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Dissertations / Theses on the topic 'Protein variants'

Author: Grafiati

Published: 14 March 2023

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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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2

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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3

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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4

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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5

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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6

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

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7

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 h

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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

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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

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10

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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11

Turk, Casey M. "Paralemmin splice variants and mRNA and protein expression in breast cancers." Connect to this title, 2008. http://scholarworks.umass.edu/theses/194/.

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12

Chivers, Claire Elizabeth. "Investigating high-affinity non-covalent protein-ligand interaction via variants of streptavidin." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:631c65ed-08d9-484e-a8df-309a4c95df45.

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The Streptomyces avidinii protein streptavidin binds the small molecule biotin (vitamin H / B₇) with extraordinary stability, resulting in the streptavidin-biotin interaction being one of the strongest non-covalent interactions known in nature (K<sub>d</sub> ~ 10<sup>-14</sup> M). The stable and rapid biotin-binding, together with high resistance to heat, pH and proteolysis, has given streptavidin huge utility, both in vivo and in vitro. Accordingly, streptavidin has become a widely used tool in many different biotechnological applications. Streptavidin has also been the subject of extensive r

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13

Efthymiou, Maria A. "Activated protein C and severe sepsis : Generation and characterisation of novel variants." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534976.

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14

Tong, Shuping. "Molecular characterization of hepatitis B virus variants unable to express HBe protein." Lyon 1, 1992. http://www.theses.fr/1992LYO1T109.

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15

Fletcher, Jessica Frances. "Novel variants of the DNA damage checkpoint protein Cds1 in Schizosaccharomyces pombe." Thesis, Bangor University, 2017. https://research.bangor.ac.uk/portal/en/theses/novel-variants-of-the-dna-damage-checkpoint-protein-cds1-in-schizosaccharomyces-pombe(9df1851b-ca3f-449f-880f-c8eb627cb786).html.

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In the model organism Schizosaccharomyces pombe, the Cds1 (checking DNA synthesis 1) kinase is activated at the S-phase checkpoint upon stalling of the replication fork during DNA synthesis. Under normal conditions (300C), the role of the full-length protein kinase is to activate downstream processes resulting in mitotic arrest,protection of the stalled replication fork, and prevention of continued DNA replication in an unfavourable environment. In this way, Cds1 acts to ensure the reversible arrest of DNA synthesis. However, under stress conditions such as raised temperature or specific DNA d

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16

Adhikari, Sandeep. "FUNCTIONAL CHARACTERIZATION OF IDENTIFIED DEAF1 VARIANTS AND SIGNIFICANCE OF HDAC1 INTERACTIONS ON DEAF1-MEDIATED TRANSCRIPTIONAL REPRESSION." OpenSIUC, 2021. https://opensiuc.lib.siu.edu/theses/2838.

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Deformed epidermal autoregulatory factor 1 (DEAF1) encodes a transcription factor essential in early embryonic and neuronal development. In humans, mutations in the DNA binding domain of DEAF1 cause intellectual disability together with clinical characteristics collectively termed DEAF1-associated neurodevelopmental disorders (DAND). The objective of this study is to 1) assess the pathogenicity of newly identified variants using established functional assays, and 2) confirm and map the interaction domain of DEAF1 with HDAC1 and evaluate the importance of DEAF1-HDAC1 interaction on DEAF1-mediat

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17

Kuthiala, Amrita. "In-vitro Studies on Aptamer - Induced FRET Between λN22 Tagged Fluorescent Protein Variants". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-124642.

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18

Panicco, Paola. "Protein engineering of human cytochromes P450 and their allelic variants for nanobiotechnological applications." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/11739.

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Human cytochromes P450 (CYP) constitute one of the most important and studied classes of phase I drug metabolizing enzymes. A small group of 6-7 isoforms of the 57 identified until now accounts for 90-95% of the metabolism of clinically used drugs and can contain mutations (single nucleotide polymorphisms) that, when located in the coding regions, can lead to absent, deficient or enhanced enzyme activity. Thanks to the development of pharmacogenetics and later on pharmacogenomics, the presence of these single nucleotide polymorphisms (SNP) has been associated to inter-individual and inter-ethn

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19

Wilson, Michael Christopher. "Comparing the thermal, chemical and mechanical stabilities of extremophilic cold shock protein variants." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/15982/.

