male tail consists of nine lateral sensory organs called rays, embedded in a fan structure. The sensory rays go through a rapid developmental… (more)

▼ C. elegans male tail consists of nine lateral sensory organs called rays, embedded in a fan structure. The sensory rays go through a rapid developmental process involving multiple steps - cell fate choice, patterning, ray lineage execution, assembly and morphogenesis. From a previous genome-wide RNAi screen for genes acting in ray development, a T-box transcription factor, tbx-2, was identified to be required for the ray assembly process. Mutation of tbx-2 results in a failure of ray constituent cells to assemble into a ray, creating a ray loss phenotype. While tbx-2 mutant displays ray loss in all rays, tbx-2 is expressed in the structural cells of ray 1, 5, and 7 and ray neuronal B of ray 4 only. We are interested in understanding how such expression pattern arises, what factors are regulating tbx-2 expression pattern and ultimately, how a regulatory cascade controlling ray lineage and ray patterning work. Previous study have identified that tbx-2 directly auto-represses its expression in all rays by binding on cis-regulatory elements on its gene. However, this by itself cannot account for the initiation of the expression as well as the generation of expression pattern of the tbx-2 which is restricted to rays 1, 5, 7. Multiple transcription factors were hypothesised to account for the pattern. A systematic mapping of the cis-regulatory elements in combination of phylogenetic mapping would be employed to identify putative transcription factor binding sites (TFBS), which would allow for the identification of candidate regulatory genes that could be tested by genetic analyses. Since ray structural cell is shown to be responsible for ray assembly process (Zhang, Emmons, 1996), I focused my study on identifying the regulatory elements responsible for tbx-2 expression in the ray structural cells. A systematic deletion mapping was carried out on the transcriptional reporter of tbx-2 to identify cis-acting elements that control the expression of tbx-2. A 138bp region region located 3’ to the tbx-2 coding region was identified to be required and sufficient to drive expression in structural cells of ray 1, 5, 7. I identified 2 conserved motifs within this 138bp region that are essential for the expression. In-silico search for TFBS in the motifs identified conserved homeobox protein biding sites (HBS) in each of them with their function verified in mutant analysis. Since HBS were identified in the cis-regulatory element, tbx-2 transcriptional reporter activity was examined in knockdown worms of homeobox genes previously known to affect ray development. Among seven homeobox genes tested, two homeobox genes, unc-62 and ceh-20, were found to be required for the activation of tbx-2 transcription reporter. Knockdown of these 2 genes result in ray loss and ray 6-4 fusion. unc-62 encodes a TALE homeodomain protein known to form heterodimer with PBX (ceh-20). We therefore hypothesize that unc-62 and ceh-20 regulate tbx-2 by forming hetero-dimer. Expression pattern of unc-62 and ceh-20 in male tail was examined. Ultimately we would…

Subjects/Keywords: Caenorhabditis elegans ; Genetics ; Genetic transcription ; Regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ip, K. K. K. (2013). Systematic analysis of cis-acting element of a transcription factor regulating C. elegans ray assembly - tbx-2. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-62361 ; https://doi.org/10.14711/thesis-b1254481 ; http://repository.ust.hk/ir/bitstream/1783.1-62361/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ip, Kelvin Ka Kay. “Systematic analysis of cis-acting element of a transcription factor regulating C. elegans ray assembly - tbx-2.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed January 17, 2021. http://repository.ust.hk/ir/Record/1783.1-62361 ; https://doi.org/10.14711/thesis-b1254481 ; http://repository.ust.hk/ir/bitstream/1783.1-62361/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ip, Kelvin Ka Kay. “Systematic analysis of cis-acting element of a transcription factor regulating C. elegans ray assembly - tbx-2.” 2013. Web. 17 Jan 2021.

Vancouver:

Ip KKK. Systematic analysis of cis-acting element of a transcription factor regulating C. elegans ray assembly - tbx-2. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Jan 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-62361 ; https://doi.org/10.14711/thesis-b1254481 ; http://repository.ust.hk/ir/bitstream/1783.1-62361/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ip KKK. Systematic analysis of cis-acting element of a transcription factor regulating C. elegans ray assembly - tbx-2. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-62361 ; https://doi.org/10.14711/thesis-b1254481 ; http://repository.ust.hk/ir/bitstream/1783.1-62361/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

25. Liu, Yunle LIFS. Transcriptional regulation of acetylcholinesterase by targeting various transcriptional factors in different cell types.

