subject:(Cellular)

Wright State University

1. Battini, Vishnu Priya Chowdary. Accurate splicing of HDAC6 requires Son.

Degree: MS, Biological Sciences, 2013, Wright State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=wright1390306890

► Pre-mRNA splicing requires proper splice site selection mediated by many factors including snRNPs and serine-arginine rich (SR) splicing factors. Son is the largest known SR… (more)

▼ Pre-mRNA splicing requires proper splice site selection mediated by many factors including snRNPs and serine-arginine rich (SR) splicing factors. Son is the largest known SR splicing factor, and it has several putative functional domains including an RS domain, a glycine rich patch (G-patch) and double stranded RNA binding domain (DSRBD). One-third of Son’s amino acid sequence consists of novel repetitive sequence motifs of unknown function (Sharma et al., 2010). Son is essential for organization of pre-mRNA processing factors in nuclear speckles and for cell cycle progression (Sharma et al., 2010; Sharma et al., 2011; Ahn et al 2011). Exon array analysis of Son-depleted HeLa cells revealed changes in 1061 transcripts showing exon inclusion or exclusion, and a total of 2067 splicing events that are potentially regulated by Son. We validated that Son is required for appropriate splice site choice in transcripts for several chromatin-modifying enzymes, including HDAC6, ADA and SETD8 (Sharma et al., 2011). However, the mechanism by which Son maintains accurate splicing is unknown. We are systematically generating model minigene cassettes for molecular and in situ analysis of Son-dependent splicing regulation. We have constructed a HDAC6 minigene reporter that contains the genomic sequence spanning exons 26 through 29. Following Son depletion in HeLa cells transiently transfected with the HDAC6 minigene reporter construct, we observed skipping of exons 27 and 28 on both the reporter and endogenous HDAC6 transcripts. Stable cell lines constructed using HDAC6 minigene reporter construct showed exclusion of exons 27 and 28 upon Son depletion. In order to study Son-dependent splicing on HDAC6 in situ, we aimed to localize splicing factor recruitment to the HDAC6 reporter minigene transcription site; however, RNA-FISH performed using probes designed to bind to HDAC6 minigene transcripts did not show reproducible labeling of the transcription locus. Finally, HEK293 cells stably expressing four different siRNA-refractory Son deletion mutants were used to show rescue splicing of HDAC6 minigene transcripts. Advisors/Committee Members: Bubulya, Paula (Advisor).

Subjects/Keywords: Cellular Biology; cellular biology

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APA (6^th Edition):

Battini, V. P. C. (2013). Accurate splicing of HDAC6 requires Son. (Masters Thesis). Wright State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=wright1390306890

Chicago Manual of Style (16^th Edition):

Battini, Vishnu Priya Chowdary. “Accurate splicing of HDAC6 requires Son.” 2013. Masters Thesis, Wright State University. Accessed January 19, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1390306890.

MLA Handbook (7^th Edition):

Battini, Vishnu Priya Chowdary. “Accurate splicing of HDAC6 requires Son.” 2013. Web. 19 Jan 2021.

Vancouver:

Battini VPC. Accurate splicing of HDAC6 requires Son. [Internet] [Masters thesis]. Wright State University; 2013. [cited 2021 Jan 19]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1390306890.

Council of Science Editors:

Battini VPC. Accurate splicing of HDAC6 requires Son. [Masters Thesis]. Wright State University; 2013. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1390306890

University of California – Berkeley

2. Acosta, Jamie. Integrating form and function in the mammary gland: crosstalk of extracellular matrix, extracellular matrix degrading enzymes and epithelial cells in 3D cultures and engineered mice.

Degree: Comparative Biochemistry, 2015, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/1zk6s482

► Tissues exist in a highly ordered three dimensional structure that is critical to inform function. When cells are explanted into culture, the tissue-specific functions are… (more)

▼ Tissues exist in a highly ordered three dimensional structure that is critical to inform function. When cells are explanted into culture, the tissue-specific functions are often lost or drastically altered suggesting that the lowest functional unit in higher organisms is not a cell but a cell associated with a particular extracellular matrix (ECM) (Bissell, 1981; Bissell and Hall, 1987). Indeed the unit of function in a larger context is the organ itself (Bissell and Hall, 1987). In our studies of the mammary gland, its ECM and ECM-degrading enzymes we have employed culture models that begin to recreate the tissue structure and aspects of the normal mammary gland microenvironment. These three dimensional (3D) culture models provided a platform to ask questions- and elucidate functions- of mammary gland development and mechanisms of tumorigenesis within a 3D structure. We examined the ultrastructural features of a progression series where cells became tumorigenic outside the human body (Briand et al., 1987; Petersen et al., 1992; Rizki et al., 2008). In 3D culture the non-malignant cells form growth arrested acinus-like structures and the malignant cells form disorganized masses that do not growth arrest. Electron microscopy imaging of the non-malignant S1 acini revealed that the cell line thought to represent highly polarized luminal epithelial cells of the human breast displayed features consistent with a luminal-basal hybrid cell line. The acini had well-organized basal polarity and basement membrane (BM). The BM is a specialized ECM that separates epithelial, endothelial and fat cells from the surrounding connective tissue and functions as a selective barrier and organizer of organs. The acini had partially apically oriented tight junctions (ZO-1 protein) suggestive of less apical polarization. They also displayed irregular microvilli projections, primary cilia and nuclear invaginations characteristic of basal cells. We found that the three dimensional acini were growth arrested and demonstrated polarized distribution of organelles and proteins (Petersen et al., 1992). Overall the features suggested that S1 cells are a hybrid of a luminal and basal cell perhaps representing a progenitor cell of the human breast. The BM protein laminin-111 has been shown to be necessary for polarization of mammary epithelium (Gudjonsson et al., 2002) and functional differentiation (Streuli et al., 1991). Here, we knocked down the unique chain of laminin-111, laminin α1, in the HMT-3522-S1 and found that polarity and growth arrest were disrupted despite the presence of laminin-111 in the 3D assay. We show endogenous laminin α1 regulates levels of the matrix degrading enzyme MMP9, activation of signaling pathways and secretion of other ECM proteins. We have shown previously that modulating malignant pathways reverts the malignant phenotype (Weaver et al., 1997; Wang et al., 2002; Beliveau et al., 2010). Expression of the laminin α1 protein in the syngeneic tumor cell line, T4, revealed that cells transfected with the LAMA1 construct…

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Acosta, J. (2015). Integrating form and function in the mammary gland: crosstalk of extracellular matrix, extracellular matrix degrading enzymes and epithelial cells in 3D cultures and engineered mice. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/1zk6s482

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):

Acosta, Jamie. “Integrating form and function in the mammary gland: crosstalk of extracellular matrix, extracellular matrix degrading enzymes and epithelial cells in 3D cultures and engineered mice.” 2015. Thesis, University of California – Berkeley. Accessed January 19, 2021. http://www.escholarship.org/uc/item/1zk6s482.

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

MLA Handbook (7^th Edition):

Acosta, Jamie. “Integrating form and function in the mammary gland: crosstalk of extracellular matrix, extracellular matrix degrading enzymes and epithelial cells in 3D cultures and engineered mice.” 2015. Web. 19 Jan 2021.

Vancouver:

Acosta J. Integrating form and function in the mammary gland: crosstalk of extracellular matrix, extracellular matrix degrading enzymes and epithelial cells in 3D cultures and engineered mice. [Internet] [Thesis]. University of California – Berkeley; 2015. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/1zk6s482.

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

Council of Science Editors:

Acosta J. Integrating form and function in the mammary gland: crosstalk of extracellular matrix, extracellular matrix degrading enzymes and epithelial cells in 3D cultures and engineered mice. [Thesis]. University of California – Berkeley; 2015. Available from: http://www.escholarship.org/uc/item/1zk6s482

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

University of California – Berkeley

3. Helmke, Kara. Interspecies Comparisons of Xenopus Egg Extracts Reveal Mechanisms for Modulating Meiotic Spindle Size and Architecture.

Degree: Molecular & Cell Biology, 2014, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/8vz146zw

► The function of the spindle to faithfully segregate chromosomes is universal among eukaryotes. A common feature of metaphase spindles is their self-organizing, bipolar structure, with… (more)

▼ The function of the spindle to faithfully segregate chromosomes is universal among eukaryotes. A common feature of metaphase spindles is their self-organizing, bipolar structure, with microtubules organized into polar arrays by the activity of motors and other proteins. However, wide variation in spindle assembly, size and morphology is observed among different cell types, presumably to optimize spindle function. While many of the hundreds of conserved spindle assembly factors have been identified, how these proteins interact to establish a particular spindle architecture is poorly understood.Xenopus provides a valuable system to study a variety of spindle types in vitro, since spindles formed in egg and embryo extracts recapitulate morphologies observed in vivo. The ellipsoidal, ~35 μm long Xenopus laevis meiotic spindle has been studied most extensively and is thought to be built from a tiled array of dynamic, overlapping microtubules. Meiotic spindles assembled in egg extracts of the smaller Xenopus tropicalis frog possess a similar anastral appearance but are significantly shorter at ~22 μm. Previously, these two extracts were used to identify proteins which regulate spindle length, and a microtubule-severing protein p60 katanin was shown to be differentially phospho-regulated between these two systems. Activity differences in p60 katanin were not sufficient to explain the size differences between X. tropicalis and X. laevis, and this study identifies TPX2 as an additional length regulator that also contributes to other features of spindle architecture.In addition to evaluating spindle length, we probed the involvement of positional microtubule nucleation, motor organization, and microtubule distribution as contributors to architectural features. Spindles formed in X. laevis extracts have been previously shown to rely heavily on both microtubule nucleation near the chromatin governed by the protein RanGTP as well as organization of antiparallel arrays by the kinesin-5 motor Eg5, resulting in a structure with a tiled array of microtubules in almost constant density pole-to-pole. Intriguingly, X. tropicalis extract spindles do not require either process, as indicated by resistance to inhibition of these pathways. Furthermore, X. tropicalis microtubule density is significantly reduced in the spindle midzone. We focused on the role of the microtubule-associated factor TPX2 in mediating these differences, since it has been shown to interact both with Ran and Eg5. Levels of TPX2 were measured to be approximately 3-fold higher in X. tropicalis. Addition of excess TPX2 to X. laevis extract recapitulated differences seen in the architectures of the two spindles: rendering spindles less sensitive to RanGTP and Eg5 inhibition and as well as reducing spindle length. These spindles also showed increased recruitment of Eg5 to the spindle poles, where…

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Helmke, K. (2014). Interspecies Comparisons of Xenopus Egg Extracts Reveal Mechanisms for Modulating Meiotic Spindle Size and Architecture. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/8vz146zw

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):

Helmke, Kara. “Interspecies Comparisons of Xenopus Egg Extracts Reveal Mechanisms for Modulating Meiotic Spindle Size and Architecture.” 2014. Thesis, University of California – Berkeley. Accessed January 19, 2021. http://www.escholarship.org/uc/item/8vz146zw.

