subject:(Genetic transcription Regulation)

Hong Kong University of Science and Technology

1. 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

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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 15, 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. 15 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 15]. 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

University of Oklahoma

2. Zhao, Tao. Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS.

Degree: PhD, 2011, University of Oklahoma

URL: http://hdl.handle.net/11244/318596

► Animal neurons dynamically change their morphologies in response to steroid hormone signaling to adapt to changing environments. The molecular mechanisms underlying animal neuronal remodeling, however,… (more)

▼ Animal neurons dynamically change their morphologies in response to steroid hormone signaling to adapt to changing environments. The molecular mechanisms underlying animal neuronal remodeling, however, remain largely unknown. Metamorphosis is an important developmental stage in insects when crawling and feeding larvae transform into reproductive and flying adults. During this period, many insect larval neurons undergo dramatic morphological and functional alterations. These neuronal changes are regulated by a arthropod-specific steroid hormone, 20-hydroxyecdysone (ecdysone). Research on the metamorphic remodeling of insect neurons, has provided insights into the general neuronal remodeling process. During the early stage of metamorphosis, the larval neurons prune their projections and then grow out adult-specific neurites. A group of Drosophila melanogaster (fruit fly) neuroendocrine cells, the crustacean cardioactive peptide (CCAP) neurons, experiences metamorphic remodeling, and I used these neurons to dissect the molecular mechanisms controlling this process. The CCAP neurons mainly produce two neuropeptides, CCAP and bursicon, to control insect molting-related behaviors, ecdysis and wing expansion. Functional disruption of the CCAP neuron remodeling leads to defective wing expansion in adults. In a genetic screen, thousands of genes were mis- or overexpressed in the CCAP neurons. The genes that produced strong wing expansion defects were identified. Fourteen of the identified genes specifically inhibited the outgrowth of adult-specific neurites during metamorphic remodeling. One of these, split ends (spen) was selected to identify the molecular pathways affected by its overexpression. I performed a deficiency modifier screen to identify mutations that modify the outgrowth defects induced by spen. A mutation of Mbs, the gene encoding the Myosin binding subunit, moderately suppressed the outgrowth defects. Since Mbs negatively regulates myosin II activity, the results suggested that spen overexpressin suppressed myosin II activity. Another myosinmodulating signaling pathway, Rac1-PAK, was also tested to confirm the observations. The Rac1-PAK signaling pathway positively regulates myosin II function, and this pathway suppressed the neurite outgrowth defects induced by spen overexpression. Furthermore, down-regulation of spen activity strongly rescued the wing expansion and neurite growth defects resulting from disrupted Rac1-PAK signaling. These results strongly support a model in which spen functions antagonistically with myosin II to regulate neuronal outgrowth during metamorphosis. Advisors/Committee Members: Hewes, Randall S (advisor).

Subjects/Keywords: Neurons; Genetic transcription – Regulation; Transcription factors

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APA (6^th Edition):

Zhao, T. (2011). Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS. (Doctoral Dissertation). University of Oklahoma. Retrieved from http://hdl.handle.net/11244/318596

Chicago Manual of Style (16^th Edition):

Zhao, Tao. “Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS.” 2011. Doctoral Dissertation, University of Oklahoma. Accessed January 15, 2021. http://hdl.handle.net/11244/318596.

MLA Handbook (7^th Edition):

Zhao, Tao. “Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS.” 2011. Web. 15 Jan 2021.

Vancouver:

Zhao T. Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS. [Internet] [Doctoral dissertation]. University of Oklahoma; 2011. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/11244/318596.

Council of Science Editors:

Zhao T. Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS. [Doctoral Dissertation]. University of Oklahoma; 2011. Available from: http://hdl.handle.net/11244/318596

Columbia University

3. 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

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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 15, 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. 15 Jan 2021.

Vancouver:

Corrigan DJ. Differential Roles of PRDM16 Isoforms in Normal and Malignant Hematopoiesis. [Internet] [Doctoral dissertation]. Columbia University; 2018. [cited 2021 Jan 15]. 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

Hong Kong University of Science and Technology

4. 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

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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 15, 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. 15 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 15]. 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

5. 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

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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 15, 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. 15 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 15]. 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

University of Texas – Austin

6. Hu, Zhanzhi. Functional transcription regulatory network reconstruction and characterization.

Degree: PhD, Microbiology, 2005, University of Texas – Austin

URL: http://hdl.handle.net/2152/2450

► The genome of yeast Saccharomyces cerevisiae encodes more than 5,800 genes with well controlled and coordinated expression patterns for normal cellular functions. Control of gene… (more)

▼ The genome of yeast Saccharomyces cerevisiae encodes more than 5,800 genes with well controlled and coordinated expression patterns for normal cellular functions. Control of gene expression occurs primarily at the transcriptional level via transcription factors. In response to various conditions, these regulators bind to promoters of target genes and recruit additional factors and the transcription machinery to activate or repress transcription. However, the genome-wide details of the transcriptional regulatory networks are largely unknown. We first mapped the genome-wide in vivo DNA binding distribution of Heat Shock Factor (HSF), one of the most highly conserved transcriptional regulators in eukaryotes. HSF mediates the response of cells to many stresses including heat shock, but little is known about its full range of biological targets. We used whole genome analyses to identify virtually all of the direct transcriptional targets of yeast HSF. The majority of the identified loci were heat-inducibly bound by HSF. The target genes encode proteins with a broad range of biological functions. This study provides novel insights into the role of HSF in growth, development, disease and aging, and in the complex metabolic reprogramming in cells in response to stress. Together with a recent study using a similar approach, this has provided a view of the potential regulatory network composed of transcription factors and their binding sites. However, it has been implicated that the binding of a transcription factor does not necessarily lead to an expression change. We therefore profiled the transcriptional response of yeast upon the individual deletion of more than 250 transcriptional regulators under normal growth as well as under heat shock for a subset of those. This enabled us to construct a functional transcription network. Solid support of the network was established. Known and novel roles of transcription factors were inferred and quantitatively verified. From the promoter regions of the target gene sets, we discovered many novel sequence motifs in addition to many previously characterized ones. In conclusion, the present study provides important insights for elucidating the specific roles of transcription factors in mediating the responses of the cells under different conditions. Advisors/Committee Members: Iyer, Vishwanath R. (advisor).

Subjects/Keywords: Genetic transcription – Regulation

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

APA (6^th Edition):

Hu, Z. (2005). Functional transcription regulatory network reconstruction and characterization. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/2450

Chicago Manual of Style (16^th Edition):

Hu, Zhanzhi. “Functional transcription regulatory network reconstruction and characterization.” 2005. Doctoral Dissertation, University of Texas – Austin. Accessed January 15, 2021. http://hdl.handle.net/2152/2450.

MLA Handbook (7^th Edition):

Hu, Zhanzhi. “Functional transcription regulatory network reconstruction and characterization.” 2005. Web. 15 Jan 2021.

Vancouver:

Hu Z. Functional transcription regulatory network reconstruction and characterization. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2005. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2152/2450.

Council of Science Editors:

Hu Z. Functional transcription regulatory network reconstruction and characterization. [Doctoral Dissertation]. University of Texas – Austin; 2005. Available from: http://hdl.handle.net/2152/2450

University of Texas – Austin

7. Killion, Patrick J., 1974-. Fungus to fibroblast: a functional genomic exploration of eukaryotic transcriptional regulation: Functional genomic exploration of eukaryotic transcriptional regulation.

Degree: PhD, Cell and Molecular Biology, 2007, University of Texas – Austin

URL: http://hdl.handle.net/2152/3616

► I have pursued a breadth of research that explored the functional genomic study of eukaryotic transcriptional regulation. I have utilized two model organisms, many experimental… (more)

▼ I have pursued a breadth of research that explored the functional genomic study of eukaryotic transcriptional regulation. I have utilized two model organisms, many experimental methodologies, and have developed a suite of computational resources to study the interaction of transcription factors with regulated targets. In Saccharomyces cerevisiae I worked with my collaborator Dr. Zhanzhi (Mike) Hu to characterize the whole-genome transcriptional response of 263 individual transcription factor deletions. We utilized a sophisticated error model and directed-weighted graphs to model a network of high-confidence targets for each transcription factor profiled. We then used regulatory epistasis to elucidate the true set of primary KO-regulated targets and construct a functional transcriptional regulatory network. This network was analyzed for ontological and sequence motif enrichment in order to gain insight into the biological functions represented by transcription factors studied. Functional validation was performed to evaluate the probability of novel functional characterizations. Significant insight was gained from this study with regard to the nature of regulatory cascades and the inability for DNA binding events to predict regulation. This set of analysis was performed with a novel bioinformatic server called ArrayPlex. ArrayPlex is a software package that centrally provides a large number of flexible toolsets useful for functional genomics including microarray data storage, quality assessments, data visualization, gene annotation retrieval, statistical tests, genomic sequence retrieval and motif analysis. It uses a client-server architecture based on open source components, provides graphical, command-line, as well as programmatic access to all needed resources, and is extensible by virtue of a documented API. Using many of the techniques and computational resources developed, I pursued the study of microRNA transcriptional abundance and targeting in H. sapiens cell cultures. Utilizing custom-fabricated microarrays, I measured the whole-genome response of both mRNAs and microRNAs under serum stimulation, c-Myc overexpression, and c-Myc siRNA-mediated knockdown. I then characterized the regulatory interactions between the sets of regulated microRNAs and coordinately regulated transcription factors. Using analytical methods sensitive to regulatory directionality of both populations I was able to determine high-confidence relationships between transcription factors and regulated microRNAs as well as microRNAs and regulated gene targets. Advisors/Committee Members: Iyer, Vishwanath R. (advisor).

