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Okada, Kouki. "CD68 on rat macrophages binds tightly to S100A8 and S100A9 and helps to regulate the cells’ immune functions." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225517.
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Stephens, Chad Louis. "Autonomic Differentiation of Emotions: A Cluster Analysis Approach." Thesis, Virginia Tech, 2007. http://hdl.handle.net/10919/79690.
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The autonomic specificity of emotion is intrinsic for many major theories of emotion. One of the goals of this study was to validate a standardized set of music clips to be used in studies of emotion and affect. This was accomplished using self-reported affective responses to 40 music pieces, noise, and silence clips in a sample of 71 college-aged individuals. Following the music selection phase of the study; the validated music clips as well as film clips previously shown to induce a wide array of emotional responses were presented to 50 college-aged subjects while a montage of autonomic variables were measured. Evidence for autonomic discrimination of emotion was found via pattern classification analysis replicating findings from previous research. It was theorized that groups of individuals could be identified based upon individual response specificity using cluster analytic techniques. Single cluster solutions for all emotion conditions indicated that stimulus response stereotypy of emotions was more powerful than individual patterns. Results from pattern classification analysis and cluster analysis support the concept of autonomic specificity of emotion.<br>Master of Science<br>[Appendix B: Beck Depression Inventory, p. 61-64, was removed Oct. 4, 2011 GMc]
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Chrysostomou, Charalambos. "Characterisation and classification of protein sequences by using enhanced amino acid indices and signal processing-based methods." Thesis, De Montfort University, 2013. http://hdl.handle.net/2086/9895.
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Protein sequencing has produced overwhelming amount of protein sequences, especially in the last decade. Nevertheless, the majority of the proteins' functional and structural classes are still unknown, and experimental methods currently used to determine these properties are very expensive, laborious and time consuming. Therefore, automated computational methods are urgently required to accurately and reliably predict functional and structural classes of the proteins. Several bioinformatics methods have been developed to determine such properties of the proteins directly from their sequence information. Such methods that involve signal processing methods have recently become popular in the bioinformatics area and been investigated for the analysis of DNA and protein sequences and shown to be useful and generally help better characterise the sequences. However, there are various technical issues that need to be addressed in order to overcome problems associated with the signal processing methods for the analysis of the proteins sequences. Amino acid indices that are used to transform the protein sequences into signals have various applications and can represent diverse features of the protein sequences and amino acids. As the majority of indices have similar features, this project proposes a new set of computationally derived indices that better represent the original group of indices. A study is also carried out that resulted in finding a unique and universal set of best discriminating amino acid indices for the characterisation of allergenic proteins. This analysis extracts features directly from the protein sequences by using Discrete Fourier Transform (DFT) to build a classification model based on Support Vector Machines (SVM) for the allergenic proteins. The proposed predictive model yields a higher and more reliable accuracy than those of the existing methods. A new method is proposed for performing a multiple sequence alignment. For this method, DFT-based method is used to construct a new distance matrix in combination with multiple amino acid indices that were used to encode protein sequences into numerical sequences. Additionally, a new type of substitution matrix is proposed where the physicochemical similarities between any given amino acids is calculated. These similarities were calculated based on the 25 amino acids indices selected, where each one represents a unique biological protein feature. The proposed multiple sequence alignment method yields a better and more reliable alignment than the existing methods. In order to evaluate complex information that is generated as a result of DFT, Complex Informational Spectrum Analysis (CISA) is developed and presented. As the results show, when protein classes present similarities or differences according to the Common Frequency Peak (CFP) in specific amino acid indices, then it is probable that these classes are related to the protein feature that the specific amino acid represents. By using only the absolute spectrum in the analysis of protein sequences using the informational spectrum analysis is proven to be insufficient, as biologically related features can appear individually either in the real or the imaginary spectrum. This is successfully demonstrated over the analysis of influenza neuraminidase protein sequences. Upon identification of a new protein, it is important to single out amino acid responsible for the structural and functional classification of the protein, as well as the amino acids contributing to the protein's specific biological characterisation. In this work, a novel approach is presented to identify and quantify the relationship between individual amino acids and the protein. This is successfully demonstrated over the analysis of influenza neuraminidase protein sequences. Characterisation and identification problem of the Influenza A virus protein sequences is tackled through a Subgroup Discovery (SD) algorithm, which can provide ancillary knowledge to the experts. The main objective of the case study was to derive interpretable knowledge for the influenza A virus problem and to consequently better describe the relationships between subtypes of this virus. Finally, by using DFT-based sequence-driven features a Support Vector Machine (SVM)-based classification model was built and tested, that yields higher predictive accuracy than that of SD. The methods developed and presented in this study yield promising results and can be easily applied to proteomic fields.