Degree: 2018, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-98261 ; https://doi.org/10.14711/thesis-991012697269203412 ; http://repository.ust.hk/ir/bitstream/1783.1-98261/1/th_redirect.html

► Acetylcholinesterase (AChE) is known to be vital in life maintenance for terminating cholinergic transmission. By alternative splicing, AChE is synthesized in four different isoforms, and… (more)

▼ Acetylcholinesterase (AChE) is known to be vital in life maintenance for terminating cholinergic transmission. By alternative splicing, AChE is synthesized in four different isoforms, and which are readthrough (AChE_R), hydrophobic (AChE_H), soluble (AChE_S) and tailed (AChE_T) forms. In the brain and muscles, AChE_T is the major form and plays an important role in nervous system. The comprehensive function of AChE_T depends on a tight interaction between its C-terminal peptide with the anchoring protein collagen tail (ColQ) to form asymmetric enzyme or proline-rich membrane anchor (PRiMA) to form tetrameric membrane bond enzyme. The expression of AChE subunits in different tissues has been studied in detail, and transcriptional regulation appears to be the major feature in controlling the expression associated with various cellular activities. The binding sites of different transcriptional factors on mammalian AChE gene have proposed various functions of this enzyme in specific cell type. However, the regulation of AChE by cAMP response element-binding protein (CREB) and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) have not been fully identified, particularly the regulation mediated by these factors in different cell types. Genistein, 4’,5,7-trihydroxyisoflavone, a major isoflavone in soybean, is known as phytoestrogen having known benefit to brain functions. In cultured PC12 cells, application of genistein significantly induced the expression of neurofilaments, markers for neuronal differentiation. In parallel, the expression of tetrameric form of proline-rich membrane anchor (PRiMA)-linked AChE (G₄ AChE), a key isoform in the brain, was induced in a dose-dependent manner: this induction included the associated protein PRiMA. The genistein-induced AChE expression was fully blocked by pre-treatment of H89 (an inhibitor of protein kinase A, PKA) and G15 (a selective G protein-coupled receptor 30 (GPR 30) antagonist) in the cultures, suggesting a direct involvement of a membrane-bound estrogen receptor, named as GPR 30 in the cultures. In parallel, the estrogen-induced activation of GPR 30 induced AChE expression in a dose-dependent manner. The genistein/estrogen-induced the phosphorylation of CREB, which subsequently triggered a cyclic AMP responding element (CRE) located on the ACHE gene promoter. The binding of this CRE site by CREB induced ACHE gene transcription. Thus, the activation of GPR 30 could be one way for estrogen or flavonoids, possessing estrogenic properties, to enhance cholinergic functions in the brain via CREB transcription factor. Protein assembly of oligomeric AChE could be affected by chaperons. Many AChE inhibitors (AChEIs) could act as chemical chaperons. In cultured neuroblastoma (NG108-15) or cortical neurons, application of AChEIs, including tacrine (Cognex), rivastigmine (Exelon), but not donepezil (Aricept), caused a beatable amount of AChE in NG108-15 cell surface by immunofluorescence…

Subjects/Keywords: Acetylcholinesterase ; Regulation ; Cellular signal transduction ; Genetic transcription

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Liu, Y. L. (2018). Transcriptional regulation of acetylcholinesterase by targeting various transcriptional factors in different cell types. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-98261 ; https://doi.org/10.14711/thesis-991012697269203412 ; http://repository.ust.hk/ir/bitstream/1783.1-98261/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Liu, Yunle LIFS. “Transcriptional regulation of acetylcholinesterase by targeting various transcriptional factors in different cell types.” 2018. Thesis, Hong Kong University of Science and Technology. Accessed January 17, 2021. http://repository.ust.hk/ir/Record/1783.1-98261 ; https://doi.org/10.14711/thesis-991012697269203412 ; http://repository.ust.hk/ir/bitstream/1783.1-98261/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Liu, Yunle LIFS. “Transcriptional regulation of acetylcholinesterase by targeting various transcriptional factors in different cell types.” 2018. Web. 17 Jan 2021.

Vancouver:

Liu YL. Transcriptional regulation of acetylcholinesterase by targeting various transcriptional factors in different cell types. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2018. [cited 2021 Jan 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-98261 ; https://doi.org/10.14711/thesis-991012697269203412 ; http://repository.ust.hk/ir/bitstream/1783.1-98261/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Liu YL. Transcriptional regulation of acetylcholinesterase by targeting various transcriptional factors in different cell types. [Thesis]. Hong Kong University of Science and Technology; 2018. Available from: http://repository.ust.hk/ir/Record/1783.1-98261 ; https://doi.org/10.14711/thesis-991012697269203412 ; http://repository.ust.hk/ir/bitstream/1783.1-98261/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Michigan State University

26. Roehl, Holger Harald Helmut. Regulation of the human thymidine kinase gene promoter in serum stimulated and SV40 infected cells.