Subjects/Keywords: Genetic transcription – Regulation

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APA (6^th Edition):

Killion, Patrick J., 1. (2007). Fungus to fibroblast: a functional genomic exploration of eukaryotic transcriptional regulation: Functional genomic exploration of eukaryotic transcriptional regulation. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/3616

Chicago Manual of Style (16^th Edition):

Killion, Patrick J., 1974-. “Fungus to fibroblast: a functional genomic exploration of eukaryotic transcriptional regulation: Functional genomic exploration of eukaryotic transcriptional regulation.” 2007. Doctoral Dissertation, University of Texas – Austin. Accessed January 15, 2021. http://hdl.handle.net/2152/3616.

MLA Handbook (7^th Edition):

Killion, Patrick J., 1974-. “Fungus to fibroblast: a functional genomic exploration of eukaryotic transcriptional regulation: Functional genomic exploration of eukaryotic transcriptional regulation.” 2007. Web. 15 Jan 2021.

Vancouver:

Killion, Patrick J. 1. Fungus to fibroblast: a functional genomic exploration of eukaryotic transcriptional regulation: Functional genomic exploration of eukaryotic transcriptional regulation. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2007. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2152/3616.

Council of Science Editors:

Killion, Patrick J. 1. Fungus to fibroblast: a functional genomic exploration of eukaryotic transcriptional regulation: Functional genomic exploration of eukaryotic transcriptional regulation. [Doctoral Dissertation]. University of Texas – Austin; 2007. Available from: http://hdl.handle.net/2152/3616

Michigan State University

8. Uygun, Sahra. Using transcriptome and data science methods to uncover gene regulatory and functional information.

Degree: 2017, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:4560

►

Thesis Ph. D. Michigan State University. Genetics 2017

Even in the well-studied model organisms, there are still genomic regions with unknown function. These genomic regions… (more)

▼

Thesis Ph. D. Michigan State University. Genetics 2017

Even in the well-studied model organisms, there are still genomic regions with unknown function. These genomic regions include protein-coding genes and regulatory elements that are key components of transcriptional regulation. With technological advances, more biological data are being generated including spatial, temporal, developmental, and conditional gene expression data. Gene expression data, and specifically co-expression analyses have been widely used to predict gene function through guilt by association. However, it remains to be seen to what degree co-expression is informative, whether it can be applied to genes involved in different biological processes, and how the choice of gene expression dataset and clustering algorithms impact inferences about gene functions. To answer these questions, I used co-expression to identify novel genes that function in a biological process, and the impact of different clustering algorithms on the ability to identify genes that function in the same pathway. Apart from the functional associations, gene co-expression analyses can also be used to identify the putative cis-regulatory elements that are over-represented in co-expressed gene promoters. These elements can be used to build models of gene regulation under changing environments and genome-wide models of how different organ and cell type gene expression are regulated under changing environments have not yet been built in plants. I used Arabidopsis thaliana organ and cell type stress responsive gene expression data and co-expression clusters to identify putative cis-regulatory elements. Using these elements and machine learning models, I predicted high salinity responsive gene expression in shoots, roots and six root cell types. I found that plant organ and cell type transcriptional response to high salinity are likely regulated by a core set of elements that we identified and built predictive models of plant spatial transcriptional responses to environmental stress. Overall, this research contributes to understanding the role of "big data" in biology, provides guidelines for effectively using gene co-expression in functional associations and shows how computational approaches help in identifying gene regulatory information.

Description based on online resource;

Advisors/Committee Members: Shiu, Shinhan, Chan, Christina, Chen, Jin, Last, Robert L.

Subjects/Keywords: Gene expression; Genetic transcription – Regulation; Bioinformatics; Genetics

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

APA (6^th Edition):

Uygun, S. (2017). Using transcriptome and data science methods to uncover gene regulatory and functional information. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:4560

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):

Uygun, Sahra. “Using transcriptome and data science methods to uncover gene regulatory and functional information.” 2017. Thesis, Michigan State University. Accessed January 15, 2021. http://etd.lib.msu.edu/islandora/object/etd:4560.

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

MLA Handbook (7^th Edition):

Uygun, Sahra. “Using transcriptome and data science methods to uncover gene regulatory and functional information.” 2017. Web. 15 Jan 2021.

Vancouver:

Uygun S. Using transcriptome and data science methods to uncover gene regulatory and functional information. [Internet] [Thesis]. Michigan State University; 2017. [cited 2021 Jan 15]. Available from: http://etd.lib.msu.edu/islandora/object/etd:4560.

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

Council of Science Editors:

Uygun S. Using transcriptome and data science methods to uncover gene regulatory and functional information. [Thesis]. Michigan State University; 2017. Available from: http://etd.lib.msu.edu/islandora/object/etd:4560

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

9. Xie, Qunhui. Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron.

Degree: 2006, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-2852 ; https://doi.org/10.14711/thesis-b938091 ; http://repository.ust.hk/ir/bitstream/1783.1-2852/1/th_redirect.html

► Acetylcholinesterase (AChE) exists as tetrameric globular (G4) form enzyme on the membrane of muscle and neuron. This G4 AChE possesses important physiological functions in cholinergic… (more)

▼ Acetylcholinesterase (AChE) exists as tetrameric globular (G4) form enzyme on the membrane of muscle and neuron. This G4 AChE possesses important physiological functions in cholinergic neurotransmission. PRiMA (P̲roline-R̲i̲ch M̲embrane A̲nchor) cDNA encoding the AChE membrane anchor has been identified and cloned. PRiMA is a transmembrane protein containing a PRAD (P̲roline-R̲ich A̲ttachment D̲omain) domain for interacting with four AChE catalytic subunits (AChET), and anchor the enzyme at the surface of muscle and neuron. However, the expression and localization of PRiMA in both muscle and neuron have not been investigated yet. In the current study, mouse C2C12 muscle cells and cultured rat cortical neurons were employed as models to investigate PRiMA regulation. The G4 AChE was expressed predominantly in the C2C12 myoblasts and mature neurons. The expression of PRiMA mRNA was decreased during the myogenesis of C2C12 muscle cells, and increased during differentiation of cultured neurons. Moreover, the assembly of G4 AChE could be driven by over expressing PRiMA and AChET cDNAs in both cell types. Therefore, the elucidation of regulatory mechanisms of PRiMA expression would be important to understand the precise control of G4 AChE. Because of the lack of a promising anti-PRiMA antibody, transcriptional regulation of PRiMA was investigated in this study. Results revealed that PRiMA mRNA in muscle was suppressed by MRFs (myogenic regulatory factors); as well as nerve-derived factors, CGRP (calcitonin gene-related peptide) and muscular activity, via the activation of CREB (cAMP-responsive element binding protein). During the differentiation of cultured cortical neurons, the activity of MAPK (mitogen-activated protein kinase) and CaMKII (calcium/calmodulin-dependent protein kinase II) could be induced. The expression of PRiMA mRNA was increased by activating these two signaling pathways; these results suggested the possible roles of MAPK and CaMKll in up regulating PRiMA expression in neurons. Similar results were observed when using the PRiMA promoter in promoter-luciferase-reporter systems of both muscle and neuron cells. These results, therefore, indicated the control of PRiMA mRNA expression was, at least, at a transcriptional level. Besides a sufficient expression level, a proper positioning of AChE is vital for its synaptic function. The subcellular localization of AChE in brain indicated that G4 AChE existed in lipid raft micro-domain. In mature cortical neurons, AChE was co-localized with synaptic proteins. The restricted localization of AChE in cultured neurons could be possibly directed by PRiMA. To further reveal the role of PRiMA in directing G4 AChE to lipid raft, a recombinant system of NG108-15 neuroblastoma cells was employed. In AChET and PRiMA co-expressed NG108-15 cells, G4 AChE was predominantly assembled and localized at lipid raft; the co-expression subsequently caused a dramatic increase of the enzymatic activity. These emerging lines of evidence suggest that PRiMA is responsible not only for…

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

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

APA (6^th Edition):

Xie, Q. (2006). Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-2852 ; https://doi.org/10.14711/thesis-b938091 ; http://repository.ust.hk/ir/bitstream/1783.1-2852/1/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):

Xie, Qunhui. “Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron.” 2006. Thesis, Hong Kong University of Science and Technology. Accessed January 15, 2021. http://repository.ust.hk/ir/Record/1783.1-2852 ; https://doi.org/10.14711/thesis-b938091 ; http://repository.ust.hk/ir/bitstream/1783.1-2852/1/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):

Xie, Qunhui. “Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron.” 2006. Web. 15 Jan 2021.