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Bian, Shumin. "Fe-S proteins : cluster assembly and degradation /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487952208109007.
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Goff, Lindsey Kate. "Cluster of differentiation 45 isoforms and murine thymic ontogeny." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333266.
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Batrakou, Dzmitry G. "Nuclear envelope transmembrane proteins in differentiation systems." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/9981.
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Historically, our perception of the nuclear envelope has evolved from a simple barrier isolating the genome from the rest of a cell to a complex system that regulates functions including transcription, splicing, DNA replication and repair and development. Several recent proteomic studies uncovered a great variety of nuclear envelope transmembrane proteins (NETs). Diseases associated with several nuclear envelope proteins, mostly NETs, affect many tissues e.g. muscle, adipose tissue, skin, bones. Many NETs of the inner nuclear membrane have been shown to interact with chromatin, suggesting that their influencing gene expression might explain NET roles in disease. This work is focused on finding novel interactions of NETs with chromatin. First, SUN2 post-translational modifications were analysed and the effect of phosphomimetic and phospho-null mutants on heterochromatin and the cytoskeleton was tested by overexpression. However, no obvious changes were found. Second, several tissue-preferential NETs were tested in an adipocyte differentiation system. NET29 changed chromosome 6 position in pre-adipocytes. This matched changes in chromosome positioning that occur during adipocyte differentiation when NET29 is normally induced. Post-translational modifications of NET29 are likely to play a vital role in this process because a phospho-null mutant dominantly blocked chromosome repositioning. The effect of over-expression and down-regulation of NET29 on transcription was tested and results suggest that NET29 negatively regulates expression of myogenic genes during adipogenesis. This thesis is split into six chapters. Chapter I is an overview of the nuclear envelope, adipogenesis and chromatin remodelling, Chapter II is a detailed description of methods used in this study. Chapter III focuses on post-translational modifications of SUN2, as well as trials to identify novel partners of SUN2. Chapter IV and V deal with a novel nuclear envelope transmembrane protein and its role in adipogenesis. Finally, the last chapter includes a discussion and recommended future directions.
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Tilley, Gareth John. "Electrochemical investigations into iron-sulfur cluster containing proteins." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365300.
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Dizin, Eric Michel. "Insights On Iron-Sulfur Cluster Assembly Donor Proteins." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1208532379.
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Ding, Shu. "Thermodynamic studies on iron-sulfur cluster assembly proteins." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1316472363.
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Trivedi, Archit. "Bromodomain Containing Proteins in Melanocyte Differentiation and Melanoma." University of Toledo Health Science Campus / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=mco1438963150.
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Smialowski, Pawel. "Structural and functional studies on photoactive proteins and proteins involved in cell differentiation." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971648379.
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Shimmin, Lawrence Charles. "An archaebacterial ribosomal protein gene cluster." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30994.
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The eubacteria, archaebacteria and eucaryota evolved from a common ancestral state, the progenote, approximately 4,000 million years ago. The archaebacteria flourish in extreme environments, exhibiting unusual macromolecular structures and metabolism of which much has recently been elucidated. Less, however, is known of the genetics of archaebacteria. In order to investigate gene structure, organization, regulation and evolution in the archaebacteria a gene cluster encoding the ribosomal proteins of the GTPase domain was cloned from the extremely halophilic archaebacterium Halobacterium cutirubrum, characterized and compared with the homologous genes and proteins from eubacteria and eucaryota.
A clone containing a 5146 basepair insert of genomic Halobacterium cutirubrum NRCC 34001 DNA encoding the GTPase domain ribosomal proteins was characterized and discovered to retain the identical gene order (i.e. L11e, Lie, L10e and L12e) as the homologous Escherichia coli genes and in addition two transcribed upstream open reading frames encoding the potential proteins ORF, of unknown function and NAB, bearing sequence similarity to nucleic acid binding proteins.