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

MLA Handbook (7^th Edition):

Helmke, Kara. “Interspecies Comparisons of Xenopus Egg Extracts Reveal Mechanisms for Modulating Meiotic Spindle Size and Architecture.” 2014. Web. 19 Jan 2021.

Vancouver:

Helmke K. Interspecies Comparisons of Xenopus Egg Extracts Reveal Mechanisms for Modulating Meiotic Spindle Size and Architecture. [Internet] [Thesis]. University of California – Berkeley; 2014. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/8vz146zw.

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

Council of Science Editors:

Helmke K. Interspecies Comparisons of Xenopus Egg Extracts Reveal Mechanisms for Modulating Meiotic Spindle Size and Architecture. [Thesis]. University of California – Berkeley; 2014. Available from: http://www.escholarship.org/uc/item/8vz146zw

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

University of California – Riverside

4. Truong, Tan Minh. Development of a Phage Display System for Engineering Peptide Inhibitors Containing Multiple Non-Canonical Amino Acids.

Degree: Cell, Molecular and Developmental Biology, 2017, University of California – Riverside

URL: http://www.escholarship.org/uc/item/46s2552t

► Phage display is a powerful screening method capable of potentially screening over 1011 unique peptide sequences for protein-protein or protein-DNA interactions. It has been extensively… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Truong, T. M. (2017). Development of a Phage Display System for Engineering Peptide Inhibitors Containing Multiple Non-Canonical Amino Acids. (Thesis). University of California – Riverside. Retrieved from http://www.escholarship.org/uc/item/46s2552t

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):

Truong, Tan Minh. “Development of a Phage Display System for Engineering Peptide Inhibitors Containing Multiple Non-Canonical Amino Acids.” 2017. Thesis, University of California – Riverside. Accessed January 19, 2021. http://www.escholarship.org/uc/item/46s2552t.

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

MLA Handbook (7^th Edition):

Truong, Tan Minh. “Development of a Phage Display System for Engineering Peptide Inhibitors Containing Multiple Non-Canonical Amino Acids.” 2017. Web. 19 Jan 2021.

Vancouver:

Truong TM. Development of a Phage Display System for Engineering Peptide Inhibitors Containing Multiple Non-Canonical Amino Acids. [Internet] [Thesis]. University of California – Riverside; 2017. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/46s2552t.

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

Council of Science Editors:

Truong TM. Development of a Phage Display System for Engineering Peptide Inhibitors Containing Multiple Non-Canonical Amino Acids. [Thesis]. University of California – Riverside; 2017. Available from: http://www.escholarship.org/uc/item/46s2552t

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

UCLA

5. Sullivan, William Juster. Hyaluronidase Promotes Glucose Metabolism: Identification of the Extracellular Matrix as a Node of Cell-Extrinsic Metabolic Regulation.

Degree: Molecular and Medical Pharmacology, 2017, UCLA

URL: http://www.escholarship.org/uc/item/4fj8f40n

► The metabolic state of a cell can be determined by cell-extrinsic factors, including nutrient availability and growth factor signaling. Here, we define extracellular matrix (ECM)… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Sullivan, W. J. (2017). Hyaluronidase Promotes Glucose Metabolism: Identification of the Extracellular Matrix as a Node of Cell-Extrinsic Metabolic Regulation. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/4fj8f40n

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):

Sullivan, William Juster. “Hyaluronidase Promotes Glucose Metabolism: Identification of the Extracellular Matrix as a Node of Cell-Extrinsic Metabolic Regulation.” 2017. Thesis, UCLA. Accessed January 19, 2021. http://www.escholarship.org/uc/item/4fj8f40n.

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

MLA Handbook (7^th Edition):

Sullivan, William Juster. “Hyaluronidase Promotes Glucose Metabolism: Identification of the Extracellular Matrix as a Node of Cell-Extrinsic Metabolic Regulation.” 2017. Web. 19 Jan 2021.

Vancouver:

Sullivan WJ. Hyaluronidase Promotes Glucose Metabolism: Identification of the Extracellular Matrix as a Node of Cell-Extrinsic Metabolic Regulation. [Internet] [Thesis]. UCLA; 2017. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/4fj8f40n.

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

Council of Science Editors:

Sullivan WJ. Hyaluronidase Promotes Glucose Metabolism: Identification of the Extracellular Matrix as a Node of Cell-Extrinsic Metabolic Regulation. [Thesis]. UCLA; 2017. Available from: http://www.escholarship.org/uc/item/4fj8f40n

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

University of California – Berkeley

6. Carroll, Susheela Yogini. Uptake of Toxin K28 and Early Endocytic Site Formation in S. cerevisiae.

Degree: Molecular & Cell Biology, 2010, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/7gz0d3vf

► K28 is an A/B toxin that targets yeast cells and depends on endocytosis and retrograde trafficking for toxicity. Knowledge of the specific proteins, lipids, and… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Carroll, S. Y. (2010). Uptake of Toxin K28 and Early Endocytic Site Formation in S. cerevisiae. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/7gz0d3vf

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):

Carroll, Susheela Yogini. “Uptake of Toxin K28 and Early Endocytic Site Formation in S. cerevisiae.” 2010. Thesis, University of California – Berkeley. Accessed January 19, 2021. http://www.escholarship.org/uc/item/7gz0d3vf.

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

MLA Handbook (7^th Edition):

Carroll, Susheela Yogini. “Uptake of Toxin K28 and Early Endocytic Site Formation in S. cerevisiae.” 2010. Web. 19 Jan 2021.

Vancouver:

Carroll SY. Uptake of Toxin K28 and Early Endocytic Site Formation in S. cerevisiae. [Internet] [Thesis]. University of California – Berkeley; 2010. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/7gz0d3vf.

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

Council of Science Editors:

Carroll SY. Uptake of Toxin K28 and Early Endocytic Site Formation in S. cerevisiae. [Thesis]. University of California – Berkeley; 2010. Available from: http://www.escholarship.org/uc/item/7gz0d3vf

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

University of California – Berkeley

7. Joyner, Ryan Preston. The Dynamic Organization of the Yeast Genome.

Degree: Molecular & Cell Biology, 2014, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/3565x0kc

► Regardless of size, shape, or function, all cells must rapidly respond to a changing environment, especially in adverse conditions. Various environmental stresses including heat shock,… (more)

▼ Regardless of size, shape, or function, all cells must rapidly respond to a changing environment, especially in adverse conditions. Various environmental stresses including heat shock, osmotic stress, and nutrient starvation consequently induce dramatic changes in the molecular composition of cellular machinery. Importantly, the cell's adjustment to a new homeostasis is accomplished through a variety of mechanisms, but most predominantly through the regulation of gene expression which is normally thought to function through the interplay of specific transcriptional repressors and activators. Recent evidence suggests, however, that more novel forms of transcriptional regulation may exist, including the repositioning of specific genes to distinct subdomains within the nucleus and through global changes in genome organization. Moreover, it has been hypothesized that such changes may function to supplement more traditional models of transcriptional regulation. Thus, upon environmental stress, cells may dramatically modify global transcriptional programs through a reorganization of their genome, facilitating a more rapid response to an adverse environment. The budding yeast Saccharomyces cerevisiae represents a remarkable model for elucidating how the organization of the genome and the repositioning of specific genes may function to regulate gene expression. In yeast, certain cellular stresses are known to stimulate the repositioning of genes within the nucleus and alter the global organization of the genome. Despite considerable research into the dynamic nature of genome organization, however, many questions remain as to the true function of gene positioning and the mechanism(s) by which cells establish specific organizational conformations of the genome.In the following dissertation, I first provide evidence on the function of repositioning a specific gene to the nuclear periphery by examining the consequences of improperly localizing the GAL locus of budding yeast. Next, I describe my attempts to discern the coordinated diffusion of co-regulated genes as well as my findings on the independent movement of loci positioned various distances apart on the same chromosome. Finally, I describe novel findings on the mechanism of chromatin mobility through experiments focused on understanding the biological determinants of intracellular diffusion. Together, my results suggest that chromatin mobility is, in part, actively driven, which may function to facilitate more rapid alterations in genome organization and thus more rapid regulation of gene expression.I first set out to understand the function of repositioning specific genes to distinct locations within the nucleus. In yeast, the GAL locus, comprised of GAL1, GAL7, and GAL10 and necessary for the metabolism of galactose, re-localizes from a central position of the nucleus when repressed to the nuclear periphery when transcriptionally active. To understand the function of this specific repositioning, I took advantage of mutants in different macromolecular…

Subjects/Keywords: Cellular biology

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

APA (6^th Edition):

Joyner, R. P. (2014). The Dynamic Organization of the Yeast Genome. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/3565x0kc

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):

Joyner, Ryan Preston. “The Dynamic Organization of the Yeast Genome.” 2014. Thesis, University of California – Berkeley. Accessed January 19, 2021. http://www.escholarship.org/uc/item/3565x0kc.

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

MLA Handbook (7^th Edition):

Joyner, Ryan Preston. “The Dynamic Organization of the Yeast Genome.” 2014. Web. 19 Jan 2021.

Vancouver:

Joyner RP. The Dynamic Organization of the Yeast Genome. [Internet] [Thesis]. University of California – Berkeley; 2014. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/3565x0kc.

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

Council of Science Editors:

Joyner RP. The Dynamic Organization of the Yeast Genome. [Thesis]. University of California – Berkeley; 2014. Available from: http://www.escholarship.org/uc/item/3565x0kc

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

University of California – Santa Cruz

8. Lim, Angeline. Axonal Transport Of Neuropeptides In Drosophila Axons.

Degree: Molecular Cell and Developmental Biology, 2014, University of California – Santa Cruz

URL: http://www.escholarship.org/uc/item/3v52j5rs

► Microtubule motor proteins are known to drive long distance organelle transport in neurons, but there are many motor species and many organelle types, so specific… (more)

Subjects/Keywords: Cellular biology

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

APA (6^th Edition):

Lim, A. (2014). Axonal Transport Of Neuropeptides In Drosophila Axons. (Thesis). University of California – Santa Cruz. Retrieved from http://www.escholarship.org/uc/item/3v52j5rs

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):

Lim, Angeline. “Axonal Transport Of Neuropeptides In Drosophila Axons.” 2014. Thesis, University of California – Santa Cruz. Accessed January 19, 2021. http://www.escholarship.org/uc/item/3v52j5rs.

