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You searched for +publisher:"Temple University" +contributor:("Kim, Seonhee"). Showing records 1 – 3 of 3 total matches.

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Temple University

1. Hughes, Lucinda Jane. Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma.

Degree: PhD, 2016, Temple University

Biomedical Sciences

The Hippo signaling pathway was first discovered in Drosophila melanogaster and is involved in organ size control by regulating cell proliferation and apoptosis. This well conserved pathway is activated by various signal inputs, including cell-cell contact, mechanotransduction, and G-protein coupled receptors, with signals converging on the downstream effector protein Yap and its homologue Taz, which are transcriptional co-activators. When the Hippo pathway is activated, Yap/Taz are phosphorylated, leading to cytoplasmic retention and degradation, and diminishing their transcriptional activity. Yap has also been recently implicated as a potential oncogene, as it is upregulated and transcriptionally active in several tumor types. Furthermore, inhibiting Yap activity in various cancer models has been shown to revert cancer cells to a normal phenotype. Although the role of Yap has been described in several organ systems, there is a paucity of information about the function of Yap in the central nervous system. I investigated the function of Yap/Taz in the murine cerebellum to determine its significance during normal development and a potential role for Yap/Taz in medulloblastoma, a tumor that arises in the cerebellum. In Chapter 2, I describe the expression pattern of Yap from embryonic through adult stages in mice, and demonstrate the functional significance of Yap/Taz in different cell populations using conditional knockout mouse models. I show that Yap plays a significant role in cell fate determination as well as in cerebellar foliation: Yap is highly expressed in the ventricular zone and is required for the proper formation of ependymal cells, and is also strongly expressed in Bergmann glia (BG) during early developmental stages, where Yap, together with Taz, plays a significant role in cerebellar foliation. Furthermore, Yap/Taz-deficient BG exhibit migrational defects, as their cell bodies can be found mislocalized to the molecular layer (ML), rather than remaining tightly associated with Purkinje Cells (PCs) in the PC layer. BG support the health of PCs, and severely defective BG positioning eventually leads to a loss of PCs. However, although Yap is highly expressed in granule neuron progenitors (GNPs) during the rapid postnatal expansion stage, it does not appear to play a major role in proliferation of these cells as conditionally knocking-out Yap/Taz in GNPs does not alter their proliferative capacity. Our observations demonstrate that in the cerebellum, Yap has a novel function in glia that is required for the development of normal foliation and organization, but plays a minimal role in GNP proliferation. Importantly, I also show that the reduction of sphingosine-1-phosphate G-protein-coupled receptor (S1P1) signal transduction activates the upstream kinase Lats with concomitant increases of phosphorylated Yap as well as a reduction of the known Yap target connective tissue growth factor (CTGF). This study identifies a novel function of Yap/Taz in cerebellar glia that is required for…

Advisors/Committee Members: Kim, Seonhee;, Graña, Xavier, Pearson, Helen E., Thomas, Gareth, Shore, Scott K.;.

Subjects/Keywords: Developmental biology; Cellular biology; Neurosciences;

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APA (6th Edition):

Hughes, L. J. (2016). Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,412035

Chicago Manual of Style (16th Edition):

Hughes, Lucinda Jane. “Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma.” 2016. Doctoral Dissertation, Temple University. Accessed October 28, 2020. http://digital.library.temple.edu/u?/p245801coll10,412035.

MLA Handbook (7th Edition):

Hughes, Lucinda Jane. “Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma.” 2016. Web. 28 Oct 2020.

Vancouver:

Hughes LJ. Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Oct 28]. Available from: http://digital.library.temple.edu/u?/p245801coll10,412035.

Council of Science Editors:

Hughes LJ. Yes-Associated Protein (YAP) and Transcriptional Co-Activator with PDZ Binding Motif (TAZ) Function in Normal Cerebellar Development and Medulloblastoma. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,412035


Temple University

2. Putatunda, Raj. HIV-1 INFECTION OF NEURAL STEM CELLS RESULTS IN COGNITIVE DEFICITS THROUGH ADULT NEUROGENIC MODULATION.

Degree: PhD, 2018, Temple University

Biomedical Sciences

While antiretroviral therapy (ART) regimens have significantly decreased the mortality rate in patients with HIV-1 infection and subsequent opportunistic infections, the co-morbidities continue to rise. Some of these co-morbidities include cardiomyopathies, metabolic dysfunction, accelerated aging, and most notably, neurocognitive deficits. HIV-1 associated neurocognitive disorders (HAND) denote a spectrum of neurocognitive deficits that are either asymptomatic in nature (asymptomatic neurocognitive impairments, ANI), mild to moderate in intensity (mild neurocognitive disorders, MND), or robust in nature (HIV-associated dementia, HAD). Thanks to the development of ART regimens, the incidence of HAD dramatically decreased. However, the emergence of ANI and MND continues to increase in the HIV-1 patient population. While the multifaceted nature behind the central nervous system (CNS) neuropathology of HIV-1 infection is not completely understood, dysregulated blood-brain barrier (BBB) integrity and the “Trojan-Horse” type mechanism of HIV-1 infection have been proposed as the cellular mechanisms underlying HAND. HIV-1 infects CD4+ T-lymphocytes and monocytes in the peripheral circulatory system. After these infected cells cross the BBB into the CNS, they release toxic viral proteins and viral particles onto microglia and astrocytes. These glial cells become activated, and release a plethora of inflammatory cytokines that further damage neurons via dysregulated neurotransmitter homeostasis, synaptodendritic damage, and calcium-mediated apoptotic pathways. At the same time, the virus may establish a state of latency in these microglia, perivascular macrophages, and astrocytes, which would allow for the long-term persistence of HIV-1 in the CNS. Recently, several studies have demonstrated that neural stem cells (NSCs) are capable of being productively and latently infected with HIV-1. This may be due to the fact that the hippocampal subgranular zone (SGZ), the subventricular zone (SVZ), and the circumventricular organs are highly vascularized, allowing potential direct contact of HIV-1 with NSCs. Additionally, the “Trojan” T-cells and macrophages could possibly release viral particles directly onto NSCs, and also transmit the virus through the formation of immunological synapses with NSCs. Therefore, the central hypothesis in this dissertation is that NSCs may serve as a novel CNS reservoir through which HIV-1 infection persists, and subsequently lead to neurocognitive impairments through dysregulating adult neurogenesis. Adult neurogenesis is a dynamic process that describes the generation of new neurons and glial cells from NSCs and neural progenitor cells (NPCs). This process mainly takes place in two areas of the brain: the SVZ around the lateral ventricles, and the SGZ within the dentate gyrus of the hippocampus. New neurons generated in these two neurogenic niches integrate into their respective circuitries to modulate olfactory stimuli and aid in memory acquisition/consolidation processes.…

Advisors/Committee Members: Hu, Wenhui;, Qin, Xuebin, Barbe, Mary F., Kim, Seonhee, Ramirez, Servio, Bethea, John R.;.

Subjects/Keywords: Neurosciences; Virology; Cellular biology;

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

APA (6th Edition):

Putatunda, R. (2018). HIV-1 INFECTION OF NEURAL STEM CELLS RESULTS IN COGNITIVE DEFICITS THROUGH ADULT NEUROGENIC MODULATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,514815

Chicago Manual of Style (16th Edition):

Putatunda, Raj. “HIV-1 INFECTION OF NEURAL STEM CELLS RESULTS IN COGNITIVE DEFICITS THROUGH ADULT NEUROGENIC MODULATION.” 2018. Doctoral Dissertation, Temple University. Accessed October 28, 2020. http://digital.library.temple.edu/u?/p245801coll10,514815.

MLA Handbook (7th Edition):

Putatunda, Raj. “HIV-1 INFECTION OF NEURAL STEM CELLS RESULTS IN COGNITIVE DEFICITS THROUGH ADULT NEUROGENIC MODULATION.” 2018. Web. 28 Oct 2020.

Vancouver:

Putatunda R. HIV-1 INFECTION OF NEURAL STEM CELLS RESULTS IN COGNITIVE DEFICITS THROUGH ADULT NEUROGENIC MODULATION. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2020 Oct 28]. Available from: http://digital.library.temple.edu/u?/p245801coll10,514815.