The predominant transcripts are monocistronic L11e and tricistronic Lie - L10e - L12e transcripts; monocistronic NAB and bicistronic NAB - L11e transcripts are present at reduced levels and the ORF is present as a very rare transcript. Common elements upstream of the transcription initiation sites include the motif TTCGA ... 4-15 bp ... TTAA ... 20-26 bp ... A or G transcription start. The NAB and some of the ORF transcripts are divergently transcribed from a single TTAA promotor element. The NAB and some of the ORF transcripts initiate 1 nucleotide before the coding region; the L11e monocistronic transcript initiates precisely at the first A of the initiator methionine ATG codon. The Lie - L10e - L12e tricistronic transcript has a 75 nucleotide leader that is probably involved in the autogenous regulation of the transcript at the translational level by the Lie protein. Termination of transcription occurs, with a single exception, within T tracts after GC rich regions. Although classic Shine-Dalgarno (eubacterial) type ribosome binding sites are present upstream of the Lie and L10e genes, the mechanism of translation initiation for transcripts with nil or negligible 5' leaders remains to be elucidated.
Alignments between the deduced amino acid sequences of the L1le, Lie, Ll0e and L12eribosomal proteins and other available homologous proteins of archaebacteria, eubacteria and eucaryota have been made and show that the L11e, Lie and L10e proteins are colinear whereas the L12e protein has suffered a rearrangement through what appears to be gene fusion events. The L11e proteins exhibit (i) sequence conservation in the region interacting with release factor 1, (ii) conserved proline residues (probably contributing to the elongated shape of the molecule) and (iii) sites of methylation in Eco L11 are not conserved in the archaebacterial L11e proteins. The Lie proteins have regions of very high sequence similarity near the center and carboxy termini of the proteins but the relationships between protein structure and function remain unknown. Intraspecies comparisons between L10e and L12e sequences indicate the archaebacterial and eucaryotic L10e proteins contain a partial copy of the L12e protein fused to their carboxy terminus. In the eubacteria most of this fusion has been removed by a carboxy terminal deletion. Within the L12e derived region a 26 amino acid long internal modular sequence reiterated thrice in the archaebacterial L10e, twice in the eucaryotic L10e and once in the eubacterial L10e was discovered. This modular sequence also appears to be present in single copy in all Ll2e proteins and may play a role in L12e dimerization, L10e - L12e complex formation and the function of L10e - L12e complex in translation. From these sequence comparisons a model depicting the evolutionary progression gene cluster and proteins from the primordial state to the contemporary archaebacterial, eucaryotic and eubacterial states is presented.<br>Medicine, Faculty of<br>Biochemistry and Molecular Biology, Department of<br>Graduate
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Wai, Carol. "Functional analysis of zinc cluster proteins in Saccharomyces cerevisiae." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98514.
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In Saccharomyces cerevisiae, zinc cluster proteins form a major family of transcriptional regulators for a variety of processes, yet many putative zinc cluster proteins have unknown functions. Previous studies assigned phenotypes to some of these proteins, a few of which showed previously unknown functions in pleiotropic drug resistance (PDR). The first study presented here focuses on a phenotypic analysis of double deletion mutants to further our understanding on functional relationships among zinc cluster proteins that mediate PDR. The second study focuses on a newly characterized zinc cluster protein, Asg1p, and its functional role in regulating stress response genes. In both studies, we found that the relationship among zinc cluster proteins is highly complex and tightly regulated.
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Mthombeni, Jabulani S. "A comparative bioinformatic analysis of zinc binuclear cluster proteins." Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1004064.
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Members of the zinc binuclear cluster family are important fungal transcriptional regulators sharing a common DNA binding domain. Da181p is a pleotropic zinc binuclear cluster protein involved in the induction of the UGA genes required for the γ-aminobutyrate nitrogen catabolic pathway in Saccharomyces cerevisiae. The zinc binuclear cluster domain is indispensable for function in Da181p and little is known about other domains in this protein. The aim of the study was to explore the zinc binuclear cluster protein family using comparative bioinformatics as a complement to biochemical and structural approaches. A database of all zinc binuclear cluster proteins was composed. A total of 118 zinc binuclear proteins are reported in this work. Thirty nine previously unidentified zinc binuclear cluster proteins were found. Four homologues of Da181p were identified by homology searching. Important sequence motifs were identified in the aligned sequences of Da181p and its homologues. The coiled coil motif found in the Ga14p zinc binuclear cluster protein could not be identified in Da181p and its homologues. This suggested that Da181p did not dimerise through this structural motif as other zinc binuclear cluster proteins. Solvent accessible site that could be phosphorylated by protein kinase C or casein kinase II and the role of such sites in the possible regulation of Da181p function were discussed.
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Sun, Daokun. "E2F Proteins Regulate Cell Proliferation and Differentiation in Development." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1562695239955401.
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Wu, Shu-Pao. "Iron-sulfur cluster biosynthesis. Iron-sulfur cluster transfer from holo ISU and ISA to apo ferredoxin." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1078866123.