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

MLA Handbook (7^th Edition):

Lim, Angeline. “Axonal Transport Of Neuropeptides In Drosophila Axons.” 2014. Web. 19 Jan 2021.

Vancouver:

Lim A. Axonal Transport Of Neuropeptides In Drosophila Axons. [Internet] [Thesis]. University of California – Santa Cruz; 2014. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/3v52j5rs.

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

Council of Science Editors:

Lim A. Axonal Transport Of Neuropeptides In Drosophila Axons. [Thesis]. University of California – Santa Cruz; 2014. Available from: http://www.escholarship.org/uc/item/3v52j5rs

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

University of California – San Diego

9. Chou, Annie Chiazong. Characterization of an internal ribosomal entry site in the coding sequence of tyrosyl-DNA phosphodiesterase 2.

Degree: Biomedical Sciences, 2018, University of California – San Diego

URL: http://www.escholarship.org/uc/item/5n965003

► Tyrosyl DNA-phosphodiesterase 2 (TDP2) is a multifunctional protein that has been implicated in a myriad of cellular pathways. While most well-known for its phosphodiesterase activity… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Chou, A. C. (2018). Characterization of an internal ribosomal entry site in the coding sequence of tyrosyl-DNA phosphodiesterase 2. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/5n965003

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):

Chou, Annie Chiazong. “Characterization of an internal ribosomal entry site in the coding sequence of tyrosyl-DNA phosphodiesterase 2.” 2018. Thesis, University of California – San Diego. Accessed January 19, 2021. http://www.escholarship.org/uc/item/5n965003.

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

MLA Handbook (7^th Edition):

Chou, Annie Chiazong. “Characterization of an internal ribosomal entry site in the coding sequence of tyrosyl-DNA phosphodiesterase 2.” 2018. Web. 19 Jan 2021.

Vancouver:

Chou AC. Characterization of an internal ribosomal entry site in the coding sequence of tyrosyl-DNA phosphodiesterase 2. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/5n965003.

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

Council of Science Editors:

Chou AC. Characterization of an internal ribosomal entry site in the coding sequence of tyrosyl-DNA phosphodiesterase 2. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/5n965003

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

Tulane University

10. Jones, Christopher. THE TRANSGENERATIONAL IMPACT OF MATERNAL EARLY LIFE ADVERSITY ON INFANT DEVELOPMENT.

Degree: 2019, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:106625

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[email protected]

The biological embedding of maternal adversity, both preconception and prenatal, can alter health trajectories of the next generation. Alterations in biological processes, including inflammation… (more)

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[email protected]

The biological embedding of maternal adversity, both preconception and prenatal, can alter health trajectories of the next generation. Alterations in biological processes, including inflammation and accelerated aging, are proposed mechanisms through which adverse environmental and experiential exposures alter disease risk over the life-course. To identify biological pathways of transgenerational risk, we describe how maternal preconception adversity, assessed by adverse childhood experience score (ACEs), influences the development of her infant’s psychopathology risk and autonomic nervous system (ANS) by examining genomic and epigenomic alterations in both the infant and the placenta. Maternal ACEs elevated her infant’s externalizing behaviors at 18-months of age. Cellular aging, indexed by telomere length (TL) erosion, modified this relation; in infants with greater TL erosion from 4- to 18-months of age, higher maternal ACEs predicted higher externalizing behaviors. At 4-months of age, we examined infant ANS stress physiology and found that higher maternal ACEs predicted lower ANS stress response. Next, we examined TL in the placenta as a pathway conferring transgenerational risk. Higher maternal ACEs predicted shorter placental TL and placental TL modified the impact of maternal ACEs on her infant’s ANS; in placentas with shorter placental TL, higher maternal ACEs predicted greater ANS stress responsivity. To understand the molecular pathways impacted by maternal ACEs and related to TL, we examined placental mRNA expression of an inflammatory gene (CCL2), a gene linked to apoptosis (BCL2), and a gene tied to cellular senescence (GLB1). CCL2 expression modified the relation between higher maternal ACEs and shorter placental TL and CCL2 expression also contributed to the relation between shorter placental TL and decreased BCL2 expression. Lastly, shorter TL moderated the relation between CCL2 expression and both BCL2 and GLB1. The demonstration of the effects of maternal ACE exposure across generations highlights the need to further define the underlying mechanisms contributing to disease risk in the next generation. Maternal ACE exposure effects the placenta, the infant’s ANS, and the infant’s behavior through the first 18-months of life, which highlights the powerful impact of maternal early life adversity across generations and compliments the known lasting health risks found within the individual.

1

Christopher Jones

Advisors/Committee Members: (author), Drury, Stacy (Thesis advisor), (Thesis advisor), School of Science & Engineering Neuroscience (Degree granting institution).

Subjects/Keywords: Cellular aging

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APA (6^th Edition):

Jones, C. (2019). THE TRANSGENERATIONAL IMPACT OF MATERNAL EARLY LIFE ADVERSITY ON INFANT DEVELOPMENT. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:106625

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):

Jones, Christopher. “THE TRANSGENERATIONAL IMPACT OF MATERNAL EARLY LIFE ADVERSITY ON INFANT DEVELOPMENT.” 2019. Thesis, Tulane University. Accessed January 19, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:106625.

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

MLA Handbook (7^th Edition):

Jones, Christopher. “THE TRANSGENERATIONAL IMPACT OF MATERNAL EARLY LIFE ADVERSITY ON INFANT DEVELOPMENT.” 2019. Web. 19 Jan 2021.

Vancouver:

Jones C. THE TRANSGENERATIONAL IMPACT OF MATERNAL EARLY LIFE ADVERSITY ON INFANT DEVELOPMENT. [Internet] [Thesis]. Tulane University; 2019. [cited 2021 Jan 19]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:106625.

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

Council of Science Editors:

Jones C. THE TRANSGENERATIONAL IMPACT OF MATERNAL EARLY LIFE ADVERSITY ON INFANT DEVELOPMENT. [Thesis]. Tulane University; 2019. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:106625

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

Temple University

11. Frara, Nagat. THE ROLE OF OSTEOACTIVIN IN MUSCULOSKELETAL TISSUES AS A REPAIR AND ANABOLIC FACTOR.

Degree: PhD, 2015, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,336629

►

Cell Biology

Osteoactivin (OA) is a novel osteogenic and repair factor. It has the ability to regulate cell proliferation, adhesion, differentiation, and synthesis and regulation… (more)

▼

Cell Biology

Osteoactivin (OA) is a novel osteogenic and repair factor. It has the ability to regulate cell proliferation, adhesion, differentiation, and synthesis and regulation of extracellular matrix proteins in various cell types under both normal and pathological conditions. Initial identification of osteoactivin (OA)/glycoprotein non-melanoma clone B (gpnmb) was demonstrated in an osteopetrotic rat model, where OA expression was increased 3-fold in mutant bones, compared to normal. OA mRNA and protein expression increase during active bone regeneration post-fracture, and primary rat osteoblasts show increased OA expression during differentiation ex vivo. To further examine OA/gpnmb as an osteoinductive agent, we characterized the skeletal phenotype of transgenic mouse overexpressing OA/gpnmb under the CMV-promoter (OA-Tg). Western blot analysis showed increased OA/gpnmb in OA-Tg osteoblasts, compared to wild-type (WT). In OA-Tg mouse femurs versus WT littermates, micro-CT analysis showed increased trabecular bone volume and thickness, and cortical bone thickness; histomorphometry showed increased osteoblast numbers, bone formation and mineral apposition rates in OA-Tg mice; and biomechanical testing showed higher peak moment and stiffness. Given that OA/gpnmb is also over-expressed in osteoclasts in OA-Tg mice, we evaluated bone resorption by ELISA and histomorphometry, and observed decreased serum CTX-1 and RANK-L, and decreased osteoclast numbers in OA-Tg, compared to WT mice, indicating decreased bone remodeling in OA-Tg mice. The proliferation rate of OA-Tg osteoblasts ex vivo was higher, compared to WT, as was alkaline phosphatase staining and activity, the latter indicating enhanced differentiation of OA-Tg osteoprogenitors. Quantitative RT-PCR analysis showed increased TGF-β1 and TGF-β receptors I and II expression in OA-Tg osteoblasts, compared to WT. Together, these data suggest that OA overexpression has an osteoinductive effect on bone mass in vivo and stimulates osteoprogenitor differentiation ex vivo. OA expression increases during tissue degeneration and regeneration, fracture repair, and after denervation-induced disuse atrophy, concomitant with increased matrix metalloproteinases (MMPs). However, OA’s expression with repetitive overuse injuries is unknown. We sought to evaluate in an animal model of upper extremity repetitive overuse, at low force loads: 1) OA expression in an operant rat model of repetitive overuse; 2) expression of MMPs; 3) inflammatory cytokines indicative of injury or inflammation; and 4) the inducible form of heat shock protein 70 (HSPA1A/HSP72), a protein known to increase during metabolic stress and be involved in cellular repair. We hypothesized that OA is functioning as a growth factor during periods of tissue repair. Young adult, female Sprague-Dawley rats performed a high repetition negligible force (HRNF) food retrieval task for up to 6 weeks, and were compared to control rats. Quantitative PCR, Western blot analyses and immunohistochemistry showed increased OA…

Advisors/Committee Members: Barbe, Mary F.;, Popoff, Steven N., Kirby, Lynn, Rizzo, Victor, Safadi, Fayez F., Tytell, Michael;.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Frara, N. (2015). THE ROLE OF OSTEOACTIVIN IN MUSCULOSKELETAL TISSUES AS A REPAIR AND ANABOLIC FACTOR. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,336629

Chicago Manual of Style (16^th Edition):

Frara, Nagat. “THE ROLE OF OSTEOACTIVIN IN MUSCULOSKELETAL TISSUES AS A REPAIR AND ANABOLIC FACTOR.” 2015. Doctoral Dissertation, Temple University. Accessed January 19, 2021. http://digital.library.temple.edu/u?/p245801coll10,336629.

MLA Handbook (7^th Edition):

Frara, Nagat. “THE ROLE OF OSTEOACTIVIN IN MUSCULOSKELETAL TISSUES AS A REPAIR AND ANABOLIC FACTOR.” 2015. Web. 19 Jan 2021.

Vancouver:

Frara N. THE ROLE OF OSTEOACTIVIN IN MUSCULOSKELETAL TISSUES AS A REPAIR AND ANABOLIC FACTOR. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2021 Jan 19]. Available from: http://digital.library.temple.edu/u?/p245801coll10,336629.