Degree: PhD, Department of Microbiology and Public Health, 1991, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:22965

Subjects/Keywords: Thymidine; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Roehl, H. H. H. (1991). Regulation of the human thymidine kinase gene promoter in serum stimulated and SV40 infected cells. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:22965

Chicago Manual of Style (16^th Edition):

Roehl, Holger Harald Helmut. “Regulation of the human thymidine kinase gene promoter in serum stimulated and SV40 infected cells.” 1991. Doctoral Dissertation, Michigan State University. Accessed January 17, 2021. http://etd.lib.msu.edu/islandora/object/etd:22965.

MLA Handbook (7^th Edition):

Roehl, Holger Harald Helmut. “Regulation of the human thymidine kinase gene promoter in serum stimulated and SV40 infected cells.” 1991. Web. 17 Jan 2021.

Vancouver:

Roehl HHH. Regulation of the human thymidine kinase gene promoter in serum stimulated and SV40 infected cells. [Internet] [Doctoral dissertation]. Michigan State University; 1991. [cited 2021 Jan 17]. Available from: http://etd.lib.msu.edu/islandora/object/etd:22965.

Council of Science Editors:

Roehl HHH. Regulation of the human thymidine kinase gene promoter in serum stimulated and SV40 infected cells. [Doctoral Dissertation]. Michigan State University; 1991. Available from: http://etd.lib.msu.edu/islandora/object/etd:22965

Michigan State University

27. Carozza, Marc A. Regulation and subcellular localization of human thymidine kinase protein.

Degree: MS, Department of Microbiology/Cell and Molecular Biology Program, 1993, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:16547

Subjects/Keywords: Thymidine; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Carozza, M. A. (1993). Regulation and subcellular localization of human thymidine kinase protein. (Masters Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:16547

Chicago Manual of Style (16^th Edition):

Carozza, Marc A. “Regulation and subcellular localization of human thymidine kinase protein.” 1993. Masters Thesis, Michigan State University. Accessed January 17, 2021. http://etd.lib.msu.edu/islandora/object/etd:16547.

MLA Handbook (7^th Edition):

Carozza, Marc A. “Regulation and subcellular localization of human thymidine kinase protein.” 1993. Web. 17 Jan 2021.

Vancouver:

Carozza MA. Regulation and subcellular localization of human thymidine kinase protein. [Internet] [Masters thesis]. Michigan State University; 1993. [cited 2021 Jan 17]. Available from: http://etd.lib.msu.edu/islandora/object/etd:16547.

Council of Science Editors:

Carozza MA. Regulation and subcellular localization of human thymidine kinase protein. [Masters Thesis]. Michigan State University; 1993. Available from: http://etd.lib.msu.edu/islandora/object/etd:16547

University of Aberdeen

28. Khanolkar, Rahul Chaitanya. Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells.

Degree: PhD, 2013, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152284350005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589494

► The leukocyte immunoglobulin like receptors (LILRs) are a group of receptors with immunomodulatory effects. Group 1 LILRs comprise of LILRB1, among others, and bind to… (more)

Subjects/Keywords: 616.07; Immunosuppression; Dendritic cells; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Khanolkar, R. C. (2013). Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152284350005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589494

Chicago Manual of Style (16^th Edition):

Khanolkar, Rahul Chaitanya. “Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells.” 2013. Doctoral Dissertation, University of Aberdeen. Accessed January 17, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152284350005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589494.

MLA Handbook (7^th Edition):

Khanolkar, Rahul Chaitanya. “Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells.” 2013. Web. 17 Jan 2021.

Vancouver:

Khanolkar RC. Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells. [Internet] [Doctoral dissertation]. University of Aberdeen; 2013. [cited 2021 Jan 17]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152284350005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589494.

Council of Science Editors:

Khanolkar RC. Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells. [Doctoral Dissertation]. University of Aberdeen; 2013. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152284350005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589494

University of Aberdeen

29. Johansson, Petronella. Characterisation of putative dendritic cell markers in salmonids and modulation of gene expression following stimulation with interleukin-4/13.

