Rozprawy doktorskie: „Protein 2”

1

Gao, Wei, i 高威. "Characterization of protein interactors of Arabidopsis acyl-coenzymea-binding protein 2". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43223837.

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Gao, Wei. "Characterization of protein interactors of Arabidopsis acyl-coenzyme a-binding protein 2". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43223837.

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3

Xu, Ping. "Sensing and analyzing unfolded protein response during heterologous protein production :". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 205 p, 2008. http://proquest.umi.com/pqdweb?did=1555621341&sid=2&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Rowell, Philip Lee. "Protein-protein interactions of the BCL-2 family". Thesis, University of Leeds, 2018. http://etheses.whiterose.ac.uk/20769/.

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The BCL-2 family of proteins are important regulators of mitochondrial apoptosis, comprising both pro- and anti-apoptotic members that interact with one another at the mitochondrial outer membrane to determine cellular fate. Dysregulation of their activities in the cell is implicated in many forms of cancer; the development of molecules able to mimic and modulate their interactions is thus highly desirable and has been the subject of a great deal of research effort. The use of techniques including structure based design and peptidomimetic approaches has produced some notable successes in this area, but few have successfully transitioned from laboratory to clinic, and the search for more and better ways to develop such molecules continues. In this thesis, I present a novel approach to identifying binding partners for BCL-2 proteins, which uses phage display experiments and the production of non-antibody scaffold proteins called Affimers. Five BCL-2 family proteins were selected as targets for study, comprising a good cross section of proand anti-apoptotic members. In the following chapters, I first describe the work undertaken to purify and characterise these target proteins, then detail the work done to identify and purify Affimer binding partners for each of them. Finally, I report on structural studies carried out to explore the mechanism by which BAX, a pro-apoptotic family member, forms death inducing oligomers. Taken together, the results of this project lay the foundations for further structural studies of BAX oligomerisation, and demonstrate that the use of phage display to generate selectively binding non-antibody scaffold proteins can provide useful additions to the existing array of BCL2 family interacting molecules.

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5

Papadopoulos, Maria. "The prion protein interacts with Bcl-2 and Bax proteins". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0026/MQ50849.pdf.

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6

Schacht, Teresa [Verfasser]. "Neuronal calcium-binding protein 2 (NECAB2): Charakterisierung eines striatalen Ca 2+ -bindenden Proteins / Teresa Schacht". Mainz : Universitätsbibliothek Mainz, 2017. http://d-nb.info/1141937689/34.

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7

Richards, Susan Diane. "Protein-protein interactions within the 2-oxoacid dehydrogenase complexes". Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299965.

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8

Funabashi, Teruki. "Roles of kinesin-2 motor proteins involved in intraciliary protein trafficking". Kyoto University, 2018. http://hdl.handle.net/2433/232321.

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9

Fang, Lin. "Mechanism of client protein binding by heat shock protein 90 /". view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1251819301&sid=2&Fmt=2&clientId=11238&RQT=309&VName=PQD.

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Thesis (Ph. D.)--University of Oregon, 2006.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 115-121). Also available for download via the World Wide Web; free to University of Oregon users.

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10

Libkind, Marianna. "SiaA: A Heme Protein". Digital Archive @ GSU, 2007. http://digitalarchive.gsu.edu/chemistry_hontheses/2.

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The protein SiaA (Streptococcal iron acquisition) is involved in heme uptake in the bacterium Streptococcus pyogenes. It is difficult to obtain this protein in its fully holo form (completely loaded with heme). To increase the concentration of heme in the growing cell, we added ä-aminolevulinic acid (ALA) and ferrous sulfate (FeSO4), precursors of heme, to the growth media. Neither increasing the concentration of heme in vivo, nor growth at lower temperature for longer times, increased the production of holoprotein. The classical method of measuring the concentration of heme in a newly discovered heme protein is cumbersome. We have developed an improved method, which gives a solution that is more stable and has a cleaner spectrum. With further development, this new technique may replace the classical assay. Background information on S. pyogenes, SiaA, ABC transporters, heme biosynthesis, and the pyridine hemochrome assay are described.