Council of Science Editors:

Frara N. THE ROLE OF OSTEOACTIVIN IN MUSCULOSKELETAL TISSUES AS A REPAIR AND ANABOLIC FACTOR. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,336629

12. Witte, Kristen. Optogenetic Investigation Reveals Robust Symmetry Breaking Mechanisms in Saccharomyces cerevisiae.

Degree: 2017, The University of Chicago

URL: http://pqdtopen.proquest.com/#viewpdf?dispub=10282229

► Cell polarization underlies many cellular and organismal functions. The GTPase Cdc42 orchestrates polarization in many contexts. In budding yeast, polarization is associated with a… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Witte, K. (2017). Optogenetic Investigation Reveals Robust Symmetry Breaking Mechanisms in Saccharomyces cerevisiae. (Thesis). The University of Chicago. Retrieved from http://pqdtopen.proquest.com/#viewpdf?dispub=10282229

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):

Witte, Kristen. “Optogenetic Investigation Reveals Robust Symmetry Breaking Mechanisms in Saccharomyces cerevisiae.” 2017. Thesis, The University of Chicago. Accessed January 19, 2021. http://pqdtopen.proquest.com/#viewpdf?dispub=10282229.

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

MLA Handbook (7^th Edition):

Witte, Kristen. “Optogenetic Investigation Reveals Robust Symmetry Breaking Mechanisms in Saccharomyces cerevisiae.” 2017. Web. 19 Jan 2021.

Vancouver:

Witte K. Optogenetic Investigation Reveals Robust Symmetry Breaking Mechanisms in Saccharomyces cerevisiae. [Internet] [Thesis]. The University of Chicago; 2017. [cited 2021 Jan 19]. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10282229.

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

Council of Science Editors:

Witte K. Optogenetic Investigation Reveals Robust Symmetry Breaking Mechanisms in Saccharomyces cerevisiae. [Thesis]. The University of Chicago; 2017. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10282229

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

Cornell University

13. Ledet, Melissa McDowell. The Mammary Gland in Health and Disease.

Degree: PhD, Biomedical and Biological Sciences, 2019, Cornell University

URL: http://hdl.handle.net/1813/67458

► The mammary gland is a conserved, defining feature among mammals; however, there is much variation between species in both healthy functions, such as lactation, and… (more)

▼ The mammary gland is a conserved, defining feature among mammals; however, there is much variation between species in both healthy functions, such as lactation, and diseases, such as mammary cancer and mastitis. Species such as the cow, for example, are expert lactators, while lactation insufficiency remains a problem for many women. Mammary cancer is common in species such as humans, dogs and cats, but is rare in other species such as horses, cows and pigs. The majority of this work focuses on mammary stem/progenitor (MaSC) cells as these are the cells thought to drive lactation and to be at least partly responsible for mammary cancer development. These cells have been successfully isolated and characterized in mice, humans, and cows; however, these methods use species-specific antibodies and thus cannot be broadly applied across species. We first describe a novel method for isolating and characterizing MaSC from many different species in an antibody-independent manner. We then describe two projects that use this method for a comparative species approach to define possible underlying mechanisms behind mammary cancer resistance. In the second project we discovered that the secretome of equine MaSC kills a subset of human breast cancer cells, establishing the potential therapeutic effects of the MaSC secretome. With this in mind, we focused on the other primary disease of the mammary gland: mastitis, an inflammatory disease most commonly caused by bacterial infections. We found that the secretome of bovine MaSC repairs epithelial and endothelial cell damage and contains antimicrobial peptides, making it a good option for complementary mastitis therapy. In our final project, we once again demonstrate the advantages of using a comparative species approach to identify potential treatments for canine and feline mammary cancer, modeled after what has previously been described for breast cancer in humans. Collectively, this work denotes two potential mechanisms for cancer resistance in domestic species and highlights the potential therapeutic benefits of the MaSC secretome. Advisors/Committee Members: Van de Walle, Gerlinde (chair), Weiss, Robert S. (committee member), Coonrod, Scott A. (committee member), Kurpios, Natasza (committee member).

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Ledet, M. M. (2019). The Mammary Gland in Health and Disease. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/67458

Chicago Manual of Style (16^th Edition):

Ledet, Melissa McDowell. “The Mammary Gland in Health and Disease.” 2019. Doctoral Dissertation, Cornell University. Accessed January 19, 2021. http://hdl.handle.net/1813/67458.

MLA Handbook (7^th Edition):

Ledet, Melissa McDowell. “The Mammary Gland in Health and Disease.” 2019. Web. 19 Jan 2021.

Vancouver:

Ledet MM. The Mammary Gland in Health and Disease. [Internet] [Doctoral dissertation]. Cornell University; 2019. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/1813/67458.

Council of Science Editors:

Ledet MM. The Mammary Gland in Health and Disease. [Doctoral Dissertation]. Cornell University; 2019. Available from: http://hdl.handle.net/1813/67458

14. Berk-Rauch, Hanna E. FMRP Regulates the Expression of Axonal Messages In Vivo.

Degree: PhD, Molecular Biology, Cell Biology, and Biochemistry, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320509/

► Fragile X syndrome, a leading cause of autism and the most common form of inherited intellectual disability, results from the loss of Fragile X mental… (more)

Subjects/Keywords: cellular biology

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APA (6^th Edition):

Berk-Rauch, H. E. (2013). FMRP Regulates the Expression of Axonal Messages In Vivo. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320509/

Chicago Manual of Style (16^th Edition):

Berk-Rauch, Hanna E. “FMRP Regulates the Expression of Axonal Messages In Vivo.” 2013. Doctoral Dissertation, Brown University. Accessed January 19, 2021. https://repository.library.brown.edu/studio/item/bdr:320509/.

MLA Handbook (7^th Edition):

Berk-Rauch, Hanna E. “FMRP Regulates the Expression of Axonal Messages In Vivo.” 2013. Web. 19 Jan 2021.

Vancouver:

Berk-Rauch HE. FMRP Regulates the Expression of Axonal Messages In Vivo. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2021 Jan 19]. Available from: https://repository.library.brown.edu/studio/item/bdr:320509/.

Council of Science Editors:

Berk-Rauch HE. FMRP Regulates the Expression of Axonal Messages In Vivo. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320509/

15. Yi, Xin. Effects of Elasticity and Geometry on Cellular Uptake of Nanoparticles.

Degree: PhD, Mechanics of Solids, 2014, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:419358/

► A fundamental understanding of cell-nanomaterial interaction is essential for biomedical diagnostics, therapeutics, and nanotoxicity. Here we perform theoretical analysis to investigate the cellular uptake of… (more)

▼ A fundamental understanding of cell-nanomaterial interaction is essential for biomedical diagnostics, therapeutics, and nanotoxicity. Here we perform theoretical analysis to investigate the cellular uptake of elastic nanoparticles and one- and two- dimensional rigid nanomaterials. We first show that the extent of adhesive wrapping of an elastic soft nanoparticle by a lipid membrane depends on the particle size, adhesion energy, membrane tension, and bending stiffness ratio between the nanoparticle and membrane. There exist five possible wrapping phases based on the stability of full wrapping, partial wrapping, and no wrapping states. Based on these wrapping phases, we determine the wrapping phase diagrams for cellular uptake of elastic nanoparticles in two and three dimensions. We find that stiffer particles can achieve full wrapping more easily than softer particles. Our results suggest that precise control of the particle elasticity can be a new way to control cellular uptake and drug delivery processes. In another study on the cell uptake of one-dimensional nanomaterials, we show that cell uptake of one-dimensional nanomaterials via receptor-mediated endocytosis is dominated by a single dimensionless parameter that scales with the membrane tension and radius of the nanomaterial and inversely with the membrane bending stiffness. As cell membrane internalizes one-dimensional nanomaterials the uptake follows a near-perpendicular entry mode at small membrane tension but it switches to a near-parallel interaction mode at large membrane tension. This tension-dependent uptake behavior is ubiquitous in the interplay between cell membranes and one-dimensional nanomaterials including nanotubes, nanowires, filamentous bacteria, and certain nanoparticle chains. It also provides a mechanism for the size maintenance of filopodia. Lastly, we investigate the interaction between cell membranes and microsized rigid two-dimensional nanomaterials such as graphene-family nanomaterials. We show that a microsized two-dimensional transmembrane nanomaterial always tends to rotate toward an orthogonal configuration with respect to cell membranes. The main driving force of such a rotation comes from both splay and membrane tension energies. In contrast, membrane wrapping of two-dimensional nanomaterials are independent of tension and surface adhering is energetically favorable compared with other inclined configurations. Advisors/Committee Members: Gao, Huajian (Director), Hurt, Robert (Reader), Kesari, Haneesh (Reader).

Subjects/Keywords: cellular uptake

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APA (6^th Edition):

Yi, X. (2014). Effects of Elasticity and Geometry on Cellular Uptake of Nanoparticles. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:419358/

Chicago Manual of Style (16^th Edition):

Yi, Xin. “Effects of Elasticity and Geometry on Cellular Uptake of Nanoparticles.” 2014. Doctoral Dissertation, Brown University. Accessed January 19, 2021. https://repository.library.brown.edu/studio/item/bdr:419358/.

MLA Handbook (7^th Edition):

Yi, Xin. “Effects of Elasticity and Geometry on Cellular Uptake of Nanoparticles.” 2014. Web. 19 Jan 2021.

Vancouver:

Yi X. Effects of Elasticity and Geometry on Cellular Uptake of Nanoparticles. [Internet] [Doctoral dissertation]. Brown University; 2014. [cited 2021 Jan 19]. Available from: https://repository.library.brown.edu/studio/item/bdr:419358/.

