Relevant bibliographies by topics / Protein variants

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Academic literature on the topic 'Protein variants'

Author: Grafiati
Published: 14 March 2023

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Dissertations / Theses on the topic "Protein variants"

1

Sadler, David Paul. "Mechanically unfolding variants of protein L." Thesis, University of Leeds, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444035.

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Jones, Kerrie Margaret. "Mutational variants of E. coli glutamate dehydrogenase." Thesis, University of Leeds, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278229.

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Lee, Seung-Joo. "Structural and functional consequences of disease-related protein variants." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1269545015.

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Veltman, Oene Robert. "Engineering high performance variants of Bacillusthermolysin-like proteases." [S.l. : [Groningen] : s.n.] ; [University Library Groningen] [Host], 1997. http://irs.ub.rug.nl/ppn/164267484.

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Bruce, Lesley J. "A study of human erythrocyte band 3 variants." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240590.

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Waterhouse, Mark Peter. "Specific targeting of FcγRIIIa using artificial scaffold protein variants". Thesis, University of Leeds, 2018. http://etheses.whiterose.ac.uk/20522/.

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Fcγ Receptors (FcγRs) are cell-surface receptors for IgG that are expressed on immune cells including macrophages, monocytes and natural killer (NK) cells. Upon binding to IgG-containing immune complexes, FcγRs trigger cell-mediated effector functions that lead to the clearance of pathogenic material and immune homeostasis. However, aberrant activation of these pathways can result in autoimmune susceptibility and, as such, FcγRs are implicated in the pathogenesis of several autoimmune disorders. For example, FcγRIIIa, expressed on macrophages and NK cells, has been functionally and genetically linked to susceptibility for rheumatoid arthritis and is a valid target for several FcγR-mediated autoimmune disorders. Despite this, FcγRIIIa is currently under-exploited due to a lack of FcγRIIIa-specific agents, which results from the expression of the near identical FcγRIIIb on neutrophils. However, several FcγRIIIa-specific Adhirons (an engineered protein scaffold) have recently been described, which inhibit IgG binding and effector functions (phagocytosis and cytokine release) of THP-1 cells. This thesis aimed to fully characterise and enhance the properties of one of these recently described Adhirons (known as AdG3) through site-directed mutagenesis (SDM); Molecular Dynamics (MD) simulations; and fusion to the IgG1- or IgG2-Fc. SDM identified several key binding residues in the AdG3 variable regions through screening of AdG3 mutants by surface plasmon resonance (SPR). SPR also identified three mutants with enhanced affinity for FcγRIIIa and showed that AdG3 possesses background binding to the highly homologous FcγRIIIbNA1, but not FcγRIIIbNA2, which was supported by MD simulations that revealed the exquisite mode of AdG3 specificity for these receptors, which was mediated through the Arg18Ser polymorphism in the AdG3 binding site. Fusion to the IgG-Fc was not detrimental to the FcγRIIIa-AdG3 interaction, and fusion to the IgG2-Fc was observed to potentially enhance the affinity and specificity of AdG3 for FcγRIIIa. These findings could subsequently be utilised for further improvement of AdG3 affinity and specificity, as well as other clinically relevant parameters such as serum half-life.
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Rivas, Cruz Manuel A. "Medical relevance and functional consequences of protein truncating variants." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:a042ca18-7b35-4a62-aef0-e3ba2e8795f7.

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Genome-wide association studies have greatly improved our understanding of the contribution of common variants to the genetic architecture of complex traits. However, two major limitations have been highlighted. First, common variant associations typically do not identify the causal variant and/or the gene that it is exerting its effect on to influence a trait. Second, common variant associations usually consist of variants with small effects. As a consequence, it is more challenging to harness their translational impact. Association studies of rare variants and complex traits may be able to help address these limitations. Empirical population genetic data shows that deleterious variants are rare. More specifically, there is a very strong depletion of common protein truncating variants (PTVs, commonly referred to as loss-of-function variants) in the genome, a group of variants that have been shown to have large effect on gene function, are enriched for severe disease-causing mutations, but in other instances may actually be protective against disease. This thesis is divided into three parts dedicated to the study of protein truncating variants, their medical relevance, and their functional consequences. First, I present statistical, bioinformatic, and computational methods developed for the study of protein truncating variants and their association to complex traits, and their functional consequences. Second, I present application of the methods to a number of case-control and quantitative trait studies discovering new variants and genes associated to breast and ovarian cancer, type 1 diabetes, lipids, and metabolic traits measured with NMR spectroscopy. Third, I present work on improving annotation of protein truncating variants by studying their functional consequences. Taken together, these results highlight the utility of interrogating protein truncating variants in medical and functional genomic studies.
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8

Baldan, Nikita <1996&gt. "Computational analysis of NaV1.7 protein variants and tool for 3D visualization of protein structures." Master's Degree Thesis, Università Ca' Foscari Venezia, 2020. http://hdl.handle.net/10579/17572.

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This thesis is composed of two parts. The first part explores the possibility to use Graph Kernels to discriminate pathogenic versus non-pathogenic variants of a specific protein. All variants are represented as Residue Interaction Networks (RIN), where nodes are amino acids and edges represent non-covalent bonds between atoms of the two involved amino acids. This part is guided by a previous Master degree thesis that considered protein NaV1.7, which is responsible for the transmission of the pain signal from the peripheral nervous system to the brain. The thesis considered 85 genetic variants of the human NaV1.7, among which 30 are known to cause neuropathic diseases and 55 are instead neutral. The results of the first part highlight that some Graph Kernels are actually able to discriminate between pathogenic and neutral variants. This prompted the idea of realizing a 3D viewer able to show the three-dimensional structure of a protein and also its non-covalent bonds. The second part of the thesis describes Spheremole, an application for the visualization of the three-dimensional structure of a protein. In particular, Spheremole allows the visualization of two proteins structures and their visual comparison, also based on their non-covalent bonds.
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9

Norman, Jane Eleanor. "Molecular mechanisms of platelet G protein-coupled receptor gene variants." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.687283.

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G protein-coupled receptors (GPCRs) are critical mediators of platelet responses to regulatory agonists and are essential drug targets. This project aimed to identify informative platelet GPCR gene variants and to characterise the mechanism of loss of receptor function for selected variants. Variants were sought in 2400 cardiac surgery patients in which preoperative platelet function test results were used to select subgroups with GPCR dysfunction potentially explained by loss of function P2Y12 receptor, thromboxane A2 receptor and protease-activated receptor 1 gene variants. This approach did not identify variants likely to affect GPCR function. Re-sequencing the protease-activated receptor 4 (PAR4) gene yielded seven different missense variants. After evaluation using computational prediction and homology modelling, the predicted tyrosine 157 to cysteine (Y157C) substitution was demonstrated to reduce PAR4 reactivity and was studied further. Compared to controls, Y157C platelets showed reduced functional responses to PAR4 activating peptide and a greater reduction in responses to a-thrombin in the presence of a PAR1 antagonist, vorapaxar, together consistent with a PAR4 defect. Y157C platelets, showed similar total PAR4 expression levels to controls but reduced surface expression, accounting at least in part for the reduced of PAR4 reactivity. HEK293 cells transfected with a PAR4 Y157C expression construct also showed reduced PAR4 surface expression and functional responses. PAR4 Y157C co-localised with an ER marker in the cell cytoplasm and had an expression pattern consistent with reduced N-glycosylation. Mutagenesis of the putative hydrogen bond partner for the substituted Y157 residue caused a similar phenotype. These findings suggest the Y157C substitution results in receptor mis-trafficking due to a disruption of an intra-molecular hydrogen bond. This first reported characterisation of a variant affecting PAR4 demonstrates that rare variants in the PAR4 gene are a potential source of inter-individual variation in the platelet haemostatic response and the effect of anti-platelet drugs that target the PAR system.
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Yang, Su jeong. "Biochemical and biophysical characterisation of allelic variants of ovine prion protein." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611255.

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