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11

Sundsten, Tea. "Protein Profiling and Type 2 Diabetes". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8458.

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Type 2 diabetes mellitus (T2DM) is a heterogeneous disease affecting millions of people worldwide. Both genetic and environmental factors contribute to the pathogenesis. The disease is characterized by alterations in many genes and their products. Historically, genomic alterations have mainly been studied at the transcriptional level in diabetes research. However, transcriptional changes do not always lead to altered translation, which makes it important to measure changes at the protein level. Proteomic techniques offer the possibility of measuring multiple protein alterations simultaneously.

In this thesis, the proteomic technique surface enhanced laser desorption ionization time-of-flight mass spectrometry (SELDI-TOF MS) has been applied and evaluated in the context of T2DM research. Protocols for pancreatic islet and serum/plasma protein profiling and identification have been developed. In addition, the technique was used to analyze the influence of genetic background versus diabetic environment by determining serum protein profiles of individuals with normal glucose tolerance (NGT) and T2DM with or without family history of diabetes. In total thirteen serum proteins displayed different levels in serum from persons with NGT versus patients with T2DM. Among these proteins, apolipoprotein CIII, albumin and one yet unidentified protein could be classified as being changed because of different genetic backgrounds. On the other hand, ten proteins for instance transthyretin, differed as a result of the diabetic environment.

When plasma protein patterns of NGT and T2DM individuals characterized by differences in early insulin responses (EIR) were compared, nine proteins were found to be varying between the two groups. Of these proteins five were identified, namely two forms of transthyretin, hemoglobin α-chain, hemoglobin β-chain and apolipoprotein H. However no individual protein alone could explain the differences in EIR. In conclusion, SELDI-TOF MS has been successfully used in the context of T2DM research to identify proteins associated with family history of diabetes and β-bell function.

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12

French, Katie. "Alpha-2-macroglobulin an abundant extracellular chaperone /". Access electronically, 2008. http://ro.uow.edu.au/theses/114.

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13

Ritchie, Sian. "Identification of cytoskeletal proteins as substrates for Ca'2'+ dependent protein kinase". Thesis, University of Reading, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240317.

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14

Tang, Norina Mei Ngon. "Regulation of protein synthesis and induction of oncogenesis by a cellular protein kinase inhibitor /". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/11501.

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15

Tentes, I. "Studies on the sarcoplasmic reticulum (Ca'2'+ + Mg'2'+) - ATPase". Thesis, University of Salford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381695.

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Tryptic digestion of SRV labelled with N-cyclohexyl-N'-(4-dimethylamino--naphthyl) carbodiimide (NCD-4), was shown to expose Ca^2+-protectable NCD-4-labelled amino acid residues, manifested by a time dependent quench (38%) of the initial fluorescence of the preparation. This finding is discussed in terms of a 3D model of the (Ca2+ + Mg2+)-ATPase. The inhibition of the sarcoplasmic reticulum (Ca2+ + Mg2+)-ATPase by the diphenolic antioxidants: 4,4'-isopropylidene diphenol, 4-hydroxy, 4'-methoxy isopropylidene diphenol, 4,4'dimethoxy isopropylidene diphenol and bis (2-hydroxy-3,5-methyl phenyl) methane, was studied, using the fluorescence response to bound NCD-4. They were shown to modulate conformational transitions of the ATPase subsequent to Ca2+ binding. It is suggested that the diphenolic antioxidants may have a target/binding site on the ATPase polypeptide via which they compete with Ca2+ ion binding and translocation. The stoichiometry of incorporation into the ATPase of tritated NCD-4 was studied. The ATPase was incubated with [3H]-NCD-4 for 4h. in the presence and in the absence of Ca2+ ions and then treated with trypsin for 35 mins. The four fragments: A(Mr= 50KD), B(Mr= 45KD), A1(Mr= 30KD) and A2(Mr= 20KD) were purified by preparative SDS-PAGE. The stoichiometry of incorporation of the radioactive label into fragments A1, A2 and the A2 subfragments SI (Mr= 13KD) and SII(Mr= 8.5KD) from CNBr cleavage, was measured by liquid scintillation counting of the gel eluates. In the absence of Ca2+, fragment A2 was found to incorporate 2.3 nmol [^3H]-NCD-4 per nmol of protein more than the equivalent preparation in the presence of Ca^2+. Subfragment S_I was shown to incorporate roughly equal amounts of label in both cases. S_II, however, in the absence of Ca^2+ was found to incorporate 1.15-2.3 nmol [^3H]-NCD-4 more than the equivalent preparation in the presence of Ca^2+. These differences were attributed to inhibitor binding at the Ca^2+-binding sites of the enzyme. However, discrepancies in the absolute incorporation values when experiments were compared, were related to loss of bound label due to nucleophilic attack. Four isomers of NCD-4 were prepared and evaluated in terms of inhibitory capacity towards the (Ca^2+ + Mg^2+)-ATPase. Preliminary evidence suggested that even related (isomeric) carbodimides can label different sites on the ATPase polypeptide. The synthesis and the evaluation of (N-cyclohexyl, N'-dimethylamino phenylazophenyl) carbodiimide (ACD) as a chromophoric probe for the Ca^2+ sites of the ATPase, is also described: this compound emerged as a relatively poor inhibitor of the enzyme, despite showing favourable chromophoric properties.