Council of Science Editors:

Yi X. Effects of Elasticity and Geometry on Cellular Uptake of Nanoparticles. [Doctoral Dissertation]. Brown University; 2014. Available from: https://repository.library.brown.edu/studio/item/bdr:419358/

16. Biron, Bethany. The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis.

Degree: Pathobiology, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:733274/

► Sepsis is a life threatening condition that elicits a dysregulated and damaging immune response, which in turn leads to tissue damage and Multiple Organ Dysfunction… (more)

▼ Sepsis is a life threatening condition that elicits a dysregulated and damaging immune response, which in turn leads to tissue damage and Multiple Organ Dysfunction (MOD). Critically ill patients that have suffered from trauma, complex surgery, gastrointestinal bleeding, obstetrical bleeding, etc., have an increased risk of developing sepsis, which may progress to Acute Respiratory Distress Syndrome (ARDS), leading in turn to an increase in mortality. Neutrophils are thought to play a role in the immune dysfunction seen in both shock and sepsis, and have been implicated in causing bystander tissue damage and organ dysfunction. Neutrophil extracellular traps (NETs) are large webs of decondensed chromatin coated with antimicrobial proteins that are released into the extracellular space. They serve as a novel effector function, regulated by the enzyme Peptidyl arginine deiminase, type IV (PAD4). NETs have been identified as an important aspect of innate immunity, but have also been linked to excessive inflammation and tissue damage. Their role in sepsis and shock/sepsis, however, is poorly understood. This dissertation examines how PAD4 (an enzyme central to NET formation) plays a role in the pathology of sepsis. It also examines whether a predispositional insult, such as severe shock antecedent to septic challenge, is affected this enzyme. Here we demonstrate that inhibition of PAD4 reduces mortality seen in a mouse polymicrobial sepsis model (CLP), as well as in a mouse model of hemorrhagic shock and sepsis (Hem/CLP). Clinically we showed that there is evidence of increased NET activity in septic patients. Together, this implies that PAD4-mediated NET formation contributes to the morbidity and mortality associated with sepsis and shock/sepsis, and that PAD4 merits further exploration as a possible therapeutic target against the damaging pro-inflammatory response seen in polymicrobial sepsis and indirect ARDS. Advisors/Committee Members: Ayala, Alfred (Advisor), Reichner, Jonathan (Reader), Lefort, Craig (Reader), Heffernan, Daithi (Reader), Levy, Bruce (Reader).

Subjects/Keywords: Cellular immunity

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APA (6^th Edition):

Biron, B. (2017). The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:733274/

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):

Biron, Bethany. “The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis.” 2017. Thesis, Brown University. Accessed January 19, 2021. https://repository.library.brown.edu/studio/item/bdr:733274/.

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

MLA Handbook (7^th Edition):

Biron, Bethany. “The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis.” 2017. Web. 19 Jan 2021.

Vancouver:

Biron B. The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis. [Internet] [Thesis]. Brown University; 2017. [cited 2021 Jan 19]. Available from: https://repository.library.brown.edu/studio/item/bdr:733274/.

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

Council of Science Editors:

Biron B. The Role of Peptidyl arginine deiminase, type IV (PAD4) in the Pathology of Shock/Sepsis. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:733274/

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

University of Johannesburg

17. Kotze, Leonie. Twee-dimensionele sellulêre outomate.

Degree: 2014, University of Johannesburg

URL: http://hdl.handle.net/10210/11919

►

M.Sc. (Computer Science)

Astudy of one- and two-dimensional cellular automata was made. Two research projects were undertaken; these are discussed in depth. One- and two-dimensional… (more)

Subjects/Keywords: Cellular automata

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APA (6^th Edition):

Kotze, L. (2014). Twee-dimensionele sellulêre outomate. (Thesis). University of Johannesburg. Retrieved from http://hdl.handle.net/10210/11919

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):

Kotze, Leonie. “Twee-dimensionele sellulêre outomate.” 2014. Thesis, University of Johannesburg. Accessed January 19, 2021. http://hdl.handle.net/10210/11919.

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

MLA Handbook (7^th Edition):

Kotze, Leonie. “Twee-dimensionele sellulêre outomate.” 2014. Web. 19 Jan 2021.

Vancouver:

Kotze L. Twee-dimensionele sellulêre outomate. [Internet] [Thesis]. University of Johannesburg; 2014. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/10210/11919.

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

Council of Science Editors:

Kotze L. Twee-dimensionele sellulêre outomate. [Thesis]. University of Johannesburg; 2014. Available from: http://hdl.handle.net/10210/11919

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

Boston University

18. Laflamme, Collette. Adiporedoxin, an upstream modulator of endoplasmic reticulum oxidative folding and protein secretion.

Degree: PhD, Medical Nutritional Sciences, 2015, Boston University

URL: http://hdl.handle.net/2144/15062

► Our laboratory identified Adiporedoxin (Adrx), an endoplasmic reticulum localized oxidoreductase whose expression in adipose tissue is many fold greater than other tissues. In gain and… (more)

▼ Our laboratory identified Adiporedoxin (Adrx), an endoplasmic reticulum localized oxidoreductase whose expression in adipose tissue is many fold greater than other tissues. In gain and loss of function experiments in cultured adipocytes Adrx knock down decreased the secretion of numerous adipokines, extracellular matrix, and transmembrane proteins and over expression increased secretion. Together, these results suggest Adrx regulates an early step in protein secretion from the ER. Immunofluorescence and proteolytic protection assays demonstrated that Adrx is located in the ER membrane with an ER luminal active site. We demonstrated that Adrx regulated protein secretion by affecting the oxidation state of ER redox chaperones. Using a cysteine-modifying PEGylation reagent, we showed Adrx oscillated between a reduced and oxidized form through the -CxxC- active site residues in response to the redox environment of the ER. Consequently, knocking down Adrx impaired the re-oxidation of protein disulfide isomerase, indicating an overlapping function with known regulators of ER redox homeostasis, namely endoplasmic reticulum oxidoreductase 1, and peroxiredoxin 4. Adrx is oxidized within the ER after treatment with hydrogen peroxide (H2O2) and can reduce H2O2 in vitro, suggesting it also acts as an antioxidant. The overexpression of Adrx in adipocytes protected the ER from oxidative stress and rescued adipokine secretion. Pancreatic islets are also highly secretory Adrx is expressed in isolated murine islets. In cultured islet cells, Adrx expression also decreased oxidative stress and correlated with the secretion of insulin, the main regulator of glucose homeostasis. In summary, Adrx expression controls secreted proteins and here we describe its ability to regulate the formation and release of disulfide-bonded proteins by reoxidizing ER chaperones and alleviating oxidative stress. Secreted proteins affect many aspects of metabolism including the control of appetite, glucose homeostasis, inflammation, and adipose tissue fibrosis. Overall, these data suggest that by mediating secreted proteins Adrx functions as important regulator of overall metabolism.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Laflamme, C. (2015). Adiporedoxin, an upstream modulator of endoplasmic reticulum oxidative folding and protein secretion. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/15062

Chicago Manual of Style (16^th Edition):

Laflamme, Collette. “Adiporedoxin, an upstream modulator of endoplasmic reticulum oxidative folding and protein secretion.” 2015. Doctoral Dissertation, Boston University. Accessed January 19, 2021. http://hdl.handle.net/2144/15062.

MLA Handbook (7^th Edition):

Laflamme, Collette. “Adiporedoxin, an upstream modulator of endoplasmic reticulum oxidative folding and protein secretion.” 2015. Web. 19 Jan 2021.

Vancouver:

Laflamme C. Adiporedoxin, an upstream modulator of endoplasmic reticulum oxidative folding and protein secretion. [Internet] [Doctoral dissertation]. Boston University; 2015. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/2144/15062.

Council of Science Editors:

Laflamme C. Adiporedoxin, an upstream modulator of endoplasmic reticulum oxidative folding and protein secretion. [Doctoral Dissertation]. Boston University; 2015. Available from: http://hdl.handle.net/2144/15062

University of California – Irvine

19. Tormanen, Kati. Re-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal Positioning.

Degree: Biological Sciences, 2018, University of California – Irvine

URL: http://www.escholarship.org/uc/item/20f55949

► Abstract of dissertationRe-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal PositioningByKati TormanenDoctor of Philosophy in Biological Sciences, University of California, Irvine Professor Christine… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Tormanen, K. (2018). Re-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal Positioning. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/20f55949

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):

Tormanen, Kati. “Re-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal Positioning.” 2018. Thesis, University of California – Irvine. Accessed January 19, 2021. http://www.escholarship.org/uc/item/20f55949.

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

MLA Handbook (7^th Edition):

Tormanen, Kati. “Re-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal Positioning.” 2018. Web. 19 Jan 2021.

Vancouver:

Tormanen K. Re-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal Positioning. [Internet] [Thesis]. University of California – Irvine; 2018. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/20f55949.

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

Council of Science Editors:

Tormanen K. Re-evaluating the Functional Significance of Golgi Ribbon Structure and Pericentrosomal Positioning. [Thesis]. University of California – Irvine; 2018. Available from: http://www.escholarship.org/uc/item/20f55949

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

University of California – San Diego

20. Nord, Matthew. Analysis of Regulation of Major Mitotic Assembly Events In Vitro by Nuclear Import and Export Receptors.

Degree: Biology, 2018, University of California – San Diego

URL: http://www.escholarship.org/uc/item/35s4b5b5

► This dissertation is an analysis of regulation of major mitotic assembly events by nuclear transport receptors, or karyopherins. Karyopherins, composed of both importins and exportins,… (more)

▼ This dissertation is an analysis of regulation of major mitotic assembly events by nuclear transport receptors, or karyopherins. Karyopherins, composed of both importins and exportins, are a large family of proteins that transport specific proteins and RNAs between the cytoplasm and nucleus of the eukaryotic cell. Each karyopherin has a distinct set of cargoes that it binds and transports through the nuclear pore complex. A high concentration of RanGTP inside the nucleus, created by the chromatin-bound enzyme RCC1, is harnessed by karyopherins to achieve transport directionality. During mitosis, upon nuclear breakdown, RCC1 continues to produce a high concentration of RanGTP around the mitotic chromosomes. Away from the chromosomes, where RanGTP is low, Importins α and β inhibit assembly factors for spindle, nuclear membrane, and nuclear pore assembly. However, near the chromosomes, where RanGTP levels are high, Importins α and β release assembly factors with the result that mitotic structures only assemble around the chromosomes. Thus, evolution has co-opted the RanGTP/karyopherin system to spatially regulate the assembly of multiple critical structures in mitosis. Much of this has been determined in Xenopus egg extracts, which are unique in that one can reconstitute cellular events in cell cycle-specific states. Chapter 2 extends the role of RanGTP/karyopherin spatial regulation by dissecting the mechanism of action by which the import receptor Transportin regulates mitotic assembly events. Using a variety of molecular tools and Xenopus egg extracts, we show that Transportin inhibits the assembly of major mitotic structures, not by titrating RanGTP, but by directly blocking proteins needed for assembly everywhere except in areas near mitotic chromosomes.Chapter 3 presents an extensive published review of karyopherins as global regulators of mitotic assembly events, both in vivo and in vitro, including protein interactions, checkpoints, and critical proteins required for proper assembly.Chapter 4 dissects whether export receptors, or exportins, play a role in mitotic assembly regulation, focusing on Crm1/Exportin-1, Exportin-tRNA, and Exportin-5. Using Xenopus egg extracts, we find that exportins are potent inhibitors of spindle assembly, nuclear membrane fusion, and nuclear pore formation, and their inhibition can be, to an extent, counteracted by RanGTP.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Nord, M. (2018). Analysis of Regulation of Major Mitotic Assembly Events In Vitro by Nuclear Import and Export Receptors. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/35s4b5b5

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):

Nord, Matthew. “Analysis of Regulation of Major Mitotic Assembly Events In Vitro by Nuclear Import and Export Receptors.” 2018. Thesis, University of California – San Diego. Accessed January 19, 2021. http://www.escholarship.org/uc/item/35s4b5b5.