Vancouver:

Xie Q. Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2006. [cited 2021 Jan 15]. Available from: http://repository.ust.hk/ir/Record/1783.1-2852 ; https://doi.org/10.14711/thesis-b938091 ; http://repository.ust.hk/ir/bitstream/1783.1-2852/1/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:

Xie Q. Transcriptional regulation and function of PRiMA (proline-rich membrane anchor), a membrane anchor of globular acetylcholinesterase, in muscle and neuron. [Thesis]. Hong Kong University of Science and Technology; 2006. Available from: http://repository.ust.hk/ir/Record/1783.1-2852 ; https://doi.org/10.14711/thesis-b938091 ; http://repository.ust.hk/ir/bitstream/1783.1-2852/1/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

10. Spooner, Chauncey J. Functional determinants of C/EBP[beta] in IL-6 and MCP-1 regulation.

Degree: PhD, Department of Microbiology and Molecular Genetics, 2003, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:32945

Subjects/Keywords: Transcription factors – Regulation; Genetic regulation

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

APA (6^th Edition):

Spooner, C. J. (2003). Functional determinants of C/EBP[beta] in IL-6 and MCP-1 regulation. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:32945

Chicago Manual of Style (16^th Edition):

Spooner, Chauncey J. “Functional determinants of C/EBP[beta] in IL-6 and MCP-1 regulation.” 2003. Doctoral Dissertation, Michigan State University. Accessed January 15, 2021. http://etd.lib.msu.edu/islandora/object/etd:32945.

MLA Handbook (7^th Edition):

Spooner, Chauncey J. “Functional determinants of C/EBP[beta] in IL-6 and MCP-1 regulation.” 2003. Web. 15 Jan 2021.

Vancouver:

Spooner CJ. Functional determinants of C/EBP[beta] in IL-6 and MCP-1 regulation. [Internet] [Doctoral dissertation]. Michigan State University; 2003. [cited 2021 Jan 15]. Available from: http://etd.lib.msu.edu/islandora/object/etd:32945.

Council of Science Editors:

Spooner CJ. Functional determinants of C/EBP[beta] in IL-6 and MCP-1 regulation. [Doctoral Dissertation]. Michigan State University; 2003. Available from: http://etd.lib.msu.edu/islandora/object/etd:32945

Michigan State University

11. MacDougald, Ormond Alexander. Trans-acting factors regulating S14 gene transcription.

Degree: PhD, Department of Physiology, 1992, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:22246

Subjects/Keywords: Genetic transcription; Transcription factors; Genetic regulation

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APA (6^th Edition):

MacDougald, O. A. (1992). Trans-acting factors regulating S14 gene transcription. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:22246

Chicago Manual of Style (16^th Edition):

MacDougald, Ormond Alexander. “Trans-acting factors regulating S14 gene transcription.” 1992. Doctoral Dissertation, Michigan State University. Accessed January 15, 2021. http://etd.lib.msu.edu/islandora/object/etd:22246.

MLA Handbook (7^th Edition):

MacDougald, Ormond Alexander. “Trans-acting factors regulating S14 gene transcription.” 1992. Web. 15 Jan 2021.

Vancouver:

MacDougald OA. Trans-acting factors regulating S14 gene transcription. [Internet] [Doctoral dissertation]. Michigan State University; 1992. [cited 2021 Jan 15]. Available from: http://etd.lib.msu.edu/islandora/object/etd:22246.

Council of Science Editors:

MacDougald OA. Trans-acting factors regulating S14 gene transcription. [Doctoral Dissertation]. Michigan State University; 1992. Available from: http://etd.lib.msu.edu/islandora/object/etd:22246

Simon Fraser University

12. Vahidi, Haleh. The organization and expression of 5S ribosomal RNA genes from the nematodes Meloidogyne arenaria and Caenorhabditis elegans.

Degree: 1991, Simon Fraser University

URL: http://summit.sfu.ca/item/4816

Subjects/Keywords: Nematoda.; Genetic transcription.; Genetic transcription – Regulation.

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

APA (6^th Edition):

Vahidi, H. (1991). The organization and expression of 5S ribosomal RNA genes from the nematodes Meloidogyne arenaria and Caenorhabditis elegans. (Thesis). Simon Fraser University. Retrieved from http://summit.sfu.ca/item/4816

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):

Vahidi, Haleh. “The organization and expression of 5S ribosomal RNA genes from the nematodes Meloidogyne arenaria and Caenorhabditis elegans.” 1991. Thesis, Simon Fraser University. Accessed January 15, 2021. http://summit.sfu.ca/item/4816.

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

MLA Handbook (7^th Edition):

Vahidi, Haleh. “The organization and expression of 5S ribosomal RNA genes from the nematodes Meloidogyne arenaria and Caenorhabditis elegans.” 1991. Web. 15 Jan 2021.

Vancouver:

Vahidi H. The organization and expression of 5S ribosomal RNA genes from the nematodes Meloidogyne arenaria and Caenorhabditis elegans. [Internet] [Thesis]. Simon Fraser University; 1991. [cited 2021 Jan 15]. Available from: http://summit.sfu.ca/item/4816.

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

Council of Science Editors:

Vahidi H. The organization and expression of 5S ribosomal RNA genes from the nematodes Meloidogyne arenaria and Caenorhabditis elegans. [Thesis]. Simon Fraser University; 1991. Available from: http://summit.sfu.ca/item/4816

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

13. Elshaarrawi, Ahmed G. Are the WNT5A isoforms functionally distinct? - promoter and signaling pathway analyses.

Degree: 2018, NC Docks

URL: http://libres.uncg.edu/ir/uncg/f/Elshaarrawi_uncg_0154M_12539.pdf

► WNT5A is a secreted glycoprotein that binds to both canonical and non-canonical Wnt receptors and has important roles in morphogenesis (e.g., anterior-posterior axis elongation and… (more)

▼ WNT5A is a secreted glycoprotein that binds to both canonical and non-canonical Wnt receptors and has important roles in morphogenesis (e.g., anterior-posterior axis elongation and limb formation) and differentiation (e.g., bone and cartilage). On a cellular level WNT5A functions in proliferation, adhesion, migration, and cell polarity. Altered WNT5A expression is associated with various human diseases, particularly cancer, but has also been linked with the inflammatory response. WNT5A has two isoforms that are derived from distinct promoters; the proteins isoforms referred to as L(A) and S(B) differ by 18 amino acids. In this project I examined the functional differences between the proteins isoforms L(A) and S(B) and the regulation of their promoters. The isoforms may have differential affinity for non-canonical receptors, selectively activating particular signaling pathways. They may also display distinct patterns of expression in particular cells, during differentiation and in development, as a consequence of their unique promoters. Conditioned medium (CM) was prepared from CHO cells expressing either isoform L(A) or S(B). Using a TOPFlash system the CML(A) and CM-S(B) were shown to be active. The CM was used to analyze the effects of the isoforms on the non-canonical Wnt signaling pathways Ca2+ and PCP/CE in HCT 116 (colon cancer) and hFOB1.19 (normal human osteoblast) cell lines by measuring levels of phospho (p)PKC and phospho (p)JNK, downstream targets of each pathway. Results showed that the CM-S(B) activated both pPKC and pJNK in HCT 116 cells whereas CML(A) had less of an effect. There was little or no effect of both CM’s in hFOB1.19 cells. AP-1 and NFAT luciferase reporter assays in HCT 116 cells confirmed the effect of CMS(B) on pJNK. Next the effect of the CM’s on apoptosis, proliferation, and migration were analyzed. Neither CMs affected the level of apoptosis in HCT 116 cells. Both isoforms were found to decrease proliferation in HCT 116 cells but CM-S(B) had a more consistent effect. CM-S(B) was found to increase migration and CM-L(A) decrease migration in HCT 116 cells. In a mouse embryonic fibroblast (MEF)-with a PORCN gene knock-out, both CMs caused a decrease in migration. Next, isoform L(A) and S(B) luciferase promoter constructs were transfected into HCT 116 and hFOB1.19 cells. The pattern of expression in the two cell types was similar for promoter L(A) and promoter S(B) but promoter S(B) showed a higher level of expression. 1707bp of upstream sequence showed a maximal expression for promoter L(A) and 1257 bp showed a maximal expression for promoter S(B) in both proliferating cell types. Analysis of the promoter L(A) and promoter S(B) reporter constructs during hFOB1.19 differentiation indicated that promoter L(A) is more highly activated than promoter S(B). Sequences within 420bp and 187bp for promoter L(A) and promoter S(B), respectively, were sufficient for activation. Putative transcription factor binding sites were identified in promoter L(A) and promoter S(B) upstream sequences. Some of…

Subjects/Keywords: Wnt proteins; Promoters (Genetics); Genetic transcription; Genetic regulation; Bones $x Growth

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

APA (6^th Edition):

Elshaarrawi, A. G. (2018). Are the WNT5A isoforms functionally distinct? - promoter and signaling pathway analyses. (Thesis). NC Docks. Retrieved from http://libres.uncg.edu/ir/uncg/f/Elshaarrawi_uncg_0154M_12539.pdf

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):

Elshaarrawi, Ahmed G. “Are the WNT5A isoforms functionally distinct? - promoter and signaling pathway analyses.” 2018. Thesis, NC Docks. Accessed January 15, 2021. http://libres.uncg.edu/ir/uncg/f/Elshaarrawi_uncg_0154M_12539.pdf.