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Proteins conduct a vast array of chemical processes and achieve this through a balance of flexibility and function. Proteins from extremophilic organisms have evolved to adjust this balance to function in extreme conditions. Research into hot-adapted proteins has been encouraged through successes in improving enzyme thermostability, though cold-adapted proteins also offer substantial potential as they can function effectively at lower temperatures. Research into cold-adapted proteins remains limited despite cold climates comprising over 80% of Earth’s biosphere. This study compares the stabili

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20

Burns, Joyce Nicole. "Development of a quantitative assay to distinguish glaucoma-causing and benign olfactomedin variants." Thesis, Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/42931.

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Myocilin, expressed in the trabecular meshwork of the eye, has been linked to inherited primary open-angle glaucoma (POAG). The biological function of myocilin is unknown, but mutant myocilin exhibits a gain-of-function mechanism, aggregating within the endoplasmic reticulum of human trabecular meshwork cells, causing cell stress and eventually apoptosis. After apoptosis occurs, the trabecular meshwork is compromised, leading to an increase in intraocular pressure, a symptom of glaucoma. In this thesis, I have expressed and purified the wild-type olfactomedin (OLF) domain and 24 reported disea

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21

Lamlum, Hanan. "Variation in human tissue inhibitor of metalloproteinase 1 gene and its effect on the control of connective tissue remodelling in cardiovascular disease." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365809.

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22

García, Alonso Luz María. "Functional profiling of human genomic data using the protein interactome." Doctoral thesis, Universitat Politècnica de València, 2015. http://hdl.handle.net/10251/55848.

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[EN] Our understanding of the biological mechanisms for most common human diseases is far from complete. Even with well established genetic landscapes, our capacity to make accurate phenotypical predictions or determine personalised disease risk using genetics alone is not possible for most diseases due to our lack of understanding of the mechanisms by which genetic alterations cause disease. Several suggestions have been proposed to explain this manifested lack of direct relation between genotype and phenotype, including interactions with other molecules, pleiotropy and environmental perturba

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23

Kalita, Ann Marie. "Comparison of the activities of two allelic variants of the human wildtype p53 protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29729.pdf.

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24

Rees, Matthew Geoffrey. "Genetic, functional, and phenotypic analysis of human variants in the glucokinase regulatory protein gene." Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589604.

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Genome-wide association (GWA) studies have provided significant insight into the underlying genetic components of common human diseases such as type 2 diabetes (T2D). However, the translation of such genetic findings into biological and clinical insight remains a major challenge. One of the genes implicated in T2D pathogenesis and effects on related glycaemic and lipidaemic traits by the GWA approach is GCKR, encoding glucokinase regulatory protein (GKRP). GKRP inhibits the glycolytic enzyme glucokinase (GCK) in the liver, sequestering it in an inactive form in the nucleus. Together, GCK and G

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25

Atkins, Elizabeth Rose. "Functional characterisation of natural variants of the hepatitis C virus p7 ion channel protein." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/6911/.

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The HCV p7 protein is a viroporin that acts to increase endosomal pH to preserve the infectivity of nascent virions. Previous work has identified several key residues in p7 that are critical for its function. A number of compounds have been found to inhibit p7 activity in vitro and genotype variation in the p7 sequence is known to have significant effects on p7 inhibitor sensitivity. This study aimed to further our understanding of the role of p7 during HCV infection. The effects of six naturally-occurring p7 variants, within a single genotype, isolated from 5 patients of varying disease sever

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26

Rossetti, Giulia. "Molecular simulation studies of the prion protein: from disease-linked variants to ligand binding." Doctoral thesis, SISSA, 2010. http://hdl.handle.net/20.500.11767/4158.