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Thesis (Ph. D.)--Ohio State University, 2004.<br>Title from first page of PDF file. Document formatted into pages; contains xx, 161 p.; also includes graphics Includes bibliographical references (p. 153-161). Available online via OhioLINK's ETD Center
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Zayas, Jennifer. "Regulation of HSC Self-Renewal and Differentiation by Pumilio Proteins." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/300.
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Evolutionarily conserved Pumilio (Pum) RNA-binding proteins act as translational repressors during embryo development and cell fate specification. Previous work in the lab has shown that over-expression of Pum2 (Pum2-EML) supports maintenance and suppresses mutilineage differentiation of murine multipotent HSC/MPP-like cell line EML. The subsequent analysis of HSC markers and functional analysis has revealed that wt EML cells share the LKS CD34 positive phenotype, whereas the majority Pum2-EML cells are similar to LKS CD34 negative. The CD34 positive wt EML cells can be divided into CD34low, CD34med and CD34high subpopulations, whereas Pum2-EML CD34 positive cells correspond to CD34low subpopulation. Colony forming assays have revealed that the overall multilineage differentiation of wt EML and Pum2-EML cells strongly correlates with the CD34 expression levels. Multiple experiments have revealed that purified CD34 negative and CD34 positive wt EML cells can generate each other and among CD34 positive wt EML cells the CD34low cells have the highest capacity to give rise to CD34 negative EML cells. We have proposed a model in which CD34 negative EML cells are more primitive cells in an "inactive" (differentiation inhibited) state, that give rise to CD3low "active" (differentiation ready) EML cells. The CD34low EML cells can revert back to the CD34 negative state or give rise to CD34med/high cells that can readily differentiate into multiple lineages. Based on that model, the over-expression of Pum2 leads to increased maintenance of cells in inactive CD34 negative state, and blocks development of CD34 positive cells past the CD34low stage. Cumulatively, these results support the notions that Pum2 could be involved in maintaining the balance between inactive and active state of multipotent hematopoietic cells. The c-kit receptor plays a vital role in self-renewal and differentiation of hematopoietic stem cells (HSC) and multipotent progenitors (MPPs). We have discovered that besides c-kit, the murine multipotent HSC/MPP-like cell line EML expresses the transcript and protein for a truncated form of c-kit, called tr-kit. Notably, the tr-kit transcript and protein levels were down-regulated during cytokine induced differentiation of HSC/MPP-like cell line EML into myelo-erythroid lineages. RT-PCR results show tr-kit is transcribed solely in cell populations enriched for LTR-HSC, STR-HSC and MPPs. The observation that tr-kit is co-expressed with c-kit only in more primitive, HSC and MPP-enriched cell populations raises an exciting possibility that tr-kit functions either as a new component of SCF/c-kit pathway, or is involved in a novel signaling pathway, present exclusively in HSC and MPPs. These findings necessitate functional characterization of tr-kit, and analysis of its potential role in the self-renewal, proliferation and/or differentiation of HSC and multipotent progenitors.
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Vogel, Katharina. "Roquin family proteins control T cell co-stimulation and differentiation." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-158244.
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Steineck, Martina. "Towards Identifying Proteins in the Synovium Promoting Articular-cartilage Differentiation." Thesis, Örebro universitet, Institutionen för medicinska vetenskaper, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-73271.
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Skeletal development begins when mesenchymal stem cells migrate, condensate and differentiate into chondrocytes. The chondrocytes differentiate in one of two ways. Either the cells form the cartilaginous template for endochondral ossification or they form the articular cartilage which express proteoglycan 4. The underlying mechanisms for articular cartilage formation are poorly understood. The purpose of this study was to assess the effect of different fractions of synoviocyte-conditioned medium on chondrocyte differentiation. We show evidence that Synovial-like fluid contains a protein which promotes chondrocytes to express proteoglycan 4, thus promoting articular cartilage formation. The synovial-like fluid was fractionized by size exclusion chromatography and reversed phase chromatography and thus, with that method, this manuscript lays the foundations for further research to identify the putative factor. Because of this study, we are now closer in identifying the proteins that promote articular cartilage formation.
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Watson, Andrea. "Heat shock proteins in leukaemia cell differentiation and cell death." Thesis, Aston University, 1990. http://publications.aston.ac.uk/12533/.