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

MLA Handbook (7^th Edition):

Elshaarrawi, Ahmed G. “Are the WNT5A isoforms functionally distinct? - promoter and signaling pathway analyses.” 2018. Web. 15 Jan 2021.

Vancouver:

Elshaarrawi AG. Are the WNT5A isoforms functionally distinct? - promoter and signaling pathway analyses. [Internet] [Thesis]. NC Docks; 2018. [cited 2021 Jan 15]. Available from: http://libres.uncg.edu/ir/uncg/f/Elshaarrawi_uncg_0154M_12539.pdf.

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

Council of Science Editors:

Elshaarrawi AG. Are the WNT5A isoforms functionally distinct? - promoter and signaling pathway analyses. [Thesis]. NC Docks; 2018. Available from: http://libres.uncg.edu/ir/uncg/f/Elshaarrawi_uncg_0154M_12539.pdf

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

Michigan State University

14. Sonnenschein, Anne. Machine learning for the study of gene regulation and complex traits.

Degree: 2017, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:6740

►

"Functional elements are found in DNA outside of protein coding regions; an important class of these elements are 'enhancers', which govern when and where transcription… (more)

Subjects/Keywords: Phenotype; Machine learning; Genetic transcription; Genetic regulation; Genetics

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APA (6^th Edition):

Sonnenschein, A. (2017). Machine learning for the study of gene regulation and complex traits. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:6740

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):

Sonnenschein, Anne. “Machine learning for the study of gene regulation and complex traits.” 2017. Thesis, Michigan State University. Accessed January 15, 2021. http://etd.lib.msu.edu/islandora/object/etd:6740.

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

MLA Handbook (7^th Edition):

Sonnenschein, Anne. “Machine learning for the study of gene regulation and complex traits.” 2017. Web. 15 Jan 2021.

Vancouver:

Sonnenschein A. Machine learning for the study of gene regulation and complex traits. [Internet] [Thesis]. Michigan State University; 2017. [cited 2021 Jan 15]. Available from: http://etd.lib.msu.edu/islandora/object/etd:6740.

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

Council of Science Editors:

Sonnenschein A. Machine learning for the study of gene regulation and complex traits. [Thesis]. Michigan State University; 2017. Available from: http://etd.lib.msu.edu/islandora/object/etd:6740

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

University of Hong Kong

15. 李耀輝. Tissue-specific transcriptional regulation of Sox2.

Degree: 2007, University of Hong Kong

URL: http://hdl.handle.net/10722/50193

Subjects/Keywords: Genetic transcription - Regulation.; Genetic regulation.; Transcription factors.

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

APA (6^th Edition):

李耀輝. (2007). Tissue-specific transcriptional regulation of Sox2. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/50193

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

Chicago Manual of Style (16^th Edition):

李耀輝. “Tissue-specific transcriptional regulation of Sox2.” 2007. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/50193.

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

MLA Handbook (7^th Edition):

李耀輝. “Tissue-specific transcriptional regulation of Sox2.” 2007. Web. 15 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

李耀輝. Tissue-specific transcriptional regulation of Sox2. [Internet] [Thesis]. University of Hong Kong; 2007. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/50193.

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

Council of Science Editors:

李耀輝. Tissue-specific transcriptional regulation of Sox2. [Thesis]. University of Hong Kong; 2007. Available from: http://hdl.handle.net/10722/50193

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

University of Texas Southwestern Medical Center

16. Schaukowitch, Katie Marie. Transcriptional Mechanisms Underlying Neuronal Activity-Dependent Plasticity.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/6150

► Impairment in learning and memory is a well-established cognitive symptom that is manifested in many psychiatric diseases including autism and schizophrenia. Studies have shown that… (more)

▼ Impairment in learning and memory is a well-established cognitive symptom that is manifested in many psychiatric diseases including autism and schizophrenia. Studies have shown that long-lasting memory formation is mediated by rapid changes in nuclear gene expression in response to learning-induced sensory experience. Despite these findings, there is a significant gap in our knowledge as to how sensory information is precisely translated into specific transcriptional outputs. Recently, a class of long noncoding RNAs that are transcribed bidirectionally from the enhancers of activity-dependent genes in neurons (eRNAs) has been identified. My first project studied the function of eRNAs of two immediate early genes Activity-regulated cytoskeletal protein (Arc) and Growth arrest and DNA-damage-inducible, beta (Gadd45b), which have been implicated in mediating synaptic plasticity. Using a knockdown approach, we found that eRNAs are necessary for the full induction of their target genes in response to membrane depolarization. eRNAs specifically regulate the early elongation stage of transcription by allowing for efficient release of paused RNA polymerase II (RNAPII) from the promoters of activity-regulated genes. Knockdown of eRNAs results in the retention of an RNAPII pausing factor, Negative Elongation Factor (NELF), at the target gene promoter. eRNAs directly bind to NELF during stimulated conditions, suggesting that eRNAs interact with NELF to facilitate its release from the promoter, thus resulting in efficient and precisely timed gene activation. These data define a new role for the spatiotemporally controlled expression of regulatory RNAs in the experience-dependent gene expression network. My second project aimed to identify the transcriptional program activated when activity levels are suppressed. Homeostatic scaling allows neurons to maintain stable activity patterns by globally altering their synaptic strength in response to changing activity levels. Decreasing activity leads to an upregulation in synaptic strength, as seen by increases in AMPA mediated mEPSCs. It was previously shown that the increase in mEPSC amplitude could be blocked by a transcription inhibitor, suggesting that transcription is necessary for the scaling response. However, little is known about the genes directly regulated by activity suppression or the signaling mechanisms underlying the transcriptional control. Using RNA-Seq, we identified nearly 100 genes that were specifically upregulated in response to activity suppression. Neuronal pentraxin-1 (Nptx1), previously shown to promote AMPAR clustering, was increased ~3 fold, and knockdown of this gene blocked the increase in mEPSC amplitudes. SRF is a key transcription factor in regulating Nptx1 induction, which is calcium-dependent, indicating the existence of an active pathway to control transcription. Taken together, this study defines a novel transcriptional program that is able to sense the absence of activity and coordinate the global increase in synaptic strength. Advisors/Committee Members: Huber, Kimberly M., Johnson, Jane E., Tamminga, Carol, Kraus, W. Lee.

Subjects/Keywords: Gene Expression Regulation; Neuronal Plasticity; Neurons; RNA, Long Noncoding; Transcription Factors; Transcription, Genetic

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APA (6^th Edition):

Schaukowitch, K. M. (2016). Transcriptional Mechanisms Underlying Neuronal Activity-Dependent Plasticity. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6150

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):

Schaukowitch, Katie Marie. “Transcriptional Mechanisms Underlying Neuronal Activity-Dependent Plasticity.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed January 15, 2021. http://hdl.handle.net/2152.5/6150.

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

MLA Handbook (7^th Edition):

Schaukowitch, Katie Marie. “Transcriptional Mechanisms Underlying Neuronal Activity-Dependent Plasticity.” 2016. Web. 15 Jan 2021.

Vancouver:

Schaukowitch KM. Transcriptional Mechanisms Underlying Neuronal Activity-Dependent Plasticity. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2152.5/6150.

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

Council of Science Editors:

Schaukowitch KM. Transcriptional Mechanisms Underlying Neuronal Activity-Dependent Plasticity. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6150

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

University of Alberta

17. Petrich, Astrid Karin. Transcriptional analysis of the isopenicillin N synthase gene of streptomyces clavuligerus.

Degree: PhD, Department of Microbiology, 1993, University of Alberta

URL: https://era.library.ualberta.ca/files/c534fr02x

Subjects/Keywords: Streptomyces clavuligerus.; Genetic transcription – Regulation.

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

APA (6^th Edition):

Petrich, A. K. (1993). Transcriptional analysis of the isopenicillin N synthase gene of streptomyces clavuligerus. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/c534fr02x

Chicago Manual of Style (16^th Edition):

Petrich, Astrid Karin. “Transcriptional analysis of the isopenicillin N synthase gene of streptomyces clavuligerus.” 1993. Doctoral Dissertation, University of Alberta. Accessed January 15, 2021. https://era.library.ualberta.ca/files/c534fr02x.

MLA Handbook (7^th Edition):

Petrich, Astrid Karin. “Transcriptional analysis of the isopenicillin N synthase gene of streptomyces clavuligerus.” 1993. Web. 15 Jan 2021.

Vancouver:

Petrich AK. Transcriptional analysis of the isopenicillin N synthase gene of streptomyces clavuligerus. [Internet] [Doctoral dissertation]. University of Alberta; 1993. [cited 2021 Jan 15]. Available from: https://era.library.ualberta.ca/files/c534fr02x.

Council of Science Editors:

Petrich AK. Transcriptional analysis of the isopenicillin N synthase gene of streptomyces clavuligerus. [Doctoral Dissertation]. University of Alberta; 1993. Available from: https://era.library.ualberta.ca/files/c534fr02x

University of Hong Kong

18. 王曉婷. A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation.

Degree: 2009, University of Hong Kong

URL: http://hdl.handle.net/10722/56671

Subjects/Keywords: Histones.; Genetic transcription - Regulation.; Chromatin.

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APA (6^th Edition):

王曉婷.. (2009). A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/56671

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

Chicago Manual of Style (16^th Edition):

王曉婷.. “A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation.” 2009. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/56671.

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

MLA Handbook (7^th Edition):

王曉婷.. “A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation.” 2009. Web. 15 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

王曉婷.. A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation. [Internet] [Thesis]. University of Hong Kong; 2009. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/56671.

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

Council of Science Editors:

王曉婷.. A role of TSPYL2, a novel nucleosome assembly protein, in transcriptional regulation. [Thesis]. University of Hong Kong; 2009. Available from: http://hdl.handle.net/10722/56671

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

Columbia University

19. Dugger, Sarah Anne. Evaluation of a precision medicine approach for hnRNP U-related developmental epileptic encephalopathy using a mouse model of disease.

Degree: 2020, Columbia University

URL: https://doi.org/10.7916/d8-qevc-mw16

► Mutations in genes that cause transcriptional dysregulation, such as genes that encode DNA and RNA-binding proteins (RNABPs), are a well-described cause of neurodevelopmental syndromes such… (more)

▼ Mutations in genes that cause transcriptional dysregulation, such as genes that encode DNA and RNA-binding proteins (RNABPs), are a well-described cause of neurodevelopmental syndromes such as autism and epilepsy. Heterozygous de novo mutations involving the gene HNRNPU, which encodes the heterogeneous nuclear ribonuclear protein U, have been implicated in a neurodevelopmental syndrome most commonly characterized by epileptic encephalopathy. Although hnRNP U is a highly-abundant and ubiquitously-expressed DNA- and RNA-binding protein involved in a variety of important nuclear processes—most notably gene expression regulation—the role it plays in neurological disease is unclear and has yet to be studied. The work presented here examines a precision medicine approach for epilepsies thought to have a transcriptomic basis, starting with a thorough neurophysiological characterization of a heterozygous loss-of-function Hnrnpu mouse model (Hnrnpu+/113DEL), followed by a comprehensive and region-specific single-cell transcriptomic study, and finally the validation of implicated brain regions. Characterization of the Hnrnpu+/113DEL mouse line revealed an increased susceptibility to seizures in Hnrnpu+/113DEL mice, along with an increased perinatal mortality, global developmental delay and gait abnormalities. Gene expression profiling, including bulk RNA-sequencing of neocortex and single cell RNA-sequencing of both neocortex and hippocampus, revealed widespread, yet modest, dysregulation of gene expression that was largely inversely correlated to gene-length, and involved important, neurodevelopmental disease genes. In particular, pyramidal neurons of the subiculum displayed greater transcriptional burden upon heterozygous loss of Hnrnpu, with the known epilepsy gene Mef2c as a clear outlier showing greater than 50% reduction in expression. Follow-up investigation into whether this region- and cell-type specific gene dysregulation correlated to differences in neuronal function using c-Fos immunostaining, revealed an overall decrease in neuronal activity within the ventral subiculum in Hnrnpu+/113DEL mice. In summary, our data validates the presence of neurodevelopmental defects upon heterozygous loss of Hnrnpu and supports the notion of transcriptional dysregulation as a likely contributing factor to hnRNP U-related disease, possibly through the dysfunction of subiculum-derived excitatory neurons. Future studies evaluating the relationship between reduced activity within the ventral subiculum and hnRNP U disease phenotypes are an important next step, and may serve as the basis for targeted therapeutic discovery.

Subjects/Keywords: Genetics; Neurosciences; Biology; Genetic transcription – Regulation; Nervous system – Diseases

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

APA (6^th Edition):

Dugger, S. A. (2020). Evaluation of a precision medicine approach for hnRNP U-related developmental epileptic encephalopathy using a mouse model of disease. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-qevc-mw16

Chicago Manual of Style (16^th Edition):

Dugger, Sarah Anne. “Evaluation of a precision medicine approach for hnRNP U-related developmental epileptic encephalopathy using a mouse model of disease.” 2020. Doctoral Dissertation, Columbia University. Accessed January 15, 2021. https://doi.org/10.7916/d8-qevc-mw16.

MLA Handbook (7^th Edition):

Dugger, Sarah Anne. “Evaluation of a precision medicine approach for hnRNP U-related developmental epileptic encephalopathy using a mouse model of disease.” 2020. Web. 15 Jan 2021.

Vancouver:

Dugger SA. Evaluation of a precision medicine approach for hnRNP U-related developmental epileptic encephalopathy using a mouse model of disease. [Internet] [Doctoral dissertation]. Columbia University; 2020. [cited 2021 Jan 15]. Available from: https://doi.org/10.7916/d8-qevc-mw16.

Council of Science Editors:

Dugger SA. Evaluation of a precision medicine approach for hnRNP U-related developmental epileptic encephalopathy using a mouse model of disease. [Doctoral Dissertation]. Columbia University; 2020. Available from: https://doi.org/10.7916/d8-qevc-mw16

Michigan State University

20. Gridasova, Anastasia Alekseevna. Regulation of human small nuclear RNA gene transcription by the tumor suppressor protein P53.

Degree: PhD, Department of Biochemistry and Molecular Biology, 2005, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:33896

Subjects/Keywords: Proteins; RNA; Genetic transcription – Regulation

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APA (6^th Edition):

Gridasova, A. A. (2005). Regulation of human small nuclear RNA gene transcription by the tumor suppressor protein P53. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:33896

Chicago Manual of Style (16^th Edition):

Gridasova, Anastasia Alekseevna. “Regulation of human small nuclear RNA gene transcription by the tumor suppressor protein P53.” 2005. Doctoral Dissertation, Michigan State University. Accessed January 15, 2021. http://etd.lib.msu.edu/islandora/object/etd:33896.

MLA Handbook (7^th Edition):

Gridasova, Anastasia Alekseevna. “Regulation of human small nuclear RNA gene transcription by the tumor suppressor protein P53.” 2005. Web. 15 Jan 2021.

Vancouver:

Gridasova AA. Regulation of human small nuclear RNA gene transcription by the tumor suppressor protein P53. [Internet] [Doctoral dissertation]. Michigan State University; 2005. [cited 2021 Jan 15]. Available from: http://etd.lib.msu.edu/islandora/object/etd:33896.

Council of Science Editors:

Gridasova AA. Regulation of human small nuclear RNA gene transcription by the tumor suppressor protein P53. [Doctoral Dissertation]. Michigan State University; 2005. Available from: http://etd.lib.msu.edu/islandora/object/etd:33896

University of Hong Kong

21. Lee, Tsz-on. Transcriptional regulation of the human secretin gene.

Degree: 2004, University of Hong Kong

URL: http://hdl.handle.net/10722/32041

Subjects/Keywords: Genetic transcription - Regulation.; Secretin.

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

APA (6^th Edition):

Lee, T. (2004). Transcriptional regulation of the human secretin gene. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/32041

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):

Lee, Tsz-on. “Transcriptional regulation of the human secretin gene.” 2004. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/32041.

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

MLA Handbook (7^th Edition):

Lee, Tsz-on. “Transcriptional regulation of the human secretin gene.” 2004. Web. 15 Jan 2021.

Vancouver:

Lee T. Transcriptional regulation of the human secretin gene. [Internet] [Thesis]. University of Hong Kong; 2004. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/32041.

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

Council of Science Editors:

Lee T. Transcriptional regulation of the human secretin gene. [Thesis]. University of Hong Kong; 2004. Available from: http://hdl.handle.net/10722/32041

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

Columbia University

22. Bailey, Elizabeth Jean. The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-1c92-rd35

► Transcription and translation are essential cellular processes that are coupled in bacteria. Though it was well-known that the rate of translation matches the rate of… (more)

▼ Transcription and translation are essential cellular processes that are coupled in bacteria. Though it was well-known that the rate of translation matches the rate of transcription, only in 2010 did evidence suggest direct physical coupling between the transcribing RNA polymerase (RNAP) and the translating ribosome. Nuclear magnetic resonance spectroscopy data showed that the RNAP-binding, transcription factor NusG could bind to the small ribosomal subunit protein, S10, through its C-terminal domain, thus, suggesting a model in which NusG simultaneously binds the transcription and translation machineries. In Chapter Two, I describe my investigations of the mechanism through which NusG-mediated transcription-translation coupling is established in bacteria, and how this coupling is regulated during gene expression. Specifically, I employed cell extract-based luciferase assays and purified C-terminal NusG mutants to show that the NusG N-terminal domain (NTD) and NusG F165A both inhibit transcription. This inhibitory effect was suppressed in an extract derived from a backtracking-resistant RNAP mutant strain, indicating that preventing backtracking by linking RNAP to the lead ribosome is a key function of NusG. While working with the cell extract-based luciferase assay system used to study NusG, I observed that deleting the cryptic rac prophage resulted in cell extracts with extremely low luciferase activity despite the strain having no phenotype in vivo. This initial observation grew into the project described in Chapter Three in which I explore the possibility of viral control of host genes by the poorly characterized rac prophage protein, RacR, through a combination of biochemical methods, structural modeling, bioinformatic analysis, and next-generation, transcriptome-wide, deep RNA sequencing. Taken together, the results reveal overlap between computationally predicted host gene targets and messenger RNA expression levels and suggest that RacR can function as a DNA-binding transcriptional regulator of host genes.

Subjects/Keywords: Biochemistry; Molecular biology; Chemistry; Genetic transcription – Regulation; Escherichia coli

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

APA (6^th Edition):

Bailey, E. J. (2019). The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-1c92-rd35

Chicago Manual of Style (16^th Edition):

Bailey, Elizabeth Jean. “The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli.” 2019. Doctoral Dissertation, Columbia University. Accessed January 15, 2021. https://doi.org/10.7916/d8-1c92-rd35.

MLA Handbook (7^th Edition):

Bailey, Elizabeth Jean. “The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli.” 2019. Web. 15 Jan 2021.

Vancouver:

Bailey EJ. The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Jan 15]. Available from: https://doi.org/10.7916/d8-1c92-rd35.

Council of Science Editors:

Bailey EJ. The Mechanism of NusG-Mediated Transcription-Translation Coupling and The Role of RacR in Transcription Regulation in Escherichia coli. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-1c92-rd35

Hong Kong University of Science and Technology

23. Choy, Siu Wah. Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans.

Degree: 2006, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-2776 ; https://doi.org/10.14711/thesis-b930671 ; http://repository.ust.hk/ir/bitstream/1783.1-2776/1/th_redirect.html

► The male tail of C. elegans is a complex structure composed of nine pairs of sensory rays embedded in a cuticular fan. Among the regulatory… (more)

▼ The male tail of C. elegans is a complex structure composed of nine pairs of sensory rays embedded in a cuticular fan. Among the regulatory genes that pattern these structures, mab-21 is required for the specification of the ray 6 identity. mab-21 mutant males show fusion of rays 4 and 6. The Mab21 gene family is highly conserved in both vertebrate and invertebrate, it is required in neural differentiation and sensory organ development. Epistatic analysis showed that mab-21 is a downstream component of the BMP pathway to regulate ray patterning. Using C. elegans as a simple model, a complete genetic network revealing the genetic relationship of mab-21 and other genes required in this process was established. SIN-3, a histone deacetylase associated corepressor molecule, has long been identified as a repression mediator in transcription. The isolation of SIN-3 through a yeast two-hybrid screen as an interacting partner of MAB-21 provides the first clue of the requirement of the corepressor molecule in ray development. The developmental role of the SIN-3 corepressor complex, as well as its regulatory relationship with MAB-21, was studied in detail in this thesis. The results supported the interaction between SIN-3 corepressor and MAB-21 is important in the ray patterning. To build upon this SIN-3-MAB-21 interaction, we further investigated the genetic relationship of mab-21 and other genes required in this process. We have identified several genes, whereby their mutants display the Mab-21-like phenotype. Mutations of these genes, egl-5, mab-18, unc-130, unc-62 and BMP pathway components, abolish the ray 6 identity. Taking advantage of the available genetic mutants and transcription reporters of these mab-21 -interacting genes, their regulatory relationship was defined. While orthologs of these genes are required in mammalian eye development, sensory ray patterning process of C. elegans serves as a simple model to uncover the genetic relationship among these genes. The finding would extend our understanding into the genetic network conserved between invertebrate and vertebrate sensory organ development.

Subjects/Keywords: Caenorhabditis elegans ; Genetic transcription – Regulation

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

APA (6^th Edition):

Choy, S. W. (2006). Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-2776 ; https://doi.org/10.14711/thesis-b930671 ; http://repository.ust.hk/ir/bitstream/1783.1-2776/1/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):

Choy, Siu Wah. “Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans.” 2006. Thesis, Hong Kong University of Science and Technology. Accessed January 15, 2021. http://repository.ust.hk/ir/Record/1783.1-2776 ; https://doi.org/10.14711/thesis-b930671 ; http://repository.ust.hk/ir/bitstream/1783.1-2776/1/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):

Choy, Siu Wah. “Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans.” 2006. Web. 15 Jan 2021.

Vancouver:

Choy SW. Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2006. [cited 2021 Jan 15]. Available from: http://repository.ust.hk/ir/Record/1783.1-2776 ; https://doi.org/10.14711/thesis-b930671 ; http://repository.ust.hk/ir/bitstream/1783.1-2776/1/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:

Choy SW. Characterization of a transcriptional repressor complex and mab-21 interacting genes in male sensory ray patterning of C. elegans. [Thesis]. Hong Kong University of Science and Technology; 2006. Available from: http://repository.ust.hk/ir/Record/1783.1-2776 ; https://doi.org/10.14711/thesis-b930671 ; http://repository.ust.hk/ir/bitstream/1783.1-2776/1/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. Zhou, Zijing. Studies of ORC dimerization and de-dimerization in the budding yeast saccharomyces cerevisiae.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-62359 ; https://doi.org/10.14711/thesis-b1254348 ; http://repository.ust.hk/ir/bitstream/1783.1-62359/1/th_redirect.html

► DNA replication is fundamental to life and for organisms to transmit their genetic information to the next generation. A crucial step in DNA replication is… (more)

▼ DNA replication is fundamental to life and for organisms to transmit their genetic information to the next generation. A crucial step in DNA replication is replication initiation [1]. This topic has been extensively studied in eukaryotes from yeast to mammalian cells, including investigation in replication initiation proteins, mechanisms controlling replication initiation, and complexes executing the function of initiating replication [2]. Despite all the understanding we have gained in this field, how does an ORC single hexamer as an asymmetric platform recruit the symmetric pre-replicative complex is still a major problem for research trying to construct the replication licensing model. Previously our lab has found evidence that ORC dimerizes, i.e., forming double hexamers. In this thesis, we performed several experiments to further study ORC dimerization and de-dimerization, as well as the potential mechanisms controlling these processes. The first experiment was to use the yeast two-hybrid assay to map the regions which are crucial for ORC dimerization. The gene expressing Orc1p and Orc6p, which are known to self-interact from the previous work of our lab, were dissected, and a series of plasmids were constructed and used to transform the yeast strains to carry out yeast two-hybrid analysis. We found out that a.a. 246-463 of Orc1p and a.a.224-333 of Orc6p have interaction with Orc1p and Orc6p, respectively, and also with the fragments themselves. The second experiment was chromatin binding essay preformed with wild type yeast cells. Based on the previous results from our lab that ORC dimerization could only occur in G1 but not S or G2/M phase, and that newly synthesized ORC could bind to chromatin only during the M-to-G1 transition, we compared the signal ratios of Orc3p/Histone H3 and Mcm2p/Histone H3 on chromatin in different time points when yeast cells were synchronized in M phase and then released into G1 phase. We found that the signal of Orc3p on chromatin began at 10-20 min after release from M phase and doubled at 50 min after release, while Mcm2p chromatin loading was delayed, starting at 20-30 min. These results indicate that ORC dimerization occurs before MCM loading onto chromatin, further supporting the conclusion from our lab that ORC dimerization is required for MCM chromatin loading. We also performed co-immunoprecipitation (co-IP) assay to examine the time course of ORC dimerization. A plasmid co-expressing Orc4-Myc and Orc4-FLAG was used to transform yeast, and cell samples were harvested at different time points during the M-to-G1 and G1-to-S transitions and subjected to co-IP assay. Using anti-FLAG and anti-Myc antibodies for co-IP followed immunobloting, we found out that the co-IP signal appeared at around 20 min after M release. Similarly, we found out that the signal of Orc1-Myc and Orc1-FLAG appeared at around 20 min after M release, and disappeared at 40 min after G1 release. From the data of chromatin binding assay with WT cells, we found out that the phosphorylation status of Orc6p is…

Subjects/Keywords: DNA replication ; Genetic transcription ; Regulation ; Saccharomyces cerevisiae ; Genetics

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

APA (6^th Edition):

Zhou, Z. (2013). Studies of ORC dimerization and de-dimerization in the budding yeast saccharomyces cerevisiae. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-62359 ; https://doi.org/10.14711/thesis-b1254348 ; http://repository.ust.hk/ir/bitstream/1783.1-62359/1/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):

Zhou, Zijing. “Studies of ORC dimerization and de-dimerization in the budding yeast saccharomyces cerevisiae.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed January 15, 2021. http://repository.ust.hk/ir/Record/1783.1-62359 ; https://doi.org/10.14711/thesis-b1254348 ; http://repository.ust.hk/ir/bitstream/1783.1-62359/1/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):

Zhou, Zijing. “Studies of ORC dimerization and de-dimerization in the budding yeast saccharomyces cerevisiae.” 2013. Web. 15 Jan 2021.

Vancouver:

Zhou Z. Studies of ORC dimerization and de-dimerization in the budding yeast saccharomyces cerevisiae. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Jan 15]. Available from: http://repository.ust.hk/ir/Record/1783.1-62359 ; https://doi.org/10.14711/thesis-b1254348 ; http://repository.ust.hk/ir/bitstream/1783.1-62359/1/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:

Zhou Z. Studies of ORC dimerization and de-dimerization in the budding yeast saccharomyces cerevisiae. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-62359 ; https://doi.org/10.14711/thesis-b1254348 ; http://repository.ust.hk/ir/bitstream/1783.1-62359/1/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. Wong, Kam Wai. Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene.

Degree: 2002, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-3889 ; https://doi.org/10.14711/thesis-b777064 ; http://repository.ust.hk/ir/bitstream/1783.1-3889/1/th_redirect.html

► Wnt signaling pathway is well known for its roles in embryonic development and oncogenesis. Frizzled related protein (Frp) is a new family of secreted proteins… (more)

▼ Wnt signaling pathway is well known for its roles in embryonic development and oncogenesis. Frizzled related protein (Frp) is a new family of secreted proteins that contain a region homologous to the extracellular cysteine-rich domain (CRD) of the Wnt receptor, the frizzled family proteins. Recent studies indicate that Frps act as Wnt antagonists in regulating or blocking the Wnt signals in the process of development and carcinogenesis. My major research project was to characterize the promoter activity and the expression patterns of secreted frizzled related protein 4 (sfrp4) gene, a homologue of the rat Frp (rFrp) found previously to be activated transcriptionally in a Rat 6 fibroblast cell line overexpressing p53val135(R6#13-8). In addition, the sfrp4 targeting vector was constructed. This targeting vector would provide the tool for the future development of sfrp4 knockout mice. Data from the early embryonic study showed that the level of sfrp4 mRNA gradually increases from E 9.5 to E 17.5 embryos. Strong signals were detected in otic vesicles, eyes, tail bud and possible other organs in the left abdominal region of the E 9.5, 10.5 and 11.5 embryos using whole mount in-situ hybridization. The results suggest that the sfrp4 gene may play a significant role in the early developmental stage of mouse embryos. At the same time, the transcriptional regulation of the gene was being explored in my study. A 1.5 kb promoter region of mouse sfrp4 was cloned and sequenced. Sequence alignments among rat, mouse and human reveal the putative transcriptional factor binding elements, some of which are well conserved among these three species. The promoter region of sfrp4 was analyzed using transient reporter assays along with site-directed mutagenesis. The Site 1, STAT3/Lyf-1/MZF1 & Site 2, C/EBP-β/GATA-1/CREB putative transcriptional factor binding sites were located in the mouse sfrp4 promoter spanning from nucleotides -238 to -144 that were found to be essential for the promoter activity of sfrp4. In addition to Sites 1 & 2, putative transcriptional factor binding sites for TFIID, SP1/GC and ATF/CREB exhibited positive, while sites for NRSE exhibited negative regulatory functions, as determined by the alkaline phosphatase activities of the reporter assay. We also demonstrated that the ATF/CREB site might cooperatively interact with the putative NRSF element in regulating sfrp4 activity. The data of this present study, the first promoter analysis of mouse Frp genes, provides the basis toward the understanding the tissue specific functions of frp and its role in regulating Wnt-signals.

Subjects/Keywords: Gene expression ; Genetic transcription – Regulation

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APA (6^th Edition):

Wong, K. W. (2002). Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-3889 ; https://doi.org/10.14711/thesis-b777064 ; http://repository.ust.hk/ir/bitstream/1783.1-3889/1/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):

Wong, Kam Wai. “Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene.” 2002. Thesis, Hong Kong University of Science and Technology. Accessed January 15, 2021. http://repository.ust.hk/ir/Record/1783.1-3889 ; https://doi.org/10.14711/thesis-b777064 ; http://repository.ust.hk/ir/bitstream/1783.1-3889/1/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):

Wong, Kam Wai. “Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene.” 2002. Web. 15 Jan 2021.

Vancouver:

Wong KW. Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2002. [cited 2021 Jan 15]. Available from: http://repository.ust.hk/ir/Record/1783.1-3889 ; https://doi.org/10.14711/thesis-b777064 ; http://repository.ust.hk/ir/bitstream/1783.1-3889/1/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:

Wong KW. Gene expression and transcriptional regulation of the mouse frizzled related protein-4 gene. [Thesis]. Hong Kong University of Science and Technology; 2002. Available from: http://repository.ust.hk/ir/Record/1783.1-3889 ; https://doi.org/10.14711/thesis-b777064 ; http://repository.ust.hk/ir/bitstream/1783.1-3889/1/th_redirect.html

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

IUPUI

26. Carbe, Christian J. GENETIC CONTROL OF EYE AND CENTRAL NERVOUS SYSTEM DEVELOPMENT.

Degree: 2011, IUPUI

URL: http://hdl.handle.net/1805/2605

►

Indiana University-Purdue University Indianapolis (IUPUI)

Aniridia, a congenital ocular disorder caused by haploinsufficiency of transcription factor PAX6, is characterized by complete or partial iris hypoplasia… (more)

▼

Indiana University-Purdue University Indianapolis (IUPUI)

Aniridia, a congenital ocular disorder caused by haploinsufficiency of transcription factor PAX6, is characterized by complete or partial iris hypoplasia with associated foveal hypoplasia. Brain imaging performed in patients heterozygous for PAX6 mutations often reveal absence of the brain anterior or posterior commissure, absence of the pineal gland, and a present but reduced in size corpus callosum. Renal coloboma syndrome, another autosomal dominant inherited disease, is characterized by hypodysplastic kidneys and optic nerve defects, and is caused by haploinsufficiency of transcription factor PAX2. In the first part of this thesis we investigated the role of these Pax genes in neural development, by generating an allelic series of knock-in models at the Pax6 locus. We showed that Pax6(5a) and Pax2 could not replace Pax6 for its auto-regulation in lens induction or for neural differentiation in retina. In brain development, however, we demonstrated that cell proliferation in the cerebral cortex and dorsoventral patterning of the telencephalon and neural tube was partially rescued in either knock-in mutant. We believe our novel findings not only reveal Pax-protein functional specificity during neural development, but may also be utilized to understand the aberrant molecular mechanism that result in aniridia and/or renal coloboma syndrome. Aphakia (lack of lens) is a rare human congenital disorder with its genetic etiology largely unknown. In the second part of this thesis, we show that homozygous deletion of Nf1, the Ras GTPase gene underlying human neurofibromatosis type 1 syndrome, caused lens dysgenesis in mouse. While early lens specification proceeded normally in Nf1 mutants, lens induction was disrupted due to deficient cell proliferation. Further analysis showed that ERK signaling was initially elevated in invaginating lens placode, but by lens vesicle stage, Ras signaling antagonist Sprouty2 was up regulated, followed by rapid decrease in ERK phosphorylation. Only after intraperitoneal treatment of U0126, an inhibitor of ERK phosphorylation, was lens development restored in Nf1 mutants. Hyperactive RAS-MAPK signaling is known to cause neuro-cardiofacial-cutaneous (NCFC) syndromes in human. As a member of NCFC family genes, Nf1 represents the first example that attenuation of Ras-MAPK kinase signaling pathway is essential for normal lens development.

Advisors/Committee Members: Zhang, Xin, White, Kenneth E., Firulli, Anthony B., Thurmond, Debbie C..

Subjects/Keywords: Eye – Diseases – Genetic aspects; Transcription factors; Genes – Regulation; Brain – Imaging

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

APA (6^th Edition):

Carbe, C. J. (2011). GENETIC CONTROL OF EYE AND CENTRAL NERVOUS SYSTEM DEVELOPMENT. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/2605

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):

Carbe, Christian J. “GENETIC CONTROL OF EYE AND CENTRAL NERVOUS SYSTEM DEVELOPMENT.” 2011. Thesis, IUPUI. Accessed January 15, 2021. http://hdl.handle.net/1805/2605.

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

MLA Handbook (7^th Edition):

Carbe, Christian J. “GENETIC CONTROL OF EYE AND CENTRAL NERVOUS SYSTEM DEVELOPMENT.” 2011. Web. 15 Jan 2021.

Vancouver:

Carbe CJ. GENETIC CONTROL OF EYE AND CENTRAL NERVOUS SYSTEM DEVELOPMENT. [Internet] [Thesis]. IUPUI; 2011. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1805/2605.

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

Council of Science Editors:

Carbe CJ. GENETIC CONTROL OF EYE AND CENTRAL NERVOUS SYSTEM DEVELOPMENT. [Thesis]. IUPUI; 2011. Available from: http://hdl.handle.net/1805/2605

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

University of Texas – Austin

27. Draper, Moon. Transcriptional regulation of the shaker homolog Kv3.

Degree: PhD, Ecology, Evolution and Behavior ; Microbiology ; Plant Biology, 2005, University of Texas – Austin

URL: http://hdl.handle.net/2152/2417

► The sequencing of entire genomes has brought into light the code of life, and along with it, many questions. Comparisons between whole genomes revealed that… (more)

Subjects/Keywords: Genetic transcription – Regulation; Genomes

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

APA (6^th Edition):

Draper, M. (2005). Transcriptional regulation of the shaker homolog Kv3. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/2417

Chicago Manual of Style (16^th Edition):

Draper, Moon. “Transcriptional regulation of the shaker homolog Kv3.” 2005. Doctoral Dissertation, University of Texas – Austin. Accessed January 15, 2021. http://hdl.handle.net/2152/2417.

MLA Handbook (7^th Edition):

Draper, Moon. “Transcriptional regulation of the shaker homolog Kv3.” 2005. Web. 15 Jan 2021.

Vancouver:

Draper M. Transcriptional regulation of the shaker homolog Kv3. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2005. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2152/2417.

Council of Science Editors:

Draper M. Transcriptional regulation of the shaker homolog Kv3. [Doctoral Dissertation]. University of Texas – Austin; 2005. Available from: http://hdl.handle.net/2152/2417

Rutgers University

28. Traldi, Eliane Zerbetto, 1975-. Modeling regulation of transcription initiation.

Degree: Computational Biology and Molecular Biophysics, 2011, Rutgers University

URL: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063670

Subjects/Keywords: Genetic transcription—Regulation; RNA—Synthesis

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

APA (6^th Edition):

Traldi, Eliane Zerbetto, 1. (2011). Modeling regulation of transcription initiation. (Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063670

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):

Traldi, Eliane Zerbetto, 1975-. “Modeling regulation of transcription initiation.” 2011. Thesis, Rutgers University. Accessed January 15, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063670.

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

MLA Handbook (7^th Edition):

Traldi, Eliane Zerbetto, 1975-. “Modeling regulation of transcription initiation.” 2011. Web. 15 Jan 2021.

Vancouver:

Traldi, Eliane Zerbetto 1. Modeling regulation of transcription initiation. [Internet] [Thesis]. Rutgers University; 2011. [cited 2021 Jan 15]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063670.

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

Council of Science Editors:

Traldi, Eliane Zerbetto 1. Modeling regulation of transcription initiation. [Thesis]. Rutgers University; 2011. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000063670

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

University of Oklahoma

29. Maddox, Scott M. Transcriptional Adaptation of Enterococcus faecalis within Macrophages and the Role of PerA in Virulence.

Degree: PhD, 2011, University of Oklahoma

URL: http://hdl.handle.net/11244/318783

► The intestinal ecosystem is comprised of bacteria that are both beneficial and detrimental to human health. The opportunistic pathogens residing within the gastrointestinal tract typically… (more)

Subjects/Keywords: Enterococcus faecalis; Virulence (Microbiology); Macrophages; Genetic regulation; Transcription factors

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APA (6^th Edition):

Maddox, S. M. (2011). Transcriptional Adaptation of Enterococcus faecalis within Macrophages and the Role of PerA in Virulence. (Doctoral Dissertation). University of Oklahoma. Retrieved from http://hdl.handle.net/11244/318783

Chicago Manual of Style (16^th Edition):

Maddox, Scott M. “Transcriptional Adaptation of Enterococcus faecalis within Macrophages and the Role of PerA in Virulence.” 2011. Doctoral Dissertation, University of Oklahoma. Accessed January 15, 2021. http://hdl.handle.net/11244/318783.

MLA Handbook (7^th Edition):

Maddox, Scott M. “Transcriptional Adaptation of Enterococcus faecalis within Macrophages and the Role of PerA in Virulence.” 2011. Web. 15 Jan 2021.

Vancouver:

Maddox SM. Transcriptional Adaptation of Enterococcus faecalis within Macrophages and the Role of PerA in Virulence. [Internet] [Doctoral dissertation]. University of Oklahoma; 2011. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/11244/318783.

Council of Science Editors:

Maddox SM. Transcriptional Adaptation of Enterococcus faecalis within Macrophages and the Role of PerA in Virulence. [Doctoral Dissertation]. University of Oklahoma; 2011. Available from: http://hdl.handle.net/11244/318783

IUPUI

30. Mullen, Rachel D. In Vivo Analysis of Human LHX3 Gene Regulation.

Degree: 2011, IUPUI

URL: http://hdl.handle.net/1805/2595

►

Indiana University-Purdue University Indianapolis (IUPUI)

LHX3 is a transcription factor important in pituitary and nervous system development. Patients with mutations in coding regions of the… (more)

▼

Indiana University-Purdue University Indianapolis (IUPUI)

LHX3 is a transcription factor important in pituitary and nervous system development. Patients with mutations in coding regions of the gene have combined pituitary hormone deficiency (CPHD) that causes growth, fertility, and metabolic problems. Promoter and intronic elements of LHX3 important for basal gene expression in vitro have been identified, but the key regulatory elements necessary for in vivo expression were unknown. With these studies, I sought to elucidate how LHX3 gene expression is regulated in vivo. Based on sequence conservation between species in non-coding regions, I identified a 7.9 kilobase (kb) region 3' of the human LHX3 gene as a potential regulatory element. In a beta galactosidase transgenic mouse model, this region directed spatial and temporal expression to the developing pituitary gland and spinal cord in a pattern consistent with endogenous LHX3 expression. Using a systematic series of deletions, I found that the conserved region contains multiple nervous system enhancers and a minimal 180 base pair (bp) enhancer that direct expression to both the pituitary and spinal cord in transgenic mice. Within this minimal enhancer, TAAT/ATTA sequences that are characteristic of homeodomain protein binding sites are required to direct expression. I performed DNA binding experiments and chromatin immunoprecipitation assays to reveal that the ISL1 and PITX1 proteins specifically recognize these elements in vitro and in vivo. Based on in vivo mutational analyses, two tandem ISL1 binding sites are required for enhancer activity in the pituitary and spine and a PITX1 binding site is required for spatial patterning of gene expression in the pituitary. Additional experiments demonstrated that these three elements cannot alone direct gene expression, suggesting a combination of factors is required for enhancer activity. This study reveals that the key regulatory elements guiding developmental regulation of the human LHX3 gene lie in this conserved downstream region. Further, this work implicates ISL1 as a new transcriptional regulator of LHX3 and describes a possible mechanism for the regulation of LHX3 by a known upstream factor, PITX1. Identification of important regulatory regions will also enable genetic screening in candidate CPHD patients and will thereby facilitate patient treatment and genetic counseling.

Advisors/Committee Members: Rhodes, Simon J., Herring, B. Paul, Skalnik, David Gordon, Thurmond, Debbie C., Walvoord, Emily C..

Subjects/Keywords: Gene Regulation; Pituitary; Combined Pituitary Hormone Deficiency; LHX3; Genetic regulation; Transcription factors; Pituitary hormones

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

APA (6^th Edition):

Mullen, R. D. (2011). In Vivo Analysis of Human LHX3 Gene Regulation. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/2595

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):

Mullen, Rachel D. “In Vivo Analysis of Human LHX3 Gene Regulation.” 2011. Thesis, IUPUI. Accessed January 15, 2021. http://hdl.handle.net/1805/2595.

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

MLA Handbook (7^th Edition):

Mullen, Rachel D. “In Vivo Analysis of Human LHX3 Gene Regulation.” 2011. Web. 15 Jan 2021.

Vancouver:

Mullen RD. In Vivo Analysis of Human LHX3 Gene Regulation. [Internet] [Thesis]. IUPUI; 2011. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1805/2595.

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

Council of Science Editors:

Mullen RD. In Vivo Analysis of Human LHX3 Gene Regulation. [Thesis]. IUPUI; 2011. Available from: http://hdl.handle.net/1805/2595

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

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Open Access Theses and Dissertations