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Dissertations / Theses on the topic 'Cell receptors'

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Published: 4 June 2021

Last updated: 1 August 2024

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1

Ferletta, Maria. "The Laminins and their Receptors." Doctoral thesis, Uppsala University, Department of Cell and Molecular Biology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1771.

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Basement membranes are thin extracellular sheets that surround muscle, fat and peripheral nerve cells and underlay epithelial and endothelial cells. Laminins are one of the main protein families of these matrices. Integrins and dystroglycan are receptors for laminins, connecting cells to basement membranes. Each laminin consists of three different chains, (α, β, γ). Laminin-1 (α1β1γ1) was the first laminin to be found and is the most frequently studied. Despite this, it was unclear where its α1 chain was expressed. A restricted distribution of the α1 chain in the adult epithelial basement membranes was demonstrated in the present study. In contrast, dystroglycan was found to have a much broader distribution. Dystroglycan is an important receptor for α2-laminins in muscle, but binds also α1-laminins. The more ubiquitous α5-laminins were also shown to bind dystroglycan, but with distinctly lower affinity than α1- and α2- laminins.

The biological roles of different laminin isoforms have been investigated. Differences were found in the capacity of various tested laminins to promote epithelial cell adhesion. The α5-laminins were potent adhesive substrates, a property shown to be dependent on α3 and α6 integrins. Each receptor alone could promote efficient epithelial cell adhesion to α5-laminins. Yet, only α6 integrin and in particular the α6A cytoplasmic splice variant could be linked to laminin-mediated activation of a mitogen-activated protein kinase (MAP kinase) pathway. Attachment to either α1- or α5-laminins activated extracellular-signal regulated kinase (ERK) in cells expressing the integrin α6A variant, but not in cells expressing α6B. A new role for dystroglycan as a suppressor of this activation was demonstrated. Dystroglycan antibodies, or recombinant fragments with high affinity for dystroglycan, decreased ERK activation induced by integrin α6 antibodies. Integrin αvβ3 was identified as a novel co-receptor for α5-laminin trimers. Cell attachment to α5-laminins was found to facilitate growth factor induced cell proliferation. This proliferation could be blocked by antibodies against integrin αvβ3 or by an inhibitor of the MEK/ERK pathway. Therefore, integrin αvβ3 binding to α5-laminins could be of biological significance.

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2

Eckl-Dorna, J. "How B cell receptors and Toll-like receptors collaborate in shaping B cell responses." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/18762/.

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Antigen recognition by B cells results in their activation followed by specific antibody production. These events are initiated by antigen binding to their surface B cell receptors (BCR) which triggers both signalling and internalization of the receptor bound antigen to the endosome. However B cells also express features of the innate immune system such as Toll like receptors (TLRs), that can be located either on the surface of the cell or intracellularly where they recognize bacterial and viral nucleic acids. Engagement of these receptors within B cells is associated with enhancement of humoral responses. The aim of my PhD project was to investigate how endosomal TLR ligands in a particulate form could gain access to their intracellular receptors in the B cell and which impact the subsequent TLR engagement had on B cell fate. To achieve this, I directly linked both antigen and TLR9 ligand to particulates. Immunisation of mice with those particulates resulted in enhanced specific antibody titers compared to stimulation with particulate antigen alone. To dissect the underlying mechanism, I employed transgenic B cells bearing BCR specificity for the same antigen and stimulated them with particulate antigen-TLR9 ligand conjugates. Particulate TLR9 ligand could not gain access to its receptor within B cells via unspecific macropinocytosis and instead depended on BCRmediated internalization. Subsequent engagement of intracellular TLR9 by its ligand present in the conjugates resulted in B cell activation and proliferation, followed by differentiation into plasma cells and antigen specific antibody secretion. The uptake of the antigen-TLR9 ligand particulates both in vitro and in vivo depended on the affinity of the antigen once a defined threshold required for internalization was surpassed. The extent of plasma cell differentiation however could be modulated by the amount of TLR9 ligand present on the particulates. Thus I observed that direct linking of antigen and TLR ligand resulted in PC differentiation through antigen specific BCR mediated internalization and subsequent TLR engagement. This reveals a mechanism that may operate during the initiation of a primary immune response.

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3

Betson, Martha Elizabeth. "Regulation of cell-cell adhesion in keratinocyes." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274930.

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4

Jorgenson, Rebecca L. "The innate immune response and toll-like receptors in the human endometrium." Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/4178.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2005.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2005" Includes bibliographical references.

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5

Jiang, Ning. "Kinetic analysis of Fcγ receptor and T cell receptor interacting with respective ligands." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/26716.

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Low affinity Fcg receptor III (FcgRIII, CD16) triggers a variety of cellular events upon binding to the Fc portion of IgG. A real-time flow cytometry method was developed to measure the affinity and kinetics of such low affinity receptor/ligand interactions, which was shown as an easily operated yet powerful tool. Results revealed an unusual temperature dependence of reverse rate of CD16aTM dissociating from IgG. Except for a few studies using mammalian cell CD16s, most kinetics analyses use purified aglycosylated extracellular portion of the molecules, making it impossible to assess the importance of the receptor anchor and glycosylation on ligand binding. We used a micropipette adhesion frequency assay to demonstrate that the anchor length affects the forward rate and affinity of CD16s for IgG in a species specific manner, most likely through conformational changes. Receptor glycosylation dramatically reduced ligand binding by 100 folds. T cell receptor (TCR) is arguably the most important receptor in the adaptive human immune system. Together with coreceptor CD4 or CD8, TCR can discriminate different antigen peptides complexed with major histocompatibility complex (MHC) molecule (pMHC), which differ by as few as only one amino acid, and trigger different T cell responses. When T cell signaling was suppressed, TCR had similar affinity and kinetics for agonist and antagonist pMHC whose binding to CD8 was undetectable. TCR on activated T cell had a higher affinity for pMHCs, suggesting that TCRs organize themselves differently on activated T cells than on naïve T cells. In the absence of inhibitors for signaling, TCR binds agonist pMHC with several orders of magnitude higher affinity than antagonist pMHC. In addition, engagement of TCR by pMHC signals an upregulation of CD8 binding to pMHC, which is much stronger than the TCR-pMHC binding. The transition from weak TCR binding to the strong CD8 binding takes place around 0.75 second after TCR in contact with pMHC and can be reduced by several inhibitors of tyrosine and lipid phosphorylation, membrane rafts, and actin cytoskeleton. These results provide new insights to understanding T cell discrimination.