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Prion diseases or transmissible spongiform encephalopathies (TSEs) are fatal neu-rodegenerative disorders (198). The crucial event in the development of these diseases is the conformational change of a membrane bound protein, the cellular PrPC in Figure 3.1, into a disease associated, bril-forming isoform (199). Despite their rare incidence, TSEs have captured very large attention from the scienti c community due to the unorthodox mechanism by which prion diseases are transmitted...

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27

Bronicki, Lucas M. "Characterization of Multiple Exon 1 Variants and Neuron-specific Transcriptional Control of Mammalian HuD." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23682.

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The RNA-binding protein (RBP) and Hu/ELAV family member HuD regulates mRNA metabolism of genes that encode proteins involved in neuronal differentiation, learning and memory, and certain neurological diseases. Given the important functions of HuD in a variety of processes, we set out to characterize the 5’ genomic region of the mammalian HuD gene and determine the mechanisms that regulate its mRNA expression in neurons using P19 cells and mouse brain as models. Bioinformatic and 5’RACE (rapid amplification of cDNA ends) analyses of the HuD 5’ genomic flanking region identified eight conserved

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28

MARRANCI, ANDREA. "Analysis of the expression of all BRAF transcript variants and of their implication in post-transcriptional regulation mediated by miRNAs in melanoma." Doctoral thesis, Università di Siena, 2017. http://hdl.handle.net/11365/1005876.

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BRAF is a widely studied oncogene and its functions are well characterized in several cellular contests and diseases. However the regulation of the expression of BRAF is mostly unknown. With the aim to understand the post-transcriptional regulation of BRAF, we performed 3’RACE in A375 melanoma cells and we found 2 different 3’UTRs: the one commonly reported in many data bases (Reference) and a new one that is only predicted (X1). The two 3’UTRs are completely different in sequence and length (120nt vs 1350nt). Furthermore, they are transcribed from exon 18 or thanks to an alternative splicin

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29

Boopathy, Sivakumar. "Investigating Structural and Functional Defects in ALS-causing Profilin 1 Variants." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/923.

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Mutations in profilin 1 (PFN1) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease that targets motor neurons. PFN1 is a 15 kDa protein that is best known for its role in actin dynamics. However, little is known about the pathological mechanisms of PFN1 in ALS. In this dissertation, it is demonstrated that certain familial ALS-linked mutations severely destabilize the native conformation of PFN1 in vitro and cause accelerated turnover of the PFN1 protein in neuronal cells. This mutation-induced destabilization can account for the high propensity of ALS-linked variants

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30

Boopathy, Sivakumar. "Investigating Structural and Functional Defects in ALS-causing Profilin 1 Variants." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/923.

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Mutations in profilin 1 (PFN1) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease that targets motor neurons. PFN1 is a 15 kDa protein that is best known for its role in actin dynamics. However, little is known about the pathological mechanisms of PFN1 in ALS. In this dissertation, it is demonstrated that certain familial ALS-linked mutations severely destabilize the native conformation of PFN1 in vitro and cause accelerated turnover of the PFN1 protein in neuronal cells. This mutation-induced destabilization can account for the high propensity of ALS-linked variants

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31

Lackman, J. (Jarkko). "Glycosylation and dimerization of the human δ-opioid receptor polymorphic variants". Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526221342.

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Abstract Cellular signaling by G protein-coupled receptors (GPCRs) governs a wide array of physiological functions throughout the body. The human δ-opioid receptor (hδOR) is a GPCR that modulates the sensation of pain and mood and has great potential for the treatment of pain and a variety of neurological disorders. A common single-nucleotide polymorphism (SNP) in the extracellular N-terminal tail of hδOR changes Phe to Cys at position 27. Using various biochemical and cell biological methods, the study demonstrates that several events during receptor biosynthesis and cell surface delivery are

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32

Gasparini, Alessandra. "From High-Throughput Analysis of Genetic Variants to the Experimental Validation of Putative Protein Function." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3426808.

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The state-of-the-art approach for the genetic molecular cause research relies on massively parallel gene sequencing, which represents a challenge both in data handling and variant prioritization. The univocal assignment of disease pathogenicity to the sequence variants is often difficult, and requires the integration of different lines of evidence for a comprehensive interpretation. During my thesis, I contributed to the development of novel approaches to evaluate rare variant contribution to the clinical phenotype. These methods were presented and evaluated at the Critical Assessment of Genom

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33

Wright, Amy Joy. "Purification and characterization of beta-protein variants of 20S proteasomes of the haloarchaeon Haloferax volcanii." [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0014370.

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34

Neueder, Andreas [Verfasser], Herbert [Akademischer Betreuer] Tschochner, and Reinhard [Akademischer Betreuer] Sterner. "Characterization of r-protein variants in Saccharomyces cerevisiae / Andreas Neueder. Betreuer: Herbert Tschochner ; Reinhard Sterner." Regensburg : Universitätsbibliothek Regensburg, 2010. http://d-nb.info/1048724115/34.

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35

Al-Mahmoud, Widad Abdulsamad Mansour. "Novel variants of the DNA damage checkpoint protein Hus1 in fission yeast and human cells." Thesis, Bangor University, 2014. https://research.bangor.ac.uk/portal/en/theses/novel-variants-of-the-dna-damage-checkpoint-protein-hus1-in-fission-yeast-and-human-cells(dee8a56b-687f-4f24-9c6d-f81d73edc877).html.

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36

Hollar, Carol M. "Estimation of Selected Milk Protein Genetic Variants by Multi-Component Analysis of Amino Acid Profiles." DigitalCommons@USU, 1992. https://digitalcommons.usu.edu/etd/5390.

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Cation-exchange fast protein liquid chromatography separated whole casein into β-casein A2, A1, and B, K-casein, αs1-casein, and αs2-casein fractions as well as γ-caseins and several unidentified peaks using a urea-acetate buffer at pH 5 and a NaCl gradient. The whole casein fractions eluted in the following order: breakdown products of β-casein and unidentified peaks; β-casein A2, Al, and B; additional breakdown products of β-casein and unidentified peaks; K-casein; αs1-casein; and αs2-casein. The calculated composition of the four major caseins correlated well with values obtained using anio

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37

Cong, Xiaojing. "Molecular Simulation Studies on the Prion Protein Variants: Insights into the Intriguing Effects of Mutations." Doctoral thesis, SISSA, 2013. http://hdl.handle.net/20.500.11767/4810.

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Prion diseases, or transmissible spongiform encephalopathies (TSE), are a group of rare fatal neurodegenerative maladies that affect humans and animals. The fundamental breakthrough in TSE research was the discovery of the "prion"⎯proteinaceous infectious particle⎯ and the verification of the “protein-only” hypothesis, which states that prions could self-propagate by converting the cellular prion protein (PrPC) into the scrapie form, PrPSc (or prions), and lead to neurodegeneration without using any nucleic acids. The concept of prions may unify neurodegenerative diseases under a common pathog

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38

Li, Jiaxie. "Effects of genetic variants of k-casein and ß-lactoglobulin on heat denaturation of milk proteins and formation of protein complex." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29741.pdf.

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39

Li, Jiaxie. "Effects of genetic variants of k-Casein and b-lactoglobulin on heat denaturation of milk proteins and formation of protein complex." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27367.

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This study was based on the 462 milk samples collected from approximately 2000 cows registered in Dairy Herd Analysis Service (DHAS). Milk samples from fresh milks were phenotyped by gel electrophoresis. Milk samples were selected according to the nine possibilities of phenotype combination of $ kappa$-casein AA, AB, BB and $ beta$-lactoglobulin AA, AB and BB. Selected milk samples from fresh milks were heated at 25$ sp circ$C, 60$ sp circ$C, 70$ sp circ$C, 80$ sp circ$C and 90$ sp circ$C, respectively. Whole casein and whey protein were separated by adjusting the pH to 4.6. Quantitative deter

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40

Gronow, Joana Verfasser], Frank [Akademischer Betreuer] [Sönnichsen та Ulrich [Gutachter] Lüning. "Structural Stabilization of α-Helical Antifreeze Protein Variants Using the Trp-cage Protein / Joana Gronow ; Gutachter: Ulrich Lüning ; Betreuer: Frank D. Sönnichsen". Kiel : Universitätsbibliothek Kiel, 2020. http://nbn-resolving.de/urn:nbn:de:gbv:8-mods-2020-00047-1.