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When HL60 cells were induced to differentiate to granulocyte-like cells with the agents N-methylformamide and tunicamycin an concentrations marginally below those which were cytotoxic, there was a decrease in the synthesis of the glucose- regulated proteins which preceded the expression of markers of a differentiated phenotype. There was a transient increase in the amount of hsp70 after 36 hours in NMF treated cells but in differentiated cells negligible amounts were detected. Inducers which were known to modulate hsp70 such as azetadine carboxylic acid did not induce differentiation suggesting early changes in the endoplasmic reticulum may be involved in the commitment to terminal differentiation of HL60 cells. These changes in group synthesis were not observed when K562 human chronic myelogenous leukemia cells were induced to differentiate to erythroid-like cells but there was a comparable increase in amounts of hsp70. When cells were treated with concentrations of drugs which brought about a loss in cell viability there was an early increase in the amount of hsp70 protein in the absence of any increase in synthesis. HL60 cells were treated with NMF (225mM), Adriamycin (1 jiM), or CB3717 (5iM) and there was an increase in the amounts of hsp70, in the absence of any new synthesis, which preceded any loss of membrane integrity and any significant changes in cell cycle but was concomitant with a later loss in viability of > 50% and a loss in proliferative potential. The amounts of hsp70 in the cell after treatment with any of the drugs was comprable to that obtained after a heat shock. Following a heat shock hsp70 was translocated from the cytoplasm to the nucleus, but treatment with toxic concentrations of drug caused hsp70 to remain localised in the cytoplasm. Changes in hsp70 turn-over was observed after a heat shock compared to NMF-treated cells. Morphological studies suggested that cells that had been treated with NMF and CB3717 were undergoing necrosis whereas the Adriamycin cells showed characteristics that were indicative of apoptosis. The data supports the hypothesis that an increase in amounts of hsp70 is an early marker of cell death.
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Olive, Joshua A. "Investigating the Roles of the Iron-Sulfur Proteins Monothiol Glutaredoxin 5, ISCA1, and ISCA2." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1503305827105994.
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Hill, Donna Monique. "Mechanism of centaurin-alpha-1 control of neuronal differentiation." Birmingham, Ala. : University of Alabama at Birmingham, 2010. https://www.mhsl.uab.edu/dt/2010m/hill.pdf.
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Thesis (M.S.)--University of Alabama at Birmingham, 2009.<br>Title from PDF t.p. (viewed June 30, 2010). Additional advisors: Lori McMahon, Stephen Watts. Includes bibliographical references (p. 31-35).
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Popov, Nikita. "Expression and activity of Myc network proteins during cell cycle progression and differentiation /." Sundbyberg, 2004. http://diss.kib.ki.se/2004/91-7349-856-4/.
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Lengner, Christopher J. "Regulation and Function of Runx2 During Chondrogenic and Osteogenic Differentiation: a Dissertation." eScholarship@UMMS, 2004. https://escholarship.umassmed.edu/gsbs_diss/80.
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Members of the Runx family of transcription factors play essential roles in the differentiation and development of several organ systems. Here we address the contribution of the osteoblast-related Runx gene, Runx2, to the osteogenic and chondrogenic differentiation of mesenchymal stem cells. Using a transgenic mouse model, we observe Runx2 transcription through one of its two known promoters (designated P1 in pre-cartilaginous mesenchymal condensations as early as E9.5. Runx2 gene activity is later repressed at the onset of cartilage formation, both in vivo and in vitro, necessitating examination of the regulation and function of Runx2 in mesenchymal stem cells. We demonstrate that Runx2 gene activity is repressed by the direct interaction of the homeodomain transcription factor Nkx3.2 with the proximal Runx2 P1 promoter. This repression was found to be required for the progression of BMP-induced chondrogenesis, thereby identifying Runx2 as a modulator of BMP activity in the chondrogenic as well as osteogenic differentiation program. To further understand the regulation of the Runx2 P1 promoter and to determine the contribution of P1-derived gene product, Runx2 Type II, to the formation of mineralized tissue, we have generated a Runx2 Type II-LacZ gene replacement mouse model in which the initial coding sequences and splice donor sites of the Type II isoform are replaced with the LacZ reporter gene. Activity of the endogenous P1 promoter can therefore be monitored by β-galactosidase production. Analysis of Runx2 Type II-LacZ mice demonstrates that the P1 promoter is transcriptionally most active in mature osteoblasts, but its product, Runx2 Type II is dispensable for embryonic skeletal formation. Lastly, we examine the link between growth control and osteogenic differentiation by tissue-specific deletion of the Mdm2 proto-oncogene in developing skeletal tissues of the mouse embryo. Loss of Mdm2 results in impaired bone formation, with skeletal elements exhibiting lower bone mineral content and higher porosity. Ex vivo cultures of calvarial osteoprogenitor cells exhibit severely decreased osteoblastogenesis and bone nodule formation accompanied by a failure to activate Runx2 gene activity. These findings suggest that Mdm2 is required for inhibition of p53 activity that ultimately allows for post-confluent proliferation and induction of Runx2 during maturation of the osteogenic phenotype. Taken together, our findings suggest that Runx2 modulates the commitment of progenitor cells to the osteogenic and chondrogenic lineages, and that Runx2 activity is inextricably linked to mechanisms that control cellular proliferation.