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6

Im, Jin Seon. "Molecular characterization of T cell receptors and non-MHC restricted T cell receptor binding peptides." Diss., The University of Arizona, 1999. http://hdl.handle.net/10150/284969.

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T cells recognize antigenic peptides presented by MHC molecules on antigen presenting cells (APC) through T cell receptors (TCRs). Since TCRs are very similar to antibodies in structure and genetics, TCRs might have the potential to bind free antigens as antibodies do. Here, peptides which bound TCRs irrespective of MHC molecules have been identified by screening "one-bead one-peptide" combinatorial libraries. Peptides: VRENAR, RTGNYV, GKMHFK, KDAVKR and RKPQAI bound recombinant Jurkat single chain T cell receptors (scTcrs). GKMHFK, KDAVKR and RKPQAI were also specific for natural TCRs on the Jurkat cell surface. Molecular modeling implies that Glu96 in the CDR3 loop of TCR alpha chain is a candidate for the peptide interaction site. However, TCR-binding peptides did not induce biological effects on parental Jurkat cells. To extend this study to a biologically relevant system, diabetogenic T cells involved in insulin-dependent diabetes mellitus (IDDM) have been characterized. GAD(524-543) responding T cells showed restricted TCR variable gene usage, which utilized preferentially Vα17 and Vβ12. Three domain single chain T cell receptors (3D scTcr) were constructed as tools to investigate potential therapies for IDDM and to identify peptides which bind to TCR without association of MHC molecules. Functional analysis has demonstrated that GAD(524-543)-specific scTcrs retained the ability to bind GAD(524-543)/IAg7 complex. This work shows that recombinant scTcrs can bind cognate peptide presented by MHC molecules, therefore they can be used as substitutes for natural TCRs in screening "one-bead one-peptide" combinatorial libraries to identify TCR-binding peptide.

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7

Ihenetu, Kenneth. "Characterisation of cannabinoid receptors on immune cells and cell lines." Thesis, University of Hertfordshire, 2003. http://hdl.handle.net/2299/14124.

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Cannabinoids may inhibit immune cell function by modulating cytokine/chemokine release but the receptors mediating these events are poorly characterised. The aim of this thesis is to characterise cannabinoid receptors mediating cytokine/chemokine release from immune and inflammatory cells by measuring the effects of cannabinoids on cytokine release using ELISA technique. Apoptosis of inflammatory cells was also assessed by visual evaluation of cells treated with cannabinoids using a nuclear fluorochrome 4'6-diamidino-2 phenyl indole dihydrochloride (DAPI). Non-selective cannabinoid receptor agonists CP55,940 (10-6 -10-4 M- 10 'S M), A? - THC (10 -10 M) and anandamide (10 M- 10-4 M) inhibited LPS-induced release of TNF-a from THP-1 cells, a monocytic cell line. The cannabinoid CB2 receptor antagonist SR144528 (10 -6 M) but not the cannabinoid CB1 receptor antagonist SR141716A (10 -6 M) antagonised the inhibitory effects of CP55,940 (pA2 = 6.1 t 0.1, n=6) on THP-1 cells. Similarly, CP55,940 (10-6-104 M -10 'S M), 09-THC (10 10 M -10 -S M) and anandamide (10 -6 M -10'4 M) inhibited PHA/PMA-induced IL-2 release from Jurkat cells, a lymphocytic cell line. However in contrast to THP-1 cells, neither SR141716A (10 -6 M) nor SR144528 (10 -6 M) antagonised the inhibitory effects of CP55,940 on this cell line. In peripheral blood mononuclear cells a nonselective cannabinoid receptor agonist WIN55212-2 (10'10 M-10'5 M) and a selective cannabinoid CB2 receptor agonist JWH 015 (10 -10 M- 10 -S M) inhibited PHAinduced release of IL-2. These effects were antagonised by SR144528 (10-6 M) (pA2 = 6.3 ± 0.1; 6.5 ± 0.1, n=5 respectively) but not by SR141716A (10 -6 M). CP55,940 (10 -10 M -10 -5 M) produced a small, non-significant (P> 0.05) inhibitory effect on IL-2 release. 09-THC (10 -10 M-10-6 M) and ACEA (10 -'0 M- 10 -6 M) had no significant inhibitory effect on the release of IL-2 from PBMC. CP55,940 (10 M) and A9- THC (10 M) antagonised the inhibitory effects of WIN55212-2 (pA2 = 6.1 ± 0.1; 6.96 ± 0.16, n=5 respectively). In HT-29 cells, CP55,940 (10"10 -10"5 M- 10 M), A9-THC (10 -10 M -10 -5 M), WIN55212-2 (10"10 M-10-5 M) and JWH 015 (10 -10 M- 10 -5 M) inhibited IL-8 release. SR141716A (10 -6 M) antagonised the inhibitory effects of CP55,940 (pA2 = 8.3 ± 0.2 n=6) but did not antagonise the effects of WIN55212-2 and JWH 015. SR144528 (10 -6 M) but not SR141716A (10 -6 M) antagonised the inhibitory effects of CP55,940 (pA2 = 8.2 ± 0.8, n=6), WIN55212-2 (pA2 = 7.1± 0.3, n=6), JWH 015 (pA2 = 7.6 ± 0.4, n=6) respectively. A protein the size of cannabinoid CB2 receptors was localised in this cell line by Western blotting. CP55,940 and WIN55212-2 inhibited basal and agonist-evoked increases in both intracellular cyclic AMP and intracellular calcium at the same concentration as that inhibiting TNF-a-induced release of IL-8. Furthermore anandamide (>1 μM) but not CP55,940 caused apoptosis in Jurkat and HT-29 cell. These data suggest that activation of cannabinoid CB2 receptors in THP-1 cells, PBMC and HT-29 cells could lead to inhibition of cytokine/chemokine release. Furthermore,c annabinoid-evokedin hibition of basal and agonist stimulated increases in HT-29 cells may be related to cannabinoid-evokedin hibition of IL-8 release. Thus data presented in this thesis suggest that cannabinoid CB2 receptor agonists with high efficacy may have potential clinical utility in the treatment of inflammatory conditions such as inflammatory bowel disease (IBD) or chronic obstructive pulmonary disease (COPD) and other inflammatory disorders where epithelial cells have a major role.