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Gronow, Joana [Verfasser], Frank D. [Akademischer Betreuer] Sönnichsen та Ulrich [Gutachter] Lüning. "Structural Stabilization of α-Helical Antifreeze Protein Variants Using the Trp-cage Protein / Joana Gronow ; Gutachter: Ulrich Lüning ; Betreuer: Frank D. Sönnichsen". Kiel : Universitätsbibliothek Kiel, 2020. http://d-nb.info/1206179678/34.

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42

Azoulay, Eric. "Induction of apoptosis or cell cycle arrest by two human wildtype variants of the p53 protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0031/MQ64313.pdf.

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43

Baugh, Evan H. "Predicting the Effects of Protein Variants using Structural Modeling, Large-Scale Data Integration, and Machine Learning." Thesis, New York University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10247644.

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<p> High-throughput sequencing technologies and new computational techniques for analyzing population genetics data are rapidly improving our understanding of disease susceptibility in humans and adaptation in a wide variety of organisms. These studies often discover nonsynonymous variation with large effects as even a single amino acid change can disrupt the folding, catalytic activity, and physical interactions of proteins. Current estimates predict that every human genome contains 10,000-11,000 nonsynonymous variations and, while we cannot currently characterize all this diversity experimen

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44

Klapper, Maja [Verfasser]. "Promoter variants and transcriptional regulation of the intestinal fatty acid binding protein gene (FABP2) / Maja Klapper." Kiel : Universitätsbibliothek Kiel, 2008. http://d-nb.info/1019630728/34.

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45

Gress, Alexander [Verfasser]. "Integration of protein three-dimensional structure into the workflow of interpretation of genetic variants / Alexander Gress." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1218075473/34.

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46

Apaja, P. (Pirjo). "Luteinizing hormone receptor:expression and post-translational regulation of the rat receptor and its ectodomain splice variant." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514279298.

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Abstract The luteinizing hormone receptor (LHR) is a G protein-coupled receptor (GPCR) that has a large N-terminal ligand binding ectodomain. The LHR ectodomain splice variant, expressed concomitantly with the full-length LHR in tissues, has an unknown biological function. GPCRs are a major pharmacological target, however, very little is known about the intracellular regulation of these receptors. In the present work, expression and maturation of the rat LHR and its variant were elucidated using both tissues and heterologous expression systems. A special effort was made to identify the role of

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47

Chu, Ge. "PCSK9 and Its Variants: An Unbiased Global Proteomic Study to Identify Interactors and Effects on Protein Trafficking." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32988.

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Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secreted glycoprotein that promotes degradation of low-density lipoprotein receptors. Gain- and loss-of-function variants of PCSK9 cause hypercholesterolemia and hypocholesterolemia, respectively. Although it has been a decade since the discovery of PCSK9, its effect in terms of global protein changes and interactions still require further understanding. This study provided a global outlook at the protein changes caused by PCSK9 and its variants in human hepatic HUH7 cell line. First, a proteomics-based method for protein subcellular d

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48

Deming, Brenda Boon. "Evaluating the role of lymphocyte radiosensitivity and variants in double-strand break repair genes, checkpoint kinase 2 (CHEK2) and nibrin (NBN), in the predisposition to prostate cancer : a dissertation /." San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1425298611&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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49

Warren, Curtis R. "Linker region of the BRCA2 protein increases chemoresistance to cisplatin: Screen for the characterization of cancer-associated variants." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 84 p, 2009. http://proquest.umi.com/pqdweb?did=1885607671&sid=3&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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50

Coghill, Lorraine Sheila. "Regulation of large conductance calcium- and voltage-activated potassium (BK) channel splice variants by protein kinase A." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23309.

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