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Mei, Hua. "The role of G[alpha]z during muscle differentiation /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20MEI.
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Moore, Carlene Drucilla. "The role of centaurin alpha-1 in the regulation of neuronal differentiation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008d/moore.pdf.
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Jagannathan, Bharadwaj Golbeck John H. "Structure-function studies on iron-sulfur cluster proteins in photosynthetic reaction centers." [University Park, Pa.] : Pennsylvania State University, 2009. http://etda.libraries.psu.edu/theses/approved/WorldWideIndex/ETD-4493/index.html.
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Akache, Bassel Ghassan. "Characterization of a family of yeast transcriptional regulators : the zine cluster proteins." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84458.
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Members of the zinc cluster (or binuclear cluster) protein family are characterized by a Zn(II)Cys6 zinc finger involved in DNA recognition and binding. These fungal proteins are transcriptional regulators of genes involved in a wide variety of cellular processes. One member, Gal4p, is involved in galactose metabolism, while others play a major role in primary and secondary metabolism, control of meiosis, and multidrug resistance. Sequencing of the Saccharomyces cerevisiae genome has revealed that 55 genes encoding putative zinc cluster proteins are present in budding yeast. However, the roles of many of these zinc cluster proteins are unknown. In order to better understand their functions, we have performed a phenotypic analysis of these putative zinc cluster proteins. We have implicated a number of them in a variety of processes in the cell, including multidrug resistance. Stb5p has been shown to be a major player in regulating the expression of multidrug resistance genes. Other zinc cluster activators of multidrug resistance genes include Pdr1p, Pdr3p, and Yrr1p. These regulators of multidrug resistance appear to interact with each other, forming many different sub-populations of homo- and heterodimers. Stb5p is found predominantly as a heterodimer with Pdr1p. It also appears that Pdr1p is a master regulator able to interact with many different partners, enabling it to mediate control over multidrug resistance genes.
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Ramage, Samuel Cowan. "The role of secreted phosphoprotein-24 in osteoblast differentiation and matrix mineralization /." Available online after August 19, 2013, 2007. http://hdl.handle.net/10156/2291.
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Sham, Mai Har. "Regulation of transcription and translation of phloem proteins in cucurbitaceae during differentiation." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329169.
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Tuxworth, Richard Ian. "The control of cell motility and differentiation by Ras pathways." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314227.
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Mansy, Sheref S. "Structure and function of iron-sulfur cluster biosynthesis proteins and the influence of oxygen ligation." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1059664189.
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Thesis (Ph. D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xxi, 250 p.; also includes graphics (some col.) Includes bibliographical references (p. 226-250). Available online via OhioLINK's ETD Center
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Noël, Josée. "Zinc cluster proteins Leu3p and Uga3p recognize highly related but distinct DNA targets." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0029/MQ64417.pdf.
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Duff, Jillian L. C. "Investigations of redox-coupled proton transfer by iron-sulfur cluster systems in proteins." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337785.
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Jiang, Hao. "Molecular analysis of penicillin-binding proteins and a gene cluster in Streptomyces Griseus /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488192960167577.
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Teo, Jia-Ling. "Presenilin-1 and TCF/[beta]-catenin signaling : effects on neuronal differentiation /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9311.
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Parker, Emma. "The role of insulin-like growth factor binding proteins (IGFBPs) in the pathogenesis of pulmonary fibrosis." Thesis, Keele University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269130.
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Malouf, Diana. "Mesenchymal stromal cell differentiation into osteoblasts on modular artificial proteins with bioactive ligands." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28155.
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Modular self-assembling de novo triblock proteins (designated CRC) that contain a central bioactive domain with associating ends allowing preferential formation bundles have been developed. These proteins subsequently self assemble into hydrogel networks. The modularity of these triblock systems allows for different combinations of end and centre domains to modulate cell