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8

Campbell, M.-A. "Functional receptors on B-cell membranes." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383704.

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9

Paramasivam, Anbalakan. "Regulation of immune cell P2X receptors." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612427.

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10

Hannan, S. B. "Cell surface mobility of GABAB receptors." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335825/.

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Type-B γ-aminobutyric acid receptors (GABABRs) are important for mediating slow inhibition in the central nervous system and the kinetics of their internalisation and lateral mobility will be a major determinant of their signalling efficacy. Functional GABABRs require R1 and R2 subunit co-assembly, but how heterodimerisation affects the trafficking kinetics of GABABRs is unknown. Here, an α-bungarotoxin binding site (BBS) was inserted into the N-terminus of R2 to monitor receptor mobility in live cells. GABABRs are internalised via clathrin- and dynamin-dependent pathways and recruited to endosomes. By mutating the BBS, a new technique was developed to differentially track R1a and R2 simultaneously, revealing the subunits internalise as heteromers and that R2 dominantly-affects constitutive internalisation of GABABRs. Notably, the internalisation profile of R1aR2 heteromers, but not R1a homomers devoid of their ER retention motif (R1ASA), is similar to R2 homomers in heterologous systems. The internalisation of R1aASA was slowed to that of R2 by mutating a di-leucine motif in the R1 C-terminus, indicating a new role for heterodimerisation, whereby R2 subunits slow the internalization of surface GABABRs. R1a and R1b are the predominant GABABR1 isoforms in the brain, differing by the two Sushi Domains (SDs) in R1a. Introduction of a BBS into the N-terminus of R1b and comparison with R1a revealed that R1bR2 internalises faster than R1aR2. Introduction of the SDs into the BBS-tagged metabotropic glutamate receptor-2 also conferred a decrease in internalisation. Finally, the lateral surface mobility of GABABRs was studied by extending the BBS-tagging method to single-particle tracking using quantum dots. R1aR2 and R1bR2 exhibited different mobility profiles on hippocampal neurons and differentially responded to baclofen. In conclusion, this study provides new and important insight into the mobility of cell surface GABABRs and the underlying mechanisms that ensure they provide efficacious slow synaptic inhibition.

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11

Gray, Phillip Neal. "Characterization of the membrane associated progesterone receptor (MAPR) homologues in Saccharomyces cervisiae and Arabidopsis thaliana." Diss., Georgia Institute of Technology, 2001. http://hdl.handle.net/1853/25589.

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12

Kalogeropoulos, Michail. "Novel mechanisms of dendritic cell regulation by leukocyte immunoglobulin-like receptor B1." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=210082.

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Dendritic cells play an essential role in activating immune responses upon recognition of pathogens. This results in maturation and migration to the lymph nodes, where T cells are stimulated by upregulated antigen presentation, co-stimulation and cytokine secretion. DCs are also considered important in inhibiting inappropriate immune responses against self-peptides which could lead to the development of autoimmunity. This has been attributed to DCs that demonstrate inhibited co-stimulation and cytokine secretion. It has been previously shown that the continuous ligation of an immunomodulatory receptor, LILRB1, during DC differentiation results in such a DC population that demonstrates an immature phenotype even after exposure to bacterial components and resulted in inhibiting primary T cell responses. The mechanisms by which LILRB1-DCs promote tolerance are, therefore, here investigated. Previous studies revealed significantly altered expression for a large number of gene targets which varied from immune to cytoskeletal and bone-related functions. One of these includes DcR3, a soluble protein with a poorly defined role in immune regulation. It is here demonstrated that DcR3 has a positive role in the induction of IL-17, a cytokine implicated in autoimmunity. However, DcR3 was not secreted by LILRB1-DCs, possibly accounting for some of their tolerogenic functions. In addition, the expression of several cytoskeletal proteins was significantly changed in response to LILRB1 ligation and was associated with decreased ability for phagocytosis and migration. Lastly, it has been recently identified that DCs are able to trans-differentiate into osteoclasts, the main cell type linked with inflammatory bone disorders, such as rheumatoid arthritis. It is here shown for the first time that ligation of LILRB1 inhibits this process and results in decreased bone resorption. Overall, these data provides evidence that ligation of LILRB1 on DCs affects normal inflammatory functions and suggests its potential for the development of new treatments against several autoimmune diseases.

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13

Burford, Neil Thornton. "Cell signalling in Chinese hamster ovary cells expressing recombinant muscarinic receptors." Thesis, University of Leicester, 1994. http://hdl.handle.net/2381/33575.

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Agonist stimulation of recombinant m1, m2, and m3 muscarinic receptors, expressed in Chinese hamster ovary (CHO) cells, was compared. Carbachol binding affinity, and its modification by cations, guanine nucleotides and PTX pretreatment, was compared in washed membrane preparations of each of the CHO cell clones. Functional responses, determined by carbachol stimulation, were: [35S]GTPS binding in membranes; Ins(l,4,5)P3 accumulation in intact cells; 45ca2+ release from permeabilized cells; and cAMP accumulation in intact cells. m2-Transfected CHO cells were found to couple to AC, mediating inhibition of forskolin-stimulated cAMP accumulation, via PTX-sensitive G proteins. After PTX pretreatment of these cells, carbachol mediated a small potentiation of forskolin-stimulated cAMP accumulation, though with a much lower carbachol potency compared with the inhibitory response. m1 and m3-transfected CHO cell clones were found to couple with both PTX-sensitive and PTX-insensitive G proteins, at relatively high levels of receptor expression. The PTX- insensitive G proteins mediated agonist-stimulated PLC activation and were involved in the activation of AC (though at a much lower potency). The mechanism, by which m1, m2 and m3 muscarinic receptors stimulated AC activity was not thought to be due to crosstalk via PLC activity. The level of m3 muscarinic receptor expression, in CHO cells, was found to markedly affect both the potency, and the maximal responsiveness, with which carbachol mediated PLC activation and AC activation. Furthermore, at lower levels of receptor expression, m3 muscarinic receptors appeared to couple to a lesser extent with PTX-sensitive G proteins. The study, therefore, concluded that comparisons of agonist-mediated responses between muscarinic receptor subtypes, expressed in CHO cells, must be performed at similar levels of receptor expression. At similar receptor densities, m1 and m3 muscarinic receptors, in CHO cells, produced very similar responses to carbachol.

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14

Burdon, Drew. "Cell growth regulation by muscarinic acetylcholine receptors." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29932.

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The growth response of Chinese hamster ovary (CHO) cells to activation of recombinantly expressed G protein-coupled muscarinic M2 or M3 acetylcholine (ACh) receptors has been assessed. Activation of these receptors leads to divergent growth responses: M2 ACh receptor activation causes an increase in DNA synthesis, whereas M3 ACh receptor activation causes a dramatic inhibition of DNA synthesis. The M3 ACh receptor-mediated growth inhibition has been characterised, and shown to comprise a G1-phase cell cycle arrest, involving an increase in p21Cip1/Waf1 protein expression. Further, a receptor-mediated increase in p21Cip1/Waf1 association with cyclin-dependent kinase 2 (CDK2) leads to a decrease in CDK2 activity and an accumulation of hypophosphorylated retinoblastoma protein (pRb). The increase p21Cip1/Waf1 expression is due at least in part to an increase p21Cip1/Waf1 mRNA although no receptor-mediated change in candidate transcription factor activities could be detected. Extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) activation profiles suggested two alternative hypotheses to account for the receptor-mediated growth arrest. However, pharmacological and biochemical data demonstrate that ERK, JNK and p38 MAPK are not involved in the growth regulation, whilst inhibition of PKC partially ablates the growth arrest. Data demonstrate that both M3 ACh receptor-mediated ERK and JNK activities may be dependent on liberated G-protein bg subunits, whilst the growth arrest is not perturbed by bg subunit sequestration. Data presented reveal a MAPK-independent mechanism of growth regulation that may involve coping of the M3 ACh receptor to heterotrimeric G-protein families other than Gq/11.

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15

Lester, Robin D. "Hypoxia activated cell signaling receptors in cancer." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3297526.

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Thesis (Ph. D.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed April 28, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 114-134).

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16

Abraham, Linda Ann. "Thrombin, protease receptors and bone cell function." Thesis, Royal Veterinary College (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287938.

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17

Joseph, Ansamma K. "DNA sequence analysis of T cell receptors." Thesis, University of Bath, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321849.

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18

Soper, David Michael. "Interleukin-2 receptor and T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8344.

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19

McLane, Jesica Mata. "Investigation of 1alpha,25-dihydroxy vitamin D3 membrane receptor ERp60 in adipocytes from male and female lean and obese mice." Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/31793.

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Thesis (M. S.)--Biomedical Engineering, Georgia Institute of Technology, 2010.
Committee Chair: Dr. Barbara Boyan; Committee Co-Chair: Dr. Zvi Schwartz; Committee Member: Dr. Hanjoong Jo. Part of the SMARTech Electronic Thesis and Dissertation Collection.

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20

Siow, Lam. "ATP and P2Y1 nucleotide receptor in cortical neurons : localization, signal transduction and transcriptional regulation /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202006%20SIOW.

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21

Dagkalis, Athanasios. "CCR2 and CX3CR1 in monocyte trafficking in experimental autoimmune uveoretinitis." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24809.

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22

Williams, Tom E. "Adhesion of membrane-bound receptors and ligands : concurrent binding and the role of microtopology." Diss., Georgia Institute of Technology, 1998. http://hdl.handle.net/1853/17335.

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23

Prevo, Remko. "Characterisation of new Link superfamily Hyaluronan receptors." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275401.

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Hauser, Jannek. "Regulation of B cell development by antigen receptors." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-40819.

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The developmental processes of lymphopoiesis generate mature B lymphocytes from hematopoietic stem cells through increasingly restricted intermediates. Networks of transcription factors regulate these cell fate choices and are composed of both ubiquitously expressed and B lineage-specific factors. E-protein transcription factors are encoded by the three genes E2A, E2-2 (SEF2-1), and HEB. The E2A gene is required for B cell development and encodes the alternatively spliced proteins E12 and E47. During B lymphocyte development, the cells have to pass several checkpoints verifying the functionality of their antigen receptors. Early in the development, the expression of a pre-B cell receptor (pre-BCR) with membrane-bound immunoglobulin (Ig) heavy chain protein associated with surrogate light chain (SLC) proteins is a critical checkpoint that monitors for functional Ig heavy chain rearrangement. Signaling from the pre-BCR induces survival and a limited clonal expansion. Here it is shown that pre-BCR signaling rapidly down-regulates the SLCs l5 and VpreB and also the co-receptor CD19. Ca2+ signaling and E2A were shown to be essential for this regulation. E2A mutated in its binding site for the Ca2+ sensor protein calmodulin (CaM), and thus with CaM-resistant DNA binding, makes l5, VpreB and CD19 expression resistant to the inhibition following pre-BCR stimulation. Thus, Ca2+ down-regulates SLC and CD19 gene expression upon pre-BCR stimulation through inhibition of E2A by Ca2+/CaM. A general negative feedback regulation of the pre-BCR proteins as well as many co-receptors and proteins in signal pathways from the receptor was also shown. After the ordered recombination of Ig heavy chain gene segments, also Ig light chain gene segments are recombined together to create antibody diversity. The recombinations are orchestrated by the recombination activating gene (RAG) enzymes, other enzymes that cleave/mutate/assemble DNA of the Ig loci, and the transcription factor Pax5. A key feature of the immune system is the concept that one lymphocyte has only one antigen specificity that can be selected for or against. This requires that only one of the alleles of genes for Ig chains is made functional. The mechanism of this allelic exclusion has however been an enigma. Here pre-BCR signaling was shown to down-regulate several components of the recombination machinery including RAG1 and RAG2 through CaM inhibition of E2A. Furthermore, E2A, Pax5 and the RAGs were shown to be in a complex bound to key sequences on the IgH gene before pre-BCR stimulation and instead bound to CaM after this stimulation. Thus, the recombination complex is directly released through CaM inhibition of E2A. Upon encountering antigens, B cells must adapt to produce a highly specific and potent antibody response. Somatic hypermutation (SH), which introduces point mutations in the variable regions of Ig genes, can increase the affinity for antigen, and antibody effector functions can be altered by class switch recombination (CSR), which changes the expressed constant region exons. Activation-induced cytidine deaminase (AID) is the mutagenic antibody diversification enzyme that is essential for both SH and CSR. The AID enzyme has to be tightly controlled as it is a powerful mutagen. BCR signaling, which signals that good antibody affinity has been reached, was shown to inhibit AID gene expression through CaM inhibition of E2A. SH increases the antigen binding strength by many orders of magnitude. Each round of SH leads to one or a few mutations, followed by selection for increased affinity. Thus, BCR signaling has to enable selection for successive improvements in antibodies (Ab) over an extremely broad range of affinities. Here the BCR is shown to be subject to general negative feedback regulation of the receptor proteins as well as many co-receptors and proteins in signal pathways from the receptor. Thus, the BCR can down-regulate itself to enable sensitive detection of successive improvements in antigen affinity. Furthermore, the feedback inhibition of the BCR signalosome and most of its protein, and most other gene regulations by BCR stimulation, is through inhibition of E2A by Ca2+/CaM. Differentiation to Ab-secreting plasmablasts and plasma cells is antigen-driven. The interaction of antigen with the membrane-bound Ab of the BCR is critical in determining which clones enter the plasma cell response. Genome-wide analysis showed that differentiation of B cells to Ab-secreting cell is induced by BCR stimulation through very fast regulatory events, and induction of IRF-4 and down-regulation of Pax5, Bcl-6, MITF, Ets-1, Fli-1 and Spi-B gene expressions were identified as immediate early events. Ca2+ signaling through CaM inhibition of E2A was essential for these rapid down-regulations of immediate early genes after BCR stimulation in initiation of plasma cell differentiation.

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Yuan, Fang. "Cell Surface Recognitions by Viral and Immune Receptors." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491598.

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Cell surface recognition is an important interaction occurring between proteins on opposite cell surfaces and transmits signals that allow cells to adapt to their environment. Viruses utilise recognition for entering host cells, and the immune system may defend against numerous attacks from environment through these interactions, by generating a protective adaptive immune response. This thesis offers insight into cell surface recognition through both viral and immune system molecules. For virus research, West Nile virus receptor binding domain was refolded and crystallized. Structural information ofthis domain was obtained and analysed. A putative receptor binding loop was identified from the structure. For immune research, T cell receptors that recognized Melan-A peptide, ELAGIGILTV, and gplOO peptide, YLEPGPVTV, were identified from several CD8+ T cell clones. Kinetic studies of these TCRs were carried out against rel<\ted human peptide-major histocompatibility complex by using surface plasmon resonance techniques. One ofthese TCRs which recognize Melan-A peptide was successfully crystallized with its ligand peptide-major histocompatibility complex. .J i Structural information obtained from X-ray diffraction studies ofviral and immune molecules indicated that protein-protein interactions are often effected by disordered/flexible regions in protein structures. For viruses, this flexible region is the binding loop and for T cell r.eceptors it is the complementarity determining regions. Such conformational flexibility allows specific protein interactions distinguishing small differences in amino acid composition. Alteration ofthe flexible regions of virus could be a potential mechanism to prevent cell entry and similarly, alteration of complementarity determining regions ofT cell receptors could lead to higher affmity for its ligand, major histocompatibility complex.

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Chang, C. "Human decidual NK cell receptors and their functions." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597450.

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In this thesis I have studied the possible receptors on decidual leukocytes which will bind to the HLA class I ligands on trophoblast. Of particular importance is the identity and function of the receptor for HLA-G as this molecule is only found on invading trophoblast cells. I have studied the expression, binding characteristics and functions of two possible HLA-G receptors, KIR2DL4 and ILT2. cDNA for these receptors was transfected into NK cell line, several functional assays were performed including cytotoxicity and cytokine production. The results showed the recognition of HLA-G by ILT2 and the functional consequences in these in vitro studies. There was no report on KIR2DL4 antigen expression in decidual NK cells. A rabbit polyclonal antibody against KIR2DL4 was made and purified. KIR2DL4 protein was detected from NK cell lysate in a Western blotting assay with this rabbit antibody. To further characterise the possible outcome of this maternal interaction in pregnancy, first I studied the cytokine profiles of decidual leukocytes, NK cells and trophoblast. In addition to previously published cytokines (GM-CSF and TNF-a), IL-6 and IFN-g have been found to be produced by decidual NK cells. These cytokines could have some major functions in the roles NK cells play in pregnancy. To dissect the change of cytokine profile after decidual leukocytes' recognition of placental cells, an in vitro culture system was developed using primary trophoblast cells and isolated decidual leukocytes. We found two cytokines (IFN-g and TNF-a) have been altered in this co-culture system. And this alteration could be due to the IL-10 and TGF-b1 produced by trophoblast. These results may shed some light on the mechanism and result of implantation.

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Melia, M. "Investigation of cell entry receptors used by morbillliviruses." Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432851.

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Summers, Andrea Eva. "Characterisation of nicotine receptors on immune cell lines." Thesis, University of Hertfordshire, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289604.

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Al-Lazikani, Bissan. "Canonical structures of immunoglobulins and T cell receptors." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624098.

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30

Border, Ellen Clare. "Structural and functional studies of cell surface receptors." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:907793da-3ba1-4a57-8bdb-c185aa84c28c.

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Receptor proteins on the surfaces of cells equip them to communicate with each other and to sense and interact with their environment. One receptor family, the αβ T-cell receptors (TCRs), allow T lymphocytes to detect and respond to pathogens via interactions with antigen-presenting major histocompatibility complex (MHC) molecules on target cells. A degree of TCR cross-reactivity (e.g. through structural similarity between peptide-MHC (pMHC) complexes) is essential to account for all possible pathogens, but can also lead to the misinterpretation of self antigens as foreign, and thereby elicit an autoimmune response, resulting in diseases such as multiple sclerosis (MS). Structural studies of pMHC and TCR-pMHC complexes have been key to developing of an understanding of the molecular basis of TCR cross reactivity, and the first strand of this thesis describes attempts to express and purify a highly cross-reactive MS patient-derived TCR for structural characterisation. The formation, purification and crystallisation of a TCR-self pMHC complex including another autoreactive TCR is also described. Another family of receptors, the fibronectin leucine-rich transmembrane proteins (FLRTs), has been implicated in roles in embryonic development including cell sorting and adhesion. In the second strand of this thesis, the nature of homotypic interactions between FLRTs, which may underlie adhesion between FLRT transfected cells, is investigated. Biophysical analyses demonstrate that these interactions may be mediated by the extracellular leucine-rich repeat (LRR) domain, and crystal structures of all three FLRT LRR domains suggest how interactions between them may underlie FLRT self-association at the cell surface. Residues which contribute to these interactions are conserved across different members of the FLRT family and different species. These findings confirm that FLRTs induce homotypic cell-cell adhesion, and suggest that this behaviour is mediated by self association at the cell surface via the LRR domain.

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Bonyanian, Zeinab. "Adenosine Receptors And Endothelial Cell Mediated Wound Healing." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/367912.

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Impaired wound healing is a common and serious complication of diabetes mellitus causing an increased risk of infection and tissue damage. Chronic wounds associated with diabetes may be caused by peripheral neuropathy, vascular complications and alterations in immune function and contributes to non-traumatic amputations. Consequently, therapeutic management of wounds in diabetes is centred on infection control and stimulating revascularization. This research will focus on the latter and investigate the effects of high glucose on endothelial function with a view of finding new strategies to improve wound healing in diabetes. This project identified the adenosine receptor subtypes in EA.hy926 endothelial cell lines that are involved in stimulating wound healing and determined whether their roles are affected in the hyperglycaemic environment associated with diabetes. As caffeine is a non-selective antagonist of the adenosine receptors, this study also investigated the effects of acute and 48 hour chronic caffeine treatments on adenosine receptor populations and on wound closure and cell proliferation. Caffeine has a crucial role in wound healing through various mechanisms such as antioxidant activity or increasing the level of cyclic adenosine monophosphate (cAMP).
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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32

Parra, Eduardo. "Molecular basis for costimulation of human T lymphocytes." Lund : Lund University, 1998. http://books.google.com/books?id=SgFrAAAAMAAJ.

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33

Kautsky, Mikael B. "The role of retinoic acid receptors in oral epithelial differentiation /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6395.

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34

Moody, Anne Marie. "T-cell receptor studies in myasthenia gravis." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337448.

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35

Tung, Kwok Kwan. "Functional roles of P2Y2 nucleotide receptor in the formation and maintenance of vertebrate neuromuscular junctions /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20TUNG.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2003.
Includes bibliographical references (leaves 127-140). Also available in electronic version. Access restricted to campus users.

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36

Yuan, Xiaohui. "Characterization of the ligand-binding specificity and transcriptional properties of estrogen receptor homodimeric/heterodimeric complexes." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3036871.

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Carson, Bryan David. "Impaired T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8337.

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38

Ravi, Janani. "CROSSTALK BETWEEN CANNABINOID RECEPTORS AND EPIDERMAL GROWTH FACTOR RECEPTOR IN NON-SMALL CELL LUNG CANCER." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1426697196.