Degree: PhD, 2014, University of Aberdeen

URL: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152796910005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633290

► Dendritic cells (DCs) are leukocytes specialized in antigen presentation. As competent stimulators of naive T lymphocytes, they link the innate and adaptive immune responses of… (more)

▼ Dendritic cells (DCs) are leukocytes specialized in antigen presentation. As competent stimulators of naive T lymphocytes, they link the innate and adaptive immune responses of vertebrates. The RAG-mediated adaptive immune system appeared approximately 500 million years ago in jawed fish and a number of studies suggest that DCs exist in bony and cartilaginous fish. However, the exact role of DCs in the fish immune system is not determined and questions remain as to whether a cell type truly homologous to DCs in homeotherms does exist. My project aimed to identify potential DCs surface markers (CD209A and LAMP3) in rainbow trout (Oncorhynchus mykiss) leukocytes for evaluation of the expression patterns by qRT-PCR under different conditions and stimuli, in vitro and in vivo. Another goal was to validate and evaluate the specificity of a produced anti-trout CD209A polyclonal antibody to further characterise antigen presenting cells (APCs) in fish. The methodology was to look for up-regulation of the predicted markers together with other markers known to be expressed by DCs in mammals and to evaluate at the mRNA and protein expression level after in vitro stimulation of trout primary leukocytes with trout rIL-4/13. Trout CD209A and LAMP3 mRNA was expressed in the main lymphoid organs of fish and could be modulated with microbial mimics. Upon in vitro stimulation of trout primary leukocytes with trout rIL-4/13, trout CD209A mRNA expression was up-regulated together with both CD83 and the MHC class II chain known to be expressed by mammalian DCs. In addition, CD209A protein expression was highly induced by trout rIL-4/13. Taken together, these results suggests that the characterisation of DCs in trout with tools such as transcript evaluation of surface markers and the anti-trout CD209A antibody, could help to more precisely define these leukocyte subsets. These findings could have further impact on fish vaccine improvements and be of importance for the aquaculture industry, by optimising stimulation of adaptive immunity.

Subjects/Keywords: 590; Dendritic cells; Salmonidae; Genetic regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Johansson, P. (2014). Characterisation of putative dendritic cell markers in salmonids and modulation of gene expression following stimulation with interleukin-4/13. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152796910005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633290

Chicago Manual of Style (16^th Edition):

Johansson, Petronella. “Characterisation of putative dendritic cell markers in salmonids and modulation of gene expression following stimulation with interleukin-4/13.” 2014. Doctoral Dissertation, University of Aberdeen. Accessed January 17, 2021. https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152796910005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633290.

MLA Handbook (7^th Edition):

Johansson, Petronella. “Characterisation of putative dendritic cell markers in salmonids and modulation of gene expression following stimulation with interleukin-4/13.” 2014. Web. 17 Jan 2021.

Vancouver:

Johansson P. Characterisation of putative dendritic cell markers in salmonids and modulation of gene expression following stimulation with interleukin-4/13. [Internet] [Doctoral dissertation]. University of Aberdeen; 2014. [cited 2021 Jan 17]. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152796910005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633290.

Council of Science Editors:

Johansson P. Characterisation of putative dendritic cell markers in salmonids and modulation of gene expression following stimulation with interleukin-4/13. [Doctoral Dissertation]. University of Aberdeen; 2014. Available from: https://eu03.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152796910005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633290

Montana State University

30. Hisey, Bennett Stephen. The role of SaeR/S in secondary Staphylococcus aureus Pneumonia.

Degree: MS, College of Agriculture, 2016, Montana State University

URL: https://scholarworks.montana.edu/xmlui/handle/1/14625

► Methicillin?resistant Staphylococcus aureus (MRSA) is a Gram?positive pathogen capable of causing diverse disease in humans. MRSA precisely controls virulence factor expression via the SaeR/S two?component… (more)

Subjects/Keywords: Staphylococcus aureus.; Lungs.; Diseases.; Genetic regulation.; Influenza.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hisey, B. S. (2016). The role of SaeR/S in secondary Staphylococcus aureus Pneumonia. (Masters Thesis). Montana State University. Retrieved from https://scholarworks.montana.edu/xmlui/handle/1/14625

Chicago Manual of Style (16^th Edition):

Hisey, Bennett Stephen. “The role of SaeR/S in secondary Staphylococcus aureus Pneumonia.” 2016. Masters Thesis, Montana State University. Accessed January 17, 2021. https://scholarworks.montana.edu/xmlui/handle/1/14625.

MLA Handbook (7^th Edition):

Hisey, Bennett Stephen. “The role of SaeR/S in secondary Staphylococcus aureus Pneumonia.” 2016. Web. 17 Jan 2021.

Vancouver:

Hisey BS. The role of SaeR/S in secondary Staphylococcus aureus Pneumonia. [Internet] [Masters thesis]. Montana State University; 2016. [cited 2021 Jan 17]. Available from: https://scholarworks.montana.edu/xmlui/handle/1/14625.

Council of Science Editors:

Hisey BS. The role of SaeR/S in secondary Staphylococcus aureus Pneumonia. [Masters Thesis]. Montana State University; 2016. Available from: https://scholarworks.montana.edu/xmlui/handle/1/14625

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations