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Molecular characterization of the chicken growth hormone receptorgeneLau, Suk-ling, Joanna., 劉淑玲. January 2005 (has links)
published_or_final_version / Zoology / Doctoral / Doctor of Philosophy
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Mechanism of antibody-dependent enhancement in severe acute respiratory syndrome coronavirus infectionLeung, Hiu-lan, Nancy., 梁曉灡. January 2012 (has links)
Severe lymphopenia is a clinical feature of Severe Acute Respiratory Syndrome
(SARS) patients. However, lymphocytes do not express receptor for SARS-CoV,
neither the widely accepted viral receptor angiotensin converting enzyme 2 (ACE2)
nor the putative receptors Dendritic Cell- and Liver/lymph-Specific Intercellular
adhesion molecule-3-Grabbing Non-integrin (DC-SIGN and L-SIGN). Our group
previously showed in vitro that, SARS-CoV Spike pseudotyped particles (SARSCoVpp)
could infect human B cells only when inoculated in presence of anti-SARSCoV
Spike immune serum. Such observations raised concerns about the possible
occurrence of antibody-dependent enhancement (ADE) of infection, a phenomenon
during which a virus bounded by antibodies could gain entry into cells through
mechanisms involving complement receptors or Fc receptors. Recently, we have
demonstrated the participation of the human Fc gamma receptor II (hFcγRII)
molecules in granting SARS-CoV an opportunity to infect human immune cells.
The aim of this study was to decipher the molecular mechanism leading to antibodymediated,
FcγRII-dependent infection of immune cells by SARS-CoV. By using
transduction experiment, I highlighted that different members of the hFcγRII family
(namely hFcγRIIA, hFcγRIIB1 and hFcγRIIB2) could confer susceptibility to ADE of
SARS-CoVpp infection. I further demonstrated that purified anti-viral
immunoglobulin G, but not other soluble factor(s) from heat-inactivated immune
serum, was the determinant for occurrence of ADE infection. Additionally, with the
development of a cell-cell fusion assay, I illustrated that in contrast to the ACE2-
dependent pathway, ADE infection did not occur at the plasma membrane, but rather
require internalization of virus/antibodies immune complexes by the target cells. In
line with this hypothesis, my results using a panel of FcγRII-expressing mutants
demonstrated that binding of immune complexes to cell surface FcγRII was a
prerequisite but was not sufficient to trigger ADE infection. In these experiments,
only FcγRII signaling-competent constructions conferred susceptibility to ADE of
SARS-CoVpp infection.
Altogether my results point toward a role of the anti-SARS-CoV Spike IgG in vitro in
granting SARS-CoV an opportunity to infect cells bearing signaling-competent
FcγRII receptors. If further confirmed, such observations could have implications for
understanding SARS-CoV tropism and SARS pathogenesis, as well as warrant for
careful design of SARS vaccines and immunotherapy based on anti-viral antibodies. / published_or_final_version / Microbiology / Master / Master of Philosophy
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Characterization of melatonin receptors in human placental trophoblasts and prostate cancerLau, Kai-wing., 劉啓榮. January 2002 (has links)
published_or_final_version / abstract / toc / Physiology / Master / Master of Philosophy
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Characterization of human secretin receptor by the cytosensor microphysiometer systemNg, Sai-ming, Samuel., 吳世明 January 1998 (has links)
published_or_final_version / Zoology / Master / Master of Philosophy
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Adhesion of membrane-bound receptors and ligands : concurrent binding and the role of microtopologyWilliams, Tom E. 12 1900 (has links)
No description available.
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Regulation of hippocampal synaptic transmission and receptor trafficking by adenosine in hypoxia and ischemia: role of protein phosphatases 1, 2A and 2B, casein kinase 2 (CK2), and equilibrative nucleoside transporters (ENTs).2014 September 1900 (has links)
The role of adenosine as an endogenous neuromodulator is well established, but the mechanism(s) mediating the extensive modulatory and regulatory actions of adenosine have not yet been fully elucidated. In fact, although adenosine, through activation of adenosine A1 and A2A receptors, has been demonstrated as neuroprotective or neurodegenerative, respectively, little is known about the mechanism by which adenosine mediates these actions. In the hippocampus, essential physiological processes rely on adenosine signaling, including regulation of long-term potentiation (LTP) and long-term depression (LTD). Neuromodulation by adenosine is dominantly inhibitory in the hippocampus, mediated by the abundant and high-affinity adenosine A1 receptor. In ischemia and hypoxia, A1 receptor activation induces rapid synaptic depression which is mediated by multiple signaling pathways including the induction of excitatory AMPA glutamate receptor internalization, which inhibits synaptic transmission in the hippocampus. Considerable effort has been devoted to investigating the role of adenosine in ischemic stroke, due to the fact that in cerebral ischemia or hypoxia, extracellular levels of adenosine increase dramatically. This thesis explores the functional consequences of adenosine signaling in hypoxia and ischemia, which mediate GluA1 AMPA receptor subunit internalization. Three major serine/threonine protein phosphatases (PPs), PP1, PP2A, and PP2B are investigated and shown to mediate A1 receptor-mediated GluA1 internalization in hypoxic conditions in the rat hippocampus. Further experiments demonstrate the role of adenosine A2A receptors in potentiating hippocampal synaptic transmission in reperfusion by increasing GluA1 surface expression through increased phosphorylation of regulatory C-terminal phosphorylation sites of GluA1. The mechanism of extracellular adenosine regulation by equilibrative nucleoside transporters (ENTs) and casein kinase 2 (CK2) are examined and shown to interact in hypoxia/reperfusion experiments on hippocampal slices. Finally, using a pial vessel disruption (PVD) permanent focal cortical ischemia stroke model, experiments demonstrate increased adenosine tone in the hippocampus, which mediates increased adenosine-induced synaptic depression. CK2 inhibition was also neuroprotective after 20min hypoxia. This shows that adenosine tone is increased in the hippocampus after a small cortical stroke, implying a potential global effect of focal ischemia. Together, these studies further reveal the paramount role of adenosine as a neuromodulator in the hippocampus during neuronal insults, furthering our understanding of the mechanism of neuronal death in hypoxic and ischemic conditions.The role of adenosine as an endogenous neuromodulator is well established, but the mechanism(s) mediating the extensive modulatory and regulatory actions of adenosine have not yet been fully elucidated. In fact, although adenosine, through activation of adenosine A1 and A2A receptors, has been demonstrated as neuroprotective or neurodegenerative, respectively, little is known about the mechanism by which adenosine mediates these actions. In the hippocampus, essential physiological processes rely on adenosine signaling, including regulation of long-term potentiation (LTP) and long-term depression (LTD). Neuromodulation by adenosine is dominantly inhibitory in the hippocampus, mediated by the abundant and high-affinity adenosine A1 receptor. In ischemia and hypoxia, A1 receptor activation induces rapid synaptic depression which is mediated by multiple signaling pathways including the induction of excitatory AMPA glutamate receptor internalization, which inhibits synaptic transmission in the hippocampus. Considerable effort has been devoted to investigating the role of adenosine in ischemic stroke, due to the fact that in cerebral ischemia or hypoxia, extracellular levels of adenosine increase dramatically. This thesis explores the functional consequences of adenosine signaling in hypoxia and ischemia, which mediate GluA1 AMPA receptor subunit internalization. Three major serine/threonine protein phosphatases (PPs), PP1, PP2A, and PP2B are investigated and shown to mediate A1 receptor-mediated GluA1 internalization in hypoxic conditions in the rat hippocampus. Further experiments demonstrate the role of adenosine A2A receptors in potentiating hippocampal synaptic transmission in reperfusion by increasing GluA1 surface expression through increased phosphorylation of regulatory C-terminal phosphorylation sites of GluA1. The mechanism of extracellular adenosine regulation by equilibrative nucleoside transporters (ENTs) and casein kinase 2 (CK2) are examined and shown to interact in hypoxia/reperfusion experiments on hippocampal slices. Finally, using a pial vessel disruption (PVD) permanent focal cortical ischemia stroke model, experiments demonstrate increased adenosine tone in the hippocampus, which mediates increased adenosine-induced synaptic depression. CK2 inhibition was also neuroprotective after 20min hypoxia. This shows that adenosine tone is increased in the hippocampus after a small cortical stroke, implying a potential global effect of focal ischemia. Together, these studies further reveal the paramount role of adenosine as a neuromodulator in the hippocampus during neuronal insults, furthering our understanding of the mechanism of neuronal death in hypoxic and ischemic conditions.
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Molecular genetic studies on prostate and penile cancer /Andersson, Patiyan, January 2008 (has links) (PDF)
Diss. (sammanfattning) Linköping : Linköpings universitet, 2008. / Härtill 4 uppsatser.
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Implantation : morphological and biochemical characterization of the receptive human endometrium /Stavréus-Evers, Anneli, January 2002 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.
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Functional studies on the orphan receptor Nurr1 and related retinoid receptors /Castro, Diogo Sampaio e, January 1900 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 4 uppsatser.
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Estrogen effects on different neurotransmitters in rat hippocampus: implications for cognitive function /El-Bakri, Nahid Karrar, January 2004 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.
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