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39

Teixeira, de Matos Cristina. "Modulation of natural killer cell and T-cell functions by CD94/NKG2A receptors /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-846-0/.

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40

Slessareva, Janna Eugenievna. "Molecular mechanisms of G protein-receptor coupling." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2907.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains vi, 200 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

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41

Ma, Hongzheng. "Molecular mechanisms of G protein-receptor coupling." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2978.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains viii, 264 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

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42

Buhler, Marc McWilliams. "Genetics of the immune cell receptors TCRB and CCR5 in human disease." University of Sydney, 2003. http://hdl.handle.net/2123/601.

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Abstract Early in the evolution of the vertebrates it is thought that two genomic duplications occurred, providing a basis for the evolution in body plan and neural crest of very early vertebrates and substantive material for further evolution of various gene families such as those making up a number of components of the adaptive vertebrate immune system. While the bony fish possibly had another, genome duplications are not generally a feature of vertebrate evolution and indeed the appearance of an antigen-adaptive immune recognition system may have served to limit the size that various vertebrate genomes, including that of the human, can in fact achieve. This initial step in vertebrate immune evolution, the establishment of recognition of non-self against the unique set of 'self' epitopes for an individual, provided an immensely powerful weapon in immune function with the ability to tailor a defense against as-yet-unseen dangers at any time albeit with the pitfall of autoimmune disease. As the recognition sites of the antigen receptor molecules such as TcR are produced by clonal modification of the segments provided in the germline and are thus not in the genome itself, pathogens have not been able to hijack this one component of the immune system in the way so many other components have been put to use throughout evolution, nor do these components necessarily reveal themselves as associated with disease through genome screens. Importantly, overall immune function is determined not just by the potential repertoire of recognition receptors but also by the ability of immunocompetent cells to migrate in a tissue specific fashion through the use of various chemokines and their receptors. Typical of the hijacking of an immune system component by a pathogen is the use of a chemokine ligand gene in the viral ancestor to SIV and HIV, allowing for virus binding to immunocompetent cells as is seen in the use of the CCR5 chemokine receptor by macrophage-tropic HIV strains. This thesis describes the allele and genotype frequencies for several TcR beta-chain variable segment polymorphisms in a population of MS patients compared with controls before and after stratification for HLA-DR15, polymorphism in the Apo-1 / Fas promoter, the DRB1 Val86/Val86 genotype, CCR5-delta32 and the HLA-DRA promoter. The thesis continues with CCR5-delta32 genotyping in IDDM, MS and SLE cohorts and then examines the question of the population of origin of the delta-32 allele of the CCR5 receptor for chemokine. Here, a case / control comparison of 122 RR-MS patients with 96 normal individuals was made for allele and genotype frequencies and for haplotypes formed by pairs of TCRB markers. Further analysis was made after HLA-DR15 stratification. Linkage disequilibrium was found between pairs of alleles of bv8s1, bv10s1, bv15s1 and bv3s1 loci in both patients and controls. In the RR-MS cohort, an increase in the allele frequency of bv8s1*2 was seen (p = 0.03) and the haplotype bv8s1*2 / bv3s1*1 was increased (p = 0.006), and both were found to be statistically significant. In the DR15-positive group, association between MS and TCRB was seen with the bv8s1*2 allele (p = 0.05) and the bv8s1*2 / bv10s1 haplotypes (p = 0.048), while the haplotype associations seen among the DR15-negative patients included the bv3s1*1 allele (bv10s1*1 / bv3s1*1, p = 0.022; bv8s1*2 / bv3s1*1, p = 0.048). While no associations were found after stratification for SDF1-3'A, Apo-1 / Fas or DRB1 there were modest interactions between bv3s1, bv10s1 and bv15s1 and the HLA-DRA promoter. These results support the involvement of the TCRB region in MS susceptibility. The further study of autoimmune disease here includes genotype analysis of CCR5-delta32 in type 1 diabetes (IDDM) and SLE. CCR5 is the major co-receptor for viral entry used by macrophage-tropic HIV strains and protection from infection is seen in homozygotes for CCR5-delta32. In diabetes, infiltration of pancreatic tissue by autoreactive T-cells involves secretion of multiple cytokines and chemokine receptor expression. Variation in the chemokine receptor CCR5 may result in differences in inflammatory cell migration in response to relevant chemokines. Adolescents with type 1 diabetes were genotyped for CCR5-delta32 (n = 626). The allele frequency was compared with that of 253 non-diabetic adolescents and with that of 92 adults with SLE. A reduced allele frequency was seen in type 1 diabetes compared with controls (0.092 vs 0.123, p = 0.05). This difference was not seen for the cohort of patients with SLE (freq = 0.114). A reduction in the number of CCR5-delta32/delta32 homozygotes, who lack CCR5, in the type 1 diabetes cohort was also seen and while not statistically significant (2 observed compared to 5.25 expected; p = 0.12) is interesting. These results suggest a partial protection from type 1 diabetes for CCR5-delta32 homozygous individuals is possible and that CCR5 has a potential role in the pathogenesis of type 1 diabetes. Global surveys of the CCR5-delta32 allele have confirmed a single mutation event in a Northeastern European population as the source of this allele. Here, Australian Ashkenazi Jews (n = 807) were found to have a CCR5-delta32 allele frequency of 14.6% while Australian Sephardic Jews (n = 35) had a frequency of 5.7% and non-Jewish Australian controls (n = 311) had an allele frequency of 11.25%. Data on birthplace of grandparents showed a gradient with highest CCR5-delta32 frequencies from Eastern European Ashkenazim (~19.5% for those whose four grandparents come only from Russia, Poland, Hungary, Austria and Czechoslovakia; n = 197) which differs significantly from the frequency seen in Ashkenazi Jews from Western Europe (n = 101, p = 0.001). Homozygotes for CCR5-delta32 were genotyped with 3p21 region microsatellites. This has defined an ancestral haplotype on which the mutation first occurred and helped to date this event to between 40 and 50 generations ago or just over a thousand years ago. The population gradient, combined with the dating of the mutation by microsatellite allele frequencies, suggests an origin for the CCR5-delta32 allele in a population ancestral to the Ashkenazim. The distribution in non-Jewish populations in northern Europe has led others to postulate spread of the mutation by Vikings. It is hypothesised here that the link between the two populations could be the kingdom of Khazaria with subsequent admixture into both Swedish Vikings and Ashkenazi Jews. The basic driving force of evolution is through selection and the immune system has a role which, through the survival pressure exerted by viruses and other pathogens, has the potential to exert a great deal of selective force on the various components of this system. The effects of this pronounced selection on an immune system component can be seen for example in the increase of the CCR5-delta32 allele over the last thousand years to the current frequency. As mentioned, some immune system components are not affected by such straightforward selection. In the case of the TCRBV segments, effects on the immune repertoire can occur through MHC interaction at the point of thymic entry and in the effects of various superantigens, but the actual binding pockets that recognise antigen are themselves unable to be selected for (or against). The findings presented in this thesis provide support for the association of TCRBV gene segments with multiple sclerosis and also provide support for the further study of the role of the CCR5-delta32 allele in type 1 diabetes. Furthermore, data presented here suggests that the CCR5-delta32 allele had an origin in the Khazar Kingdom just over a thousand years ago, accounting for the allele frequencies in both the Ashkenazi Jews and in lands frequented by the Vikings. The definition of an extended ancestral haplotype for the CCR5-delta32 allele shows how the effect of selection of an allele of one gene can carry with it specific alleles of a large number of other genes as well.