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

MLA Handbook (7^th Edition):

Nord, Matthew. “Analysis of Regulation of Major Mitotic Assembly Events In Vitro by Nuclear Import and Export Receptors.” 2018. Web. 19 Jan 2021.

Vancouver:

Nord M. Analysis of Regulation of Major Mitotic Assembly Events In Vitro by Nuclear Import and Export Receptors. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/35s4b5b5.

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

Council of Science Editors:

Nord M. Analysis of Regulation of Major Mitotic Assembly Events In Vitro by Nuclear Import and Export Receptors. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/35s4b5b5

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

University of California – San Diego

21. Ornelas, Lilia. Discovery and Analysis of Genes Required for Protein Quality Control.

Degree: Biology, 2018, University of California – San Diego

URL: http://www.escholarship.org/uc/item/8956h9bj

► Protein-based life faces constant and dynamic stress caused by protein mis-folding. This can cause a variety of potentially lethal alterations in cell physiology that underlie… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Ornelas, L. (2018). Discovery and Analysis of Genes Required for Protein Quality Control. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/8956h9bj

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):

Ornelas, Lilia. “Discovery and Analysis of Genes Required for Protein Quality Control.” 2018. Thesis, University of California – San Diego. Accessed January 19, 2021. http://www.escholarship.org/uc/item/8956h9bj.

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

MLA Handbook (7^th Edition):

Ornelas, Lilia. “Discovery and Analysis of Genes Required for Protein Quality Control.” 2018. Web. 19 Jan 2021.

Vancouver:

Ornelas L. Discovery and Analysis of Genes Required for Protein Quality Control. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/8956h9bj.

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

Council of Science Editors:

Ornelas L. Discovery and Analysis of Genes Required for Protein Quality Control. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/8956h9bj

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

Harvard University

22. Oak, Youbean. Filopodia-independent roles of the actin bundling protein fascin in promoting cell motility.

Degree: PhD, Biology, Molecular and Cellular, 2014, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13104236

► Fascin is an actin bundling protein whose overexpression has in recent years been systematically linked to increased metastasis and poor outcome in cancer patients. It… (more)

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Oak, Y. (2014). Filopodia-independent roles of the actin bundling protein fascin in promoting cell motility. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:13104236

Chicago Manual of Style (16^th Edition):

Oak, Youbean. “Filopodia-independent roles of the actin bundling protein fascin in promoting cell motility.” 2014. Doctoral Dissertation, Harvard University. Accessed January 19, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13104236.

MLA Handbook (7^th Edition):

Oak, Youbean. “Filopodia-independent roles of the actin bundling protein fascin in promoting cell motility.” 2014. Web. 19 Jan 2021.

Vancouver:

Oak Y. Filopodia-independent roles of the actin bundling protein fascin in promoting cell motility. [Internet] [Doctoral dissertation]. Harvard University; 2014. [cited 2021 Jan 19]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13104236.

Council of Science Editors:

Oak Y. Filopodia-independent roles of the actin bundling protein fascin in promoting cell motility. [Doctoral Dissertation]. Harvard University; 2014. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13104236

University of California – San Diego

23. Farber-Katz, Suzette Elena. DNA Damage Triggers Golgi Dispersal via GOLPH3 and DNA-PK.

Degree: Biomedical Sciences, 2012, University of California – San Diego

URL: http://www.escholarship.org/uc/item/0p0476db

► Golgi morphology and function has fascinated scientists for decades; however, it was unclear how the two were related. Our research delving into the function of… (more)

▼ Golgi morphology and function has fascinated scientists for decades; however, it was unclear how the two were related. Our research delving into the function of GOLPH3 provides evidence for how Golgi morphology relates to Golgi trafficking. We identified GOLPH3 as a novel PtdIns(4)P-binding protein. We found that GOLPH3 requires PtdIns(4)P for its localization at the Golgi. We also showed that GOLPH3 binds to MYO18A, which results in a tensile force that pulls vesicles off the trans-Golgi. We showed that GOLPH3, MYO18A, and F-actin are all required for trafficking from the Golgi. The tensile force also stretches the Golgi and creates the Golgi ribbon that extends around the nucleus. Therefore, we identified a novel mechanism that explains how Golgi trafficking results in the extended Golgi ribbon.While we have an understanding of how GOLPH3 functions, it was unclear how GOLPH3 is regulated. To better understand its regulation, we performed immunoprecipitation-mass spectrometry experiments to identify its phosphorylation sites. We found that T143 and T148 were phosphorylated. By analyzing the sequences surrounding these sites, we noticed that T143 and Q144 comprise a "TQ" motif, which are recognized by kinases in the DNA damage pathway. Thus, we examined whether DNA damage has any effect on Golgi morphology, and we found that it causes Golgi dispersal. We showed that DNA damage-induced Golgi dispersal requires phosphorylation of GOLPH3, as well as MYO18A and F-actin. Our extensive data argue that DNA-PK is the kinase that phosphorylates GOLPH3 on the TQ motif. We also demonstrated that DNA damage increases the interaction between GOLPH3 and MYO18A, thereby increasing the tensile force pulling on the Golgi membranes to elicit a dispersed Golgi. Because GOLPH3 was previously identified as an oncogene, we measured survival after DNA damage, and we found that GOLPH3, MYO18A, and DNA-PK are required for survival after DNA damage. Furthermore, knockdown of GOLPH3 or MYO18A increases apoptosis levels after DNA damage. Our data provide new insight into how the DNA-PK/GOLPH3/MYO18A/F-actin pathway causes dramatic Golgi reorganization. These results will have implications for cancer therapy, as inhibition of this pathway in the presence of DNA damage strikingly increases cell death.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Farber-Katz, S. E. (2012). DNA Damage Triggers Golgi Dispersal via GOLPH3 and DNA-PK. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/0p0476db

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):

Farber-Katz, Suzette Elena. “DNA Damage Triggers Golgi Dispersal via GOLPH3 and DNA-PK.” 2012. Thesis, University of California – San Diego. Accessed January 19, 2021. http://www.escholarship.org/uc/item/0p0476db.

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

MLA Handbook (7^th Edition):

Farber-Katz, Suzette Elena. “DNA Damage Triggers Golgi Dispersal via GOLPH3 and DNA-PK.” 2012. Web. 19 Jan 2021.

Vancouver:

Farber-Katz SE. DNA Damage Triggers Golgi Dispersal via GOLPH3 and DNA-PK. [Internet] [Thesis]. University of California – San Diego; 2012. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/0p0476db.

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

Council of Science Editors:

Farber-Katz SE. DNA Damage Triggers Golgi Dispersal via GOLPH3 and DNA-PK. [Thesis]. University of California – San Diego; 2012. Available from: http://www.escholarship.org/uc/item/0p0476db

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

University of California – Berkeley

24. Smoligovets, Alexander Alexandrovich. From actin to Zap70: the outcomes of the interaction of the actin cytoskeleton with T-cell receptors.

Degree: Molecular & Cell Biology, 2012, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/0cn4f9zp

► The actin cytoskeleton has for decades been known to be important in the process of T-cell recognition of antigen. Upon receiving stimulus from T-cell receptors… (more)

▼ The actin cytoskeleton has for decades been known to be important in the process of T-cell recognition of antigen. Upon receiving stimulus from T-cell receptors (TCRs), the T-cell cytoskeleton adopts a pattern of radially symmetric, centripetal flow that imposes multi-micrometer scale organization on the protein complement of a T-cell membrane. Many of the details of the interactions between actin and cell surface receptors remain unknown; of particular interest are the connections to TCRs themselves. The actin cytoskeleton appears to modulate TCR-mediated signaling, and thus T-cell behaviors, on a number of levels. On the level of single TCR molecules and oligomers, the presence of actin affects TCR-antigen recognition by altering binding kinetics through mechanisms that are still unclear. On a larger spatial and longer temporal level, actin drives the formation and centripetal movement of small TCR assemblies whose radial distribution correlates with their signaling state. Little is known about the local organization and dynamics of the actin cytoskeleton around these assemblies. A more complete understanding of the process of T-cell activation depends on the ability to characterize the involvement of actin in detail.This thesis describes how the T-cell actin cytoskeleton locally reacts to TCR assemblies, how it modulates the kinetics of the TCR-antigen interaction, and what role myosin IIA plays in organization of and signaling by TCRs. Direct imaging of actin reveals that the cytoskeletal network transiently slows and compresses at sites of mobility-limited T-cell receptors. Actin disruption during direct observation of antigen peptide binding to TCRs shows that the presence of a functional cytoskeleton increases the rate of antigen unbinding from these receptors. Tracking and disruption of labeled myosin IIA indicates that the motor protein helps but is not required for proper establishment of T-cell membrane organization, but it is necessary for appropriate calcium influx into the T-cell cytoplasm during activation. For all of these observations and others, new experimental and analytical methods are developed or applied.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Smoligovets, A. A. (2012). From actin to Zap70: the outcomes of the interaction of the actin cytoskeleton with T-cell receptors. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/0cn4f9zp

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):

Smoligovets, Alexander Alexandrovich. “From actin to Zap70: the outcomes of the interaction of the actin cytoskeleton with T-cell receptors.” 2012. Thesis, University of California – Berkeley. Accessed January 19, 2021. http://www.escholarship.org/uc/item/0cn4f9zp.

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

MLA Handbook (7^th Edition):

Smoligovets, Alexander Alexandrovich. “From actin to Zap70: the outcomes of the interaction of the actin cytoskeleton with T-cell receptors.” 2012. Web. 19 Jan 2021.

Vancouver:

Smoligovets AA. From actin to Zap70: the outcomes of the interaction of the actin cytoskeleton with T-cell receptors. [Internet] [Thesis]. University of California – Berkeley; 2012. [cited 2021 Jan 19]. Available from: http://www.escholarship.org/uc/item/0cn4f9zp.

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

Council of Science Editors:

Smoligovets AA. From actin to Zap70: the outcomes of the interaction of the actin cytoskeleton with T-cell receptors. [Thesis]. University of California – Berkeley; 2012. Available from: http://www.escholarship.org/uc/item/0cn4f9zp

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

West Virginia University

25. Beezhold, Kevin John. Repression of PHLPP by miR-190 Contributes to Arsenic-Induced Akt Activation and Carcinogenesis.

Degree: PhD, Microbiology, Immunology, and Cell Biology, 2011, West Virginia University

URL: https://doi.org/10.33915/etd.3421 ; https://researchrepository.wvu.edu/etd/3421

► Arsenic is a well-studied human carcinogen. The mechanism by which arsenic induces cancer, however, is not fully understood. It is known that as a general… (more)

▼ Arsenic is a well-studied human carcinogen. The mechanism by which arsenic induces cancer, however, is not fully understood. It is known that as a general stress inducer, arsenic can activate kinases, such as mitogen-activated protein kinases, leading to over activation of transcription factors. These transcription factors, including AP-1, NF-kB and Myc, are known to regulate the expression of early response genes, and likely to regulate miRNAs. The expression of miRNAs is often altered in cancer and other proliferative disorders. It is highly probable that miRNAs whose expressions are altered by arsenic will play a significant role in carcinogenesis. To test this hypothesis, we investigated: (1) the role of arsenic in the generation of miRNAs in the human bronchial epithelial cell line, BEAS-2B, using a microRNA array; (2) detailed the concentration-dependent regulation of the selected individual miRNA, such as miR-190, by arsenic using real-time PCR; (3) co-transcription of the intronic miRNA, miR-190, and its host gene, talin2, by a dual luciferase reporter gene assay and real-time PCR; (4) the potential target genes of miR-190 using in silico analysis, western blot, and 3'UTR reporter assays, and (5) the overall carcinogenic potential or cellular responses to arsenic-induced miR-190 through transient and stable overexpression of miR-190, followed by analytical tests such as western blot, proliferation assay and soft agar assay. The data obtained from this study show that arsenic is capable of inducing expression of several miRNAs, most remarkably miRNA-190 whose expression correlated with that of its host gene talin 2. In silico analysis of possible miR-190 targets indicated that this miRNA may be involved in tumor formation by targeting multiple proteins including PHLPP, an Akt phosphatase, and TP53INP1, a key cell apoptosis regulator. PHLPP is a known tumor suppressor that inactivates Akt by dephosphorylating serine 473, leading to decreased cell growth and enhanced apoptosis. PHLPP reporter assays indicate that miR-190 is a genuine PHLPP repressor that binds to the 3'UTR of the PHLPP mRNA. Kinase activation analysis demonstrated that miR-190 is able to mediate arsenic-induced Akt activation in a PHLPP dependant manner. Furthermore, overexpression of a miR-190 precursor could enhance the expression of VEGF, a growth factor downstream of Akt signaling responsible for enhancing tumor growth through neoangiogenesis and epithelial cell proliferation. Stable over expression of miR-190 led to an increase in colony number and size in a soft agar assay. This increase in colonies was accompanied by an increase in basal Akt phosphorylation and VEGF expression.;Taken together, these data suggest that arsenic is capable of inducing expression of miRNAs that may play critical roles in arsenic-induced carcinogenesis. Specifically, arsenic-induced miR-190 expression led to increased Akt activation and overall proliferation through repression of PHLPP. Accordingly, these findings not only revealed a novel mechanism of… Advisors/Committee Members: Michael Ruppert..

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Beezhold, K. J. (2011). Repression of PHLPP by miR-190 Contributes to Arsenic-Induced Akt Activation and Carcinogenesis. (Doctoral Dissertation). West Virginia University. Retrieved from https://doi.org/10.33915/etd.3421 ; https://researchrepository.wvu.edu/etd/3421

Chicago Manual of Style (16^th Edition):

Beezhold, Kevin John. “Repression of PHLPP by miR-190 Contributes to Arsenic-Induced Akt Activation and Carcinogenesis.” 2011. Doctoral Dissertation, West Virginia University. Accessed January 19, 2021. https://doi.org/10.33915/etd.3421 ; https://researchrepository.wvu.edu/etd/3421.

MLA Handbook (7^th Edition):

Beezhold, Kevin John. “Repression of PHLPP by miR-190 Contributes to Arsenic-Induced Akt Activation and Carcinogenesis.” 2011. Web. 19 Jan 2021.

Vancouver:

Beezhold KJ. Repression of PHLPP by miR-190 Contributes to Arsenic-Induced Akt Activation and Carcinogenesis. [Internet] [Doctoral dissertation]. West Virginia University; 2011. [cited 2021 Jan 19]. Available from: https://doi.org/10.33915/etd.3421 ; https://researchrepository.wvu.edu/etd/3421.

Council of Science Editors:

Beezhold KJ. Repression of PHLPP by miR-190 Contributes to Arsenic-Induced Akt Activation and Carcinogenesis. [Doctoral Dissertation]. West Virginia University; 2011. Available from: https://doi.org/10.33915/etd.3421 ; https://researchrepository.wvu.edu/etd/3421

West Virginia University

26. Arnold, Kimberly M. The role of focal adhesion kinase in nonmuscle cell contraction.

Degree: PhD, Microbiology, Immunology, and Cell Biology, 2013, West Virginia University

URL: https://doi.org/10.33915/etd.4949 ; https://researchrepository.wvu.edu/etd/4949

► Focal adhesions are specialized cell contact sites of distinct molecular composition and structure that bridge the actin cytoskeleton to the extracellular matrix and provide for… (more)

▼ Focal adhesions are specialized cell contact sites of distinct molecular composition and structure that bridge the actin cytoskeleton to the extracellular matrix and provide for efficient bidirectional transmission of biochemical and mechanical signals between the intra- and extracellular compartment. Many proteins within the focal adhesion have been discovered to be an integral component of the adhesion structure and function; however, a key molecule in the organization and physiological activity of focal adhesions is focal adhesion kinase (FAK). FAK is a nonreceptor tyrosine kinase that is essential for cell processes including cell migration, growth, and survival. Due to its connection between the cytoskeleton and extracellular matrix, FAK has been proposed to be a key component of integrin downstream signaling that regulates the organization of actin for transduction of cellular forces from inside to outside of the cell. While many studies have focused on determining FAK's role in sensing mechanical forces and regulating contractile signaling pathways, very few studies have attempted to determine the role of FAK in cell contraction through direct measurement of cellular tension. Therefore, the role of FAK in fibroblast and endothelial cell contractility was determined.;To investigate the role of FAK in endothelial cell tension and monolayer permeability, a stable FAK knockdown human pulmonary microvessel endothelial cell line (FAK-KD) was generated. Knockdown of FAK altered both cell morphology and actin distribution, and increased focal adhesion formation and VE-cadherin localization to cell-cell contacts. Measurement of tension produced by cells embedded within a three-dimensional (3-D) collagen matrix revealed that loss of FAK increased basal tension without alterations in basal myosin phosphorylation. Agonist-induced force was unaffected. However, loss of FAK enhanced endothelial monolayer barrier function. Thus, FAK is responsible for the balance between cellmatrix and cell-cell cohesion in order to regulate endothelial cell tension and monolayer permeability.;In order to determine the role of FAK in fibroblast cell contractility, FAK knockout (FAK-KO) mouse embryonic fibroblasts (MEFs) embedded in 3-D collagen gels were utilized. FAK null MEFs produced a decrease in basal tension and minimal agonist induced force compared to controls (FAK-WT). However, myosin II phosphorylation was comparable between FAK-KO and FAK-WT MEFs. Investigation of the collagen matrix revealed that FAKKO MEFs had an inability to organize their collagen matrix. Inhibition of FAK kinase activity or expression of FAK mutants revealed that FAK kinase activity was dispensable for tension generation. Thus, FAK localization to the focal adhesion was critical in the transmission of internal force to the collagen matrix resulting in cell contraction.;Collectively, these data show that FAK is an integral part in nonmuscle cellular tension. Although the loss of FAK altered tension generation differently in fibroblasts and endothelial cells,… Advisors/Committee Members: Robert Wysolmerski.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Arnold, K. M. (2013). The role of focal adhesion kinase in nonmuscle cell contraction. (Doctoral Dissertation). West Virginia University. Retrieved from https://doi.org/10.33915/etd.4949 ; https://researchrepository.wvu.edu/etd/4949

Chicago Manual of Style (16^th Edition):

Arnold, Kimberly M. “The role of focal adhesion kinase in nonmuscle cell contraction.” 2013. Doctoral Dissertation, West Virginia University. Accessed January 19, 2021. https://doi.org/10.33915/etd.4949 ; https://researchrepository.wvu.edu/etd/4949.

MLA Handbook (7^th Edition):

Arnold, Kimberly M. “The role of focal adhesion kinase in nonmuscle cell contraction.” 2013. Web. 19 Jan 2021.

Vancouver:

Arnold KM. The role of focal adhesion kinase in nonmuscle cell contraction. [Internet] [Doctoral dissertation]. West Virginia University; 2013. [cited 2021 Jan 19]. Available from: https://doi.org/10.33915/etd.4949 ; https://researchrepository.wvu.edu/etd/4949.

Council of Science Editors:

Arnold KM. The role of focal adhesion kinase in nonmuscle cell contraction. [Doctoral Dissertation]. West Virginia University; 2013. Available from: https://doi.org/10.33915/etd.4949 ; https://researchrepository.wvu.edu/etd/4949

Washington State University

27. [No author]. The Role of Stress Response Factors in the Development and Stress Resistance of the Zebrafish, Danio rerio .

Degree: 2011, Washington State University

URL: http://hdl.handle.net/2376/2860

► Cells respond to physiological and chemical insults by the upregulation and activation of the stress response. This response, also termed the heat shock response, is… (more)

Subjects/Keywords: Cellular Biology

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APA (6^th Edition):

author], [. (2011). The Role of Stress Response Factors in the Development and Stress Resistance of the Zebrafish, Danio rerio . (Thesis). Washington State University. Retrieved from http://hdl.handle.net/2376/2860

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):

author], [No. “The Role of Stress Response Factors in the Development and Stress Resistance of the Zebrafish, Danio rerio .” 2011. Thesis, Washington State University. Accessed January 19, 2021. http://hdl.handle.net/2376/2860.

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

MLA Handbook (7^th Edition):

author], [No. “The Role of Stress Response Factors in the Development and Stress Resistance of the Zebrafish, Danio rerio .” 2011. Web. 19 Jan 2021.

Vancouver:

author] [. The Role of Stress Response Factors in the Development and Stress Resistance of the Zebrafish, Danio rerio . [Internet] [Thesis]. Washington State University; 2011. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/2376/2860.

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

Council of Science Editors:

author] [. The Role of Stress Response Factors in the Development and Stress Resistance of the Zebrafish, Danio rerio . [Thesis]. Washington State University; 2011. Available from: http://hdl.handle.net/2376/2860

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

Temple University

28. Michael, James. Regulation of Ras signaling and oncogenesis by plasma membrane microdomains.

Degree: PhD, 2016, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,377230

►

Cell Biology

In this study, we assessed the contributions of plasma membrane (PM) microdomain targeting to the functions of H-Ras and R-Ras. These paralogues have… (more)

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Cell Biology

In this study, we assessed the contributions of plasma membrane (PM) microdomain targeting to the functions of H-Ras and R-Ras. These paralogues have identical effector-binding regions, but variant C-terminal targeting domains (tDs) which are responsible for lateral microdomain distribution: activated H-Ras targets to lipid ordered/disordered (Lo/Ld) domain borders, and R-Ras to Lo domains (rafts). We hypothesized that PM distribution regulates Ras effector interactions and downstream signaling. We used tD swap mutants, and assessed effects on signal transduction, cell proliferation, transformation, and tumorigenesis. R-Ras harboring the H-Ras tD (R-Ras-tH) interacted with Raf, and induced Raf and ERK phosphorylation similar to H-Ras. R-Ras-tH stimulated proliferation and transformation in vitro, and these effects were blocked by both MEK and PI3K inhibition. Conversely, the R-Ras tD suppressed H-Ras-mediated Raf activation and ERK phosphorylation, proliferation, and transformation. Thus, Ras access to Raf at the PM is sufficient for MAPK activation and is a principal component of Ras mitogenesis and transformation. Fusion of the R-Ras extended N-terminal domain to H-Ras had no effect on proliferation, but inhibited transformation and tumor progression, indicating that the R-Ras N-terminus also contributes negative regulation to these Ras functions. PI3K activation was tD-independent; however, H-Ras was a stronger activator of PI3K than R-Ras, with either tD. PI3K inhibition nearly ablated transformation by R-Ras-tH, H-Ras, and H-Ras-tR, whereas MEK inhibition had a modest effect on Ras-tH-driven transformation but no effect on H-Ras-tR transformation. R-Ras-tH supported tumor initiation, but not tumor progression. Whereas H-Ras-tR-induced transformation was reduced relative to H-Ras, tumor progression was robust and similar to H-Ras. H-Ras tumor growth was moderately suppressed by MEK inhibition, which had no effect on H-Ras-tR tumor growth. In contrast, PI3K inhibition markedly suppressed tumor growth by H-Ras and H-Ras-tR, indicating that sustained PI3K signaling is a critical pathway for H-Ras-driven tumor progression, independent of microdomains. In the second phase of the study, we investigated the combinatorial use of two drugs currently either in active use as anti-cancer agents (Rapamycin) or in clinical trials (OTX008), as a novel strategy to inhibit H-Ras-driven tumor progression. H-Ras anchored to the plasma membrane shuttles from the lipid ordered (Lo) domain to the lipid ordered/lipid disordered border upon activation, and retention of H-Ras at these sites requires Galectin-1 (Gal-1). We have previously found that genetically-mediated Lo sequestration of H-Ras inhibited MAPK signaling but not PI3K activation. Here we show that inhibition of Gal-1 with OTX008 sequestered H-Ras in the Lo domain, blocked H-Ras-mediated MAPK signaling, and attenuated H-Ras-driven tumor progression in mice. H-Ras-driven tumor growth was also attenuated by treatment with mTOR inhibitor Rapamycin, and this…

Advisors/Committee Members: Goldfinger, Lawrence;, Rizzo, Victor, Abood, Mary Ellen, Grana-Amat, Xavier, Golemis, Erica;.

Subjects/Keywords: Cellular biology

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APA (6^th Edition):

Michael, J. (2016). Regulation of Ras signaling and oncogenesis by plasma membrane microdomains. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,377230

Chicago Manual of Style (16^th Edition):

Michael, James. “Regulation of Ras signaling and oncogenesis by plasma membrane microdomains.” 2016. Doctoral Dissertation, Temple University. Accessed January 19, 2021. http://digital.library.temple.edu/u?/p245801coll10,377230.

MLA Handbook (7^th Edition):

Michael, James. “Regulation of Ras signaling and oncogenesis by plasma membrane microdomains.” 2016. Web. 19 Jan 2021.

Vancouver:

Michael J. Regulation of Ras signaling and oncogenesis by plasma membrane microdomains. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2021 Jan 19]. Available from: http://digital.library.temple.edu/u?/p245801coll10,377230.

Council of Science Editors:

Michael J. Regulation of Ras signaling and oncogenesis by plasma membrane microdomains. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,377230

29. Zinno, John Peter. The in vivo Detection of Outer Membrane Lysis during Spore Wall Assembly in Saccharomyces Cerevisiae Using a Novel Split GFP Assay.

Degree: 2018, State University of New York at Stony Brook

URL: http://pqdtopen.proquest.com/#viewpdf?dispub=10686038

► The regulation and mechanism of outer membrane (OM) lysis during spore wall assembly is not well understood. Although the timing of OM lysis has… (more)

Subjects/Keywords: Cellular biology

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

APA (6^th Edition):

Zinno, J. P. (2018). The in vivo Detection of Outer Membrane Lysis during Spore Wall Assembly in Saccharomyces Cerevisiae Using a Novel Split GFP Assay. (Thesis). State University of New York at Stony Brook. Retrieved from http://pqdtopen.proquest.com/#viewpdf?dispub=10686038

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):

Zinno, John Peter. “The in vivo Detection of Outer Membrane Lysis during Spore Wall Assembly in Saccharomyces Cerevisiae Using a Novel Split GFP Assay.” 2018. Thesis, State University of New York at Stony Brook. Accessed January 19, 2021. http://pqdtopen.proquest.com/#viewpdf?dispub=10686038.

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

MLA Handbook (7^th Edition):

Zinno, John Peter. “The in vivo Detection of Outer Membrane Lysis during Spore Wall Assembly in Saccharomyces Cerevisiae Using a Novel Split GFP Assay.” 2018. Web. 19 Jan 2021.

Vancouver:

Zinno JP. The in vivo Detection of Outer Membrane Lysis during Spore Wall Assembly in Saccharomyces Cerevisiae Using a Novel Split GFP Assay. [Internet] [Thesis]. State University of New York at Stony Brook; 2018. [cited 2021 Jan 19]. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10686038.

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

Council of Science Editors:

Zinno JP. The in vivo Detection of Outer Membrane Lysis during Spore Wall Assembly in Saccharomyces Cerevisiae Using a Novel Split GFP Assay. [Thesis]. State University of New York at Stony Brook; 2018. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=10686038

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

Boston University

30. Vakhshoorzadeh, Jasmine. Defining YAP/TAZ-dependency in human breast cancer cells.

Degree: MS, Medical Sciences, 2016, Boston University

URL: http://hdl.handle.net/2144/17028

► OVERVIEW: Hyperactivation and amplification of the oncogenic transcriptional co-factors YAP and TAZ are common in breast cancer. However, it is unknown if breast cancer cells… (more)

▼ OVERVIEW: Hyperactivation and amplification of the oncogenic transcriptional co-factors YAP and TAZ are common in breast cancer. However, it is unknown if breast cancer cells are dependent on YAP/TAZ for growth and survival. In addition, key transcriptional targets of YAP/TAZ that enable breast cancer growth have yet to be defined. To address these unresolved questions, we will define YAP/TAZ-dependencies across a large cohort of breast cancer cells and generate gene expression signatures for both YAP/TAZ-dependent and YAP/TAZ-independent lines. We aim to identify YAP/TAZ-target genes that are essential for the growth and survival of YAP/TAZ-dependent breast cancer cells. This approach may reveal genetic dependencies in breast cancer that can then be therapeutically exploited. METHODS: A comprehensive cohort of breast cancer cells (45 cell lines) was obtained from the American Type Culture Collection (ATCC). The majority of time allotted for this thesis was spent culturing and expanding the cell lines. Five complete breast cancer cell line libraries were successfully generated and annotated. These libraries will be a useful resource for the Boston University School of Medicine Cancer Research Community. Protein and RNA extracts were collected from all cell lines. RNA extraction was performed in all cell lines with the Qiagen RNase Kit as per the manufacturer’s instructions. Protein extracts were collected from the cell lines with RIPA lysis buffer. Protein lysates were then run on an acrylamide gel and the relative abundance of YAP and TAZ was quantified. RNA extracts were sent for microarray analysis to obtain gene expression profiles. Cell lines were also fixed and stained for YAP and TAZ at subconfluence (50%) and confluence (90%) and visualized through immunofluorescence to assess the relative subcellular localization of YAP and TAZ. RESULTS: Our results indicate that YAP/TAZ levels and activity are highly variable across breast cancer cell lines. Seven cell lines were found to overexpress only YAP, nineteen cell lines were found to overexpress only TAZ, and two cell lines (BT-474 and HCC 1599) were found to overexpress both YAP and TAZ. Two cell lines (MDA-MB-134-VI and DU4475) had negligible protein expression levels of YAP/TAZ. We were also able to identify a subset of cells as being resistant to Hippo pathway activation, as seen in MCF 10A, MCF 10F, and MCF-12A cells, which maintained nuclear YAP and TAZ even under confluent conditions, and with MDA-MB-231 cells, which maintained only nuclear YAP under confluence. Given the importance of YAP and TAZ in cellular proliferation and survival, these results suggest that these Hippo pathway inactive cell lines may be dependent on YAP and TAZ for survival, which will be assessed at a future time point. We plan to complete our analysis of the subcellular localization of YAP and TAZ for all 45 breast cancer cell lines. Microarray profiling and gene expression signature analysis of all 45 cell lines are also ongoing. DISCUSSION: We surmise that increased…

Subjects/Keywords: Cellular biology

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

APA (6^th Edition):

Vakhshoorzadeh, J. (2016). Defining YAP/TAZ-dependency in human breast cancer cells. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/17028

Chicago Manual of Style (16^th Edition):

Vakhshoorzadeh, Jasmine. “Defining YAP/TAZ-dependency in human breast cancer cells.” 2016. Masters Thesis, Boston University. Accessed January 19, 2021. http://hdl.handle.net/2144/17028.

MLA Handbook (7^th Edition):

Vakhshoorzadeh, Jasmine. “Defining YAP/TAZ-dependency in human breast cancer cells.” 2016. Web. 19 Jan 2021.

Vancouver:

Vakhshoorzadeh J. Defining YAP/TAZ-dependency in human breast cancer cells. [Internet] [Masters thesis]. Boston University; 2016. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/2144/17028.

Council of Science Editors:

Vakhshoorzadeh J. Defining YAP/TAZ-dependency in human breast cancer cells. [Masters Thesis]. Boston University; 2016. Available from: http://hdl.handle.net/2144/17028

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Open Access Theses and Dissertations