Council of Science Editors:

Putatunda R. HIV-1 INFECTION OF NEURAL STEM CELLS RESULTS IN COGNITIVE DEFICITS THROUGH ADULT NEUROGENIC MODULATION. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,514815


Temple University

3. Skuba, Andrew. In vivo imaging analysis of the regeneration failure of dorsal root axons in adult mice.

Degree: PhD, 2014, Temple University

Cell Biology

After injury, dorsal root (DR) axons regenerate in the peripheral nervous system (PNS), but turn around or stop at the dorsal root entry zone (DREZ), the entrance into the central nervous system (CNS). Examination of the dynamic axon regeneration that occurs following injury to the DR provides the opportunity to advance our understanding of what happens to sensory axons as they approach and arrive at the DREZ and expands our knowledge of sensory axon regeneration failure at the entrance to the spinal cord. Additionally, findings from these studies may offer potential avenues to provide insight into regeneration failure elsewhere in the central nervous system. Nevertheless, our understanding of the cellular and molecular processes underlying the failure of DR axons to regenerate through the DREZ is incomplete. The goal of my thesis work was to determine whether application of the time lapse-in vivo imaging technique is feasible and useful in studying dorsal root regeneration. I have also applied recently developed post-mortem analyses to the axons monitored in vivo, which provided additional insights into the mechanisms that prevent axon regeneration at the DREZ. Results in Chapters 2 and 3 demonstrate that wide-field microscopy is indeed feasible and useful for monitoring regenerating sensory axons immediately before, during, and in the days to weeks after lumbar (L5) DR crush. I was surprised to find that most axons were immobilized abruptly and chronically at the CNS portion of the DREZ, with their axon tips and shafts exhibiting features of differentiated nerve terminals. This observation raises the possibility, which has not been appreciated previously, that DR axons stop at the DREZ because their regeneration is terminated prematurely by forming synaptic contacts with unidentified postsynaptic cells. To confirm the immobilization of DR axons at the DREZ, I applied two-photon microscopy to examine the axon behavior at the DREZ at high resolution. Results described in Chapter 4 confirm those obtained with the time-lapse imaging performed with wide-field microscopy: axons arrested soon after their arrival at the DREZ did not exhibit even subtle movements. Light microscopic analyses of the failed axon tips monitored in vivo demonstrated that almost all axons stopped at the CNS territory of the DREZ, and that axon tips and adjacent shafts intensely immunolabeled with synapse markers. Ultrastructural analyses revealed that numerous axonal profiles had the characteristic features of pre- but not postsynaptic endings. Findings from these studies lead us to speculate that most, if not all, dorsal root axons become arrested as they enter the CNS territory of the DREZ by forming presynaptic terminals on non-neuronal cellular elements that differ from the dystrophic-like endings formed by a few axons. In the chapter 5, I discuss what I have found to be the key factors for successful monitoring of regenerating dorsal root axons in living animals; the feasibility, usefulness and limitations of the available…

Advisors/Committee Members: Son, Young-Jin, Barbe, Mary F.;, Son, Young-Jin, Barbe, Mary F., Gallo, Gianluca, Kim, Seonhee, Smith, George M., Ramirez, Servio;.

Subjects/Keywords: Cellular biology; Neurosciences;

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

APA (6th Edition):

Skuba, A. (2014). In vivo imaging analysis of the regeneration failure of dorsal root axons in adult mice. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,292900

Chicago Manual of Style (16th Edition):

Skuba, Andrew. “In vivo imaging analysis of the regeneration failure of dorsal root axons in adult mice.” 2014. Doctoral Dissertation, Temple University. Accessed October 28, 2020. http://digital.library.temple.edu/u?/p245801coll10,292900.

MLA Handbook (7th Edition):

Skuba, Andrew. “In vivo imaging analysis of the regeneration failure of dorsal root axons in adult mice.” 2014. Web. 28 Oct 2020.

Vancouver:

Skuba A. In vivo imaging analysis of the regeneration failure of dorsal root axons in adult mice. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Oct 28]. Available from: http://digital.library.temple.edu/u?/p245801coll10,292900.

Council of Science Editors:

Skuba A. In vivo imaging analysis of the regeneration failure of dorsal root axons in adult mice. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,292900

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