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16

Li, Xiaoman. "Study on memapsin 2 cleavage properties and its interacting proteins". Oklahoma City : [s.n.], 2010.

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17

Kanke, Toru. "Regulation of stress-activated protein kinases (SAPKs) mediated by proteinase-activated receptor-2 (PAR-2)". Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248779.

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18

Spatara, Michelle L. "Protein folding and aggregation in vitro and in vivo". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 162 p, 2009. http://proquest.umi.com/pqdweb?did=1892027491&sid=2&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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19

Zeng, Xuehuo. "The Physiological Function of Beclin, a Novel BCL-2 Interacting Protein in Protein Trafficking". Connect to full-text via OhioLINK ETD Center, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1116806533.

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Thesis (Ph.D.)--Medical College of Ohio, 2005.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: William Maltese. Includes abstract. Document formatted into pages: iv, 134 p. Title from title page of PDF document. Bibliography: pages 107-132.

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20

Streicher, John Michael. "The role of mitogen activated protein kinase activated protein kinase-2 in regulating p38 mitogen activated protein kinase induced cyclooxygenase-2 induction and heart failure". Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1872200951&sid=6&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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21

Garrey, Stephen M. "Characterization of the specificity and affinity of the splicing factor BBP/SF1 /". view abstract or download file of text, 2007. http://proquest.umi.com/pqdweb?did=1324375731&sid=2&Fmt=2&clientId=11238&RQT=309&VName=PQD.

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Thesis (Ph. D.)--University of Oregon, 2007.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 81-88). Also available for download via the World Wide Web; free to University of Oregon users.

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22

Tian, Wang, la Vega Montserrat Rojo de, Cody J. Schmidlin, Aikseng Ooi i Donna D. Zhang. "Kelch-like ECH-associated protein 1 (KEAP1) differentially regulates nuclear factor erythroid-2–related factors 1 and 2 (NRF1 and NRF2)". AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2018. http://hdl.handle.net/10150/627124.

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Nuclear factor erythroid-2-related factor 1 (NRF1) and NRF2 are essential for maintaining redox homeostasis and coordinating cellular stress responses. They are highly homologous transcription factors that regulate the expression of genes bearing antioxidant-response elements (AREs). Genetic ablation of NRF1 or NRF2 results in vastly different phenotypic outcomes, implying that they play different roles and may be differentially regulated. Kelch-like ECH-associated protein 1 (KEAP1) is the main negative regulator of NRF2 and mediates ubiquitylation and degradation of NRF2 through its NRF2-ECH homology-like domain 2 (Neh2). Here, we report that KEAP1 binds to the Neh2-like (Neh2L) domain of NRF1 and stabilizes it. Consistently, NRF1 is more stable in KEAP1(+/+) than in KEAP1(-/-) isogenic cell lines, whereas NRF2 is dramatically stabilized in KEAP1(-/-) cells. Replacing NRF1's Neh2L domain with NRF2's Neh2 domain renders NRF1 sensitive to KEAP1-mediated degradation, indicating that the amino acids between the DLG and ETGE motifs, not just the motifs themselves, are essential for KEAP1-mediated degradation. Systematic site-directed mutagenesis identified the core amino acid residues required for KEAP1-mediated degradation and further indicated that the DLG and ETGE motifs with correct spacing are insufficient as a KEAP1 degron. Our results offer critical insights into our understanding of the differential regulation of NRF1 and NRF2 by KEAP1 and their different physiological roles.

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23

Campbell, Sean Thomas. "Protein Engineering for Biochemical Interrogation and System Design". Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/560940.

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Proteins are intimately involved in almost every cellular phenomenon, from life to death. Understanding the interactions of proteins with each other and other macromolecules and the ability to rationally redesign them to improve their activities or control their function are of considerable current interest. Split-protein methodologies provide an avenue for achieving many of these goals. Since the original discovery of conditionally activated split-ubiquitin, the field has grown exponentially to include the activities of over a dozen different proteins. The flexibility of the systems has resulted in their use across a wide spectrum, both literally and figuratively, to primarily screen, visualize and quantitate macromolecular interactions in a variety of biological systems. In another arena, there is significant interest the apoptosis-regulating proteins: the Bcl-2 family. These proteins are found in many cell types and control, through expression levels as well as other mechanisms, the apoptotic state of a protein as governed by intrinsic death signals generated from such sources as DNA damage and viral infection. The apoptotic function of these proteins are mainly governed by a single type of interaction: the helix:receptor binding of the BH3-Only helices to the anti-apoptotic receptor proteins. While this often promiscuous helix:receptor interaction has received much scrutiny, the nature of the anti-apoptotic binding pocket, especially with regard to the specific residues that govern the interaction, has been lacking. With the high sensitivity and rapid analysis platform afforded by the cell-free split-luciferase analysis methodology, we devised and carried out the first systematic and large scale alanine mutagenesis of all five major anti-apoptotic members of the Bcl-2 family, validated these results both with biophysical methods as well as correlation with previous studies. Our results help explain how different receptors can bind a wide range of helices and also uncovered details regarding binding that are not possible with structural or computational analysis alone. In a second area of research, we have utilized the interaction of BH3 helices and their receptors for designing small molecule controlled protein kinases and phosphatases. In this protein design area, BH3-Only helices were inserted using a knowledge based approach into particular loops within both a protein kinase and a protein phosphatase. The BH3-Only helix interaction with added receptors, such as Bcl-xL provided an allosteric switch for turning-off the activity of the helix-inserted enzymes. The activity of the enzymes could then be turned-on by the addition of a cell-permeable small molecule that is known to bind the receptor. This plug-and-play design was demonstrated to be successful for two very different enzyme classes and likely provides a general and tunable biological element for controlling the activity of one or more proteins and enzymes in a biochemical networks.

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24

Blackler, Alissa N. "Design of bone morphogenetic protein 2/nodal chimeras". Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/fullcit?p1477885.

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Thesis (M. S.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed July 12, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (leaves 34-36).

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25

Hansen, David Donald. "FEM-2 is a rapidly evolving protein phosphatase". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0002/NQ39536.pdf.

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26

Côté, Richard Gaston. "Characterization of the retinoblastoma binding protein 2 (RBP2)". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33388.

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The retinoblastoma (RB) family of proteins plays a pivotal role in cell cycle regulation. Its members, p105/Rb, p107 and p130, interact with the E2F and DP family of transcription factors to regulate transcription of essential cell cycle and DNA synthesis genes. Several reports have mapped the regulation of E217 by RB family members to the "pocket" domain of these proteins. We demonstrate here that RBP2, a pocket-binding protein that encodes multiple DNA-binding and protein-protein interaction domains, is a transcriptional repressor. Overexpression of RBP2 inhibits E2F-dependent transcription and inhibits cellular growth. The growth suppression activity of RBP2 could not be associated with a single domain within the protein but the transcriptional repression activity can be mapped to a minimal 17 kDa fragment located at the extreme N-terminus of RBP2 that can repress transcription when expressed alone but requires the C-terminus in the context of the full-length protein.

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27

Trebilcock, Anna E. "An investigation of 2#mu# plasmid protein function". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309348.

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28

Desai, Vibhuti H. "Biotechnological applications of a surfactant protein, ranaspumin-2". Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8609/.

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Surfactant activity is generally associated with small molecules rather than biological macromolecules like proteins. Only a few proteins have good intrinsic surfactant activity, an example being the natural surfactant ranaspumin 2 (Rsn2) from the foam nests of the túngara frog. In solution, Rsn2 has a hydrophobic core and hydrophilic exterior, but when Rsn2 comes in contact with an air-water interface, it changes conformation to expose its hydrophobic core to interact with the air and present a hydrophilic face to the water. The unique combination of biocompatibility along with surface activity offers the possibility of developing biomedical applications based on Rsn2. Some of the possible applications, including cell patterning, functionalising scaffolds and stabilising droplets, have been explored in the work described in this thesis. The ability of Rsn2 to coat hydrophobic surfaces persistently, rendering them wettable and the nature of coating and interaction with the surfaces were investigated. This formed the basis for the development of a method to coat a range of hydrophobic polymers, which are commonly used for biomedical applications. These Rsn2 coated surfaces were tested for their capability to control cell adhesion on surfaces which usually do not support cell adhesion. Rsn2 coating was demonstrated to promote, and thus allowed the spatial control over, cell adhesion on otherwise non-cell compatible surfaces. The potential of Rsn2 to be used as a protein fusion partner for the production of further functionalised cell engineering substrates was explored by constructing five different integrin binding sequence (IBS)-Rsn2 conjugates. Specific IBS-Rsn2 proteins proved successful in increasing the adhesion and biomineralising potential of osteoblasts isolated from neonatal rats. In addition, Rsn2's ability to stabilise microscopic oil droplets were investigated. Rsn2 stabilised oil droplets were stable for more than six months. Thus, the surfactant properties of Rsn2 can be used for many potential biomedical applications.

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29

Hardy, Matthew Philip 1974. "The molecular and functional characterization of soluble Ifnar-2". Monash University, Institute of Reproduction and Development, 2001. http://arrow.monash.edu.au/hdl/1959.1/8852.

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30

Schulze, Nahrup Adriane. "Endotheliale Wirkmechanismen von rekombinantem aktiviertem Protein C am Beispiel von Fractalkine, Transforming Growth Factor-beta 2 und Cyclooxygenase-2 /". Giessen : VVB Laufersweiler, 2007. http://geb.uni-giessen.de/geb/volltexte/2007/4732/index.html.

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31

Khosravi, Afra. "Age-dependent antibody response to Plasmodium falciparum merozoite surface protein-2 (MSP-2)". Thesis, University of Liverpool, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411584.

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32

Adams, Phillip. "Heterologous expression and structure-function analysis of the fast twitch (Ca'2'+-Mg'2'+)-ATPase". Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295901.

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33

Tan, Pauline H. "Sequence Specificity of Src Homology-2 Domains". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1324406526.

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34

Wavreille, Anne-Sophie Marie. "SRC homology 2 domain proteins binding specificity from combinatorial chemistry to cell-permeable inhibitors /". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1164738844.

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35

Yost, Cynthia Haycox. "Regulation of the dorsal-ventral axis in Xenopus embryos by intracellular components of the Wnt pathway /". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/9224.

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36

Chiu, Peng-hang Raymond, i 趙炳铿. "Identification of protein-interacting partners of testis-specific protein y-encoded like 2 (TSPYL2)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508725.

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37

Chiu, Peng-hang Raymond. "Identification of protein-interacting partners of testis-specific protein y-encoded like 2 (TSPYL2)". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41508725.

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38

Lundén, Amanda. "Can Sterol Carrie Protein-2 function as a solubility tag in E.coli?" Thesis, Linköpings universitet, Biologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-129803.

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Expressing foreign proteins in E.coli is a major challenge because they often tend to develop into unsolvable and inactive proteins. They aggregate into so called inclusion bodies which prevent expression of the protein. This problem might be avoided by fusing the gene of the foreign protein with a soluble protein called solubility tags, which function is to enhance the solubility of the foreign protein. This report investigates whether Sterol Carrier Protein-2 (SCP-2) could function as a solubility tag. The experiment was carried out by fusing SCP-2 to two recombinant proteins, Green fluorescent protein (GFP) and a form of chloroamphenicol acetyl transferase (CATΔ9). The gene fusion was then inserted into a pET-15 vector and transformed into the E.coli strain BL21(DE3) to be expressed. The results obtained from Western blot and PageBlue staining indicates that SCP-2 does not enhance the solubility of GFP or CATΔ9 since neither of them was expressed. Furthermore, previous studies have shown that GFP can in fact be expressed usingmaltose binding protein (MBP) as a solubility tag. Unfortunately, no success has been made regarding CATΔ9. In conclusion, regarding the results from this report, SCP-2 does not function as a solubility tag. However, further studies should be carried out on SCP-2 with more experiments before rejecting the possibility to use SCP-2 as a solubility tag.

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39

Jackson, Sophie Elizabeth. "Studies on subtilisin BPN' and chymotrypsin inhibitor 2". Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386194.

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40

Beaumont, Ellen Sarah. "Refolding studies on 2-oxoacid dehydrogenase multienzyme complexes". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360171.

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41

Rheinnecker, Michael. "Subtilisin BPN' and chymotrypsin inhibitor 2 : model systems for the study of protein function and protein - protein interaction". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308125.

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42

Maitra, Sushmit. "The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase 2". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008r/maitra.pdf.

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43

Zepeck, Ferdinand. "Charakterisierung der 1-Hydroxy-2-methyl-2-(E)-butenyl-4-diphosphat-Synthase (IspG-Protein)". [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=980363721.

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44

Schwartz, Daniel. "Development of an Aqueous Suspension of Recombinant Human Bone Morphogenetic Protein-2 (rhBMP-2)". Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-44316.

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45

Takao, Keizo. "Visualization of synaptic Ca[2+]/calmodulin dependent protein kinase 2 activity in living neurons". 京都大学 (Kyoto University), 2006. http://hdl.handle.net/2433/144322.

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46

Li, Wei. "Roles for activator protein 2 (AP-2) transcription factors in zebrafish neural crest development". Diss., University of Iowa, 2008. https://ir.uiowa.edu/etd/207.

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Neural crest is a vertebrate-specific population of embryonic precursor cells thought to have been essential in vertebrate evolution. During development, a group of naïve ectoderm cells are induced to become neural crest and then undergo series of developmental events to give rise to diverse derivatives. Failure of these events often leads to malfunction of neural crest derived tissues and organs. This thesis focuses on the genetic regulation of two events during neural crest development, induction and differentiation. Neural crest induction refers to the specification of ectoderm cells to the neural crest lineage. It is believed that combinatorial activity of transcription factors governs neural crest induction, but the function of specific transcription factors in this process are not yet clear. The AP-2 family of transcription factors is implicated in control of neural crest development, but whether there is a cell autonomous role of AP-2 transcription factors in neural crest induction has remained uncertain. Here I show that in zebrafish, two AP-2 family members, Tfap2a and Tfap2c, are required redundantly for neural crest induction, and that this requirement is cell autonomous. Failure of neural crest induction in the zebrafish embryos that are devoid of Tfap2a and Tfap2c is not caused by defects in cell survival or cell proliferation, but rather appears to result from a failure neural crest cell fate specification. Simultaneous knockdown of Tfap2a and Tfap2c is one of the only known genetic manipulations that result in failure of neural crest induction. Thus the Tfap2a/c double knockdown embryos will be useful for further studies on the emergence of neural crest during both development and evolution. The second section of my thesis concerns differentiation of neural crest derived zebrafish melanophores. This study reveals that Tfap2a and another AP-2 family member, Tfap2e, redundantly and autonomously regulate melanophore differentiation. This is the first report on the function of Tfap2e in any animal. Given that the expression of AP-2 transcription factors is tightly associated with the metastasis potential of human melanoma, my study reinforces the view that cancer cells co-opt regulatory pathways employed in embryonic development.

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47

Noblett, Nathaniel. "A Role for the Caenorhabditis Elegans Adenylate Gorming Domain Protein Disco-Interacting Protein 2 (DIP-2) in the Maintenance of Neuron Morphology". Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38083.

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Post-developmentally, neurons are very long lived and, while shown to be capable of plasticity-promoting remodeling of dendritic structures, are thought to maintain relatively stable morphologies over long animal lifespans. The molecular mechanisms that maintain neuronal morphology remain poorly understood. Members of the highly conserved DIP2 protein family contain an N-terminal DNA methyltransferase-associated protein 1 (DMAP1) binding domain and two adenylate-forming (AFD) domains. Using two loss-of-function alleles, we show that DIP-2 acts to maintain neuronal morphology in C. elegans. dip-2 mutants display a progressive increase in ectopic neurite sprouting and branching post-development. DIP-2 acts in a DMAP1 binding-domain-independent manner to maintain neuronal morphology post-developmentally and DIP-2 overexpression can suppress the normal increase in neuronal sprouting defects observed in aging worms. Endogenous DIP-2 is widely expressed in neuronal and epithelial tissue but acts cell-autonomously in neurons. Finally, dip-2 neuronal defects are modified by loss of insulin/IGF-1 signalling (IIS) and DIP-2 acts in parallel with the SAX-2/Furry-SAX-1/NDR kinase pathway to regulate neuronal morphology.

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48

Hower, Amy Elizabeth. "Receptor Functions of the Receptor-Type Protein Tyrosine Phosphatase PTPRO". Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/303.

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Protein tyrosine phosphorylation regulates many aspects of cell growth and differentiation. Since cellular tyrosine phosphorylation levels are controlled by the antagonizing actions of the protein tyrosine kinases (PTKs) and the protein tyrosine phosphatases (PTPs), these enzymes play a direct role in regulating processes as diverse as oncogenesis and neuronal development. In particular, the transmembrane group of PTPs, known as the receptor-type protein tyrosine phosphatases (RPTPs), has been linked to regulation of axon growth and guidance during development and regeneration. The regulation of activity of these RPTPs is of clear importance, yet the fundamental mechanisms underlying this regulation are poorly understood. While extracellular ligands are well known to dimerize and activate the receptor protein tyrosine kinases, the extent to which RPTP regulation parallels this scenario is largely unknown. We have examined the dimerization state and the relationship this state has with the phosphatase activity of the neuronal RPTP, PTPRO. We have found that PTPRO, a Type III RPTP, can exist in a dimerized state, likely regulated by disulfide linkages in the intracellular domain. Ligand addition to a chimeric PTPRO increases dimerization of the transmembrane and intracellular domains. Ligand addition to the chimeric PTPRO also decreases its phosphatase activity towards artificial peptides and a putative substrate, TrkC, a protein also known to be important in neuronal development. PTPRO's regulation of TrkC may be physiologically relevant as the proteins can be co-precipitated from transfected cells and PTPRO's dephosphorylation of TrkC is efficient compared to that of other RPTPs. The decrease in PTPRO's activity upon ligand-induced dimerization was unexpected as dimerization of a structurally-similar RPTP family member suggested the opposite functional outcome. This work suggests a complex relationship between dimerization and activity for the Type III RPTPs, which include PTPRO. The results presented in this dissertation will extend the current knowledge on RPTP functions and the cellular processes they regulate.

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Gros, Robert. "Regulation of G-protein-coupled receptor function, a role for increased G-protein-coupled receptor kinase-2 protein content". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0019/NQ58133.pdf.

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Liang, Ying. "Characterization of Sad1/UNC-84 domain protein 2 (SUN2)". Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36616515.

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