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43

Zhang, Min, and 張敏. "The role of B cell activating factor in B cell development and autoimmunity." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37659807.

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44

Conway, Ann Marie. "Growth factor receptor tyrosine kinase-, G-protein coupled receptor- and sphingolipid-dependent regulation of the extracellular signal-regulated kinase cascade in cultured airway smooth muscle cells." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366970.

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45

Asamaphan, Patawee. "Exploring the structure and function of MelLec, a C-type lectin-like receptor that recognises DHN melanin." Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=239859.

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46

Dorning, Ashley J. "The pharmacology, signalling and expression of the lipid-sensing receptor GPR92." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=201860.

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G protein-coupled receptors (GPCRs) are 7 transmembrane domain proteins capable of initiating cellular responses following ligand binding. GPR92 is expressed in the central nervous system (CNS) and is demonstrated to be involved in pain signalling via neurons of the spinal cord and dorsal root ganglion (DRG). Activated by the endogenous lipid lysophosphatidic acid (LPA), GPR92 is now considered the 5th LPA receptor. There remains controversy regarding GPR92 pharmacology however, as studies show another endogenous lipid, farnesyl pyrophosphate (FPP), also activates GPR92 with similar potency and efficacy to LPA. LPA-induced activation of GPR92 results in increased intracellular calcium (Ca2+) and cAMP. Furthermore, GPR92 mediates neurite retraction via Rho kinase and activates the cAMP responsive element-binding (CREB) protein. This transcription factor is important in synaptic plasticity and regulates the expression of many neuronal genes including brain derived neurotrophic factor (BDNF), yet the role of GPR92 in the brain has not been explored. Here, I describe the pharmacology and signalling of GPR92, with preliminary data describing its expression. I utilise a cell line lacking endogenous LPA responsiveness (B103 rat neuroblastoma) in which I stably express GPR92. Using intracellular Ca2+ changes and CREB phosphorylation as read-outs, I find FPP to be the most potent and efficacious ligand. The similarly structured lipid geranylgeranyl pyrophosphate (GGPP) produced comparable results to FPP. GPR92-mediated CREB phosphorylation has been described in a mouse model of pain. The ligands which induce this response however, have not been assessed. I describe for the first time, ligand-induced CREB phosphorylation via GPR92, and found that FPP causes the most robust CREB response. LPA and GGPP also induced GPR92-mediated CREB phsphorylation. Furthermore, I find that GPR92 mediates a novel Gq-dependent, Ca2+ independent, signalling pathway resulting in CREB phosphorylation. In addition, I examine GPR92 expression in the CNS using reverse-transcriptase polymerase chain reaction (RT-PCR) and in situ hybridisation. GPR92 is expressed throughout the brain, with particularly high expression in 7 the brain stem, DRG, and hippocampus. In situ hybridisation revealed a distinct expression pattern confirming high levels of GPR92 mRNA in the hippocampal region. GPR92 mRNA is also observed in the cortex, habenula, thalamus and hypothalamus. I also report the expression of the FPP synthesising enzyme FPP synthase (FPPS). Relative expression levels of FPPS between CNS regions are similar to GPR92. Preliminary data suggests FPP is capable of mobilising Ca2+ in hippocampal neuronal and non-neuronal cells. These data suggest an important role for GPR92 in the brain where it, and the enzyme involved in generating one of its endogenous ligands, are highly expressed.

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Clark, Alexandra Elsie. "Characterisation of the C-type lectin-like receptor 1 (CLEC-1)." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=210080.

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48

Cheng, Wai, and 鄭蔚. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010614.

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Hussein, Mohamed Osman. "Hormonal modulation of Leydig cell membrane luteinizing hormone receptors /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487267024995937.

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50

Ammoun, Sylwia. "Orexin Receptors in Recombinant CHO Cells : Signaling to Short- and Long-Term Cell Responses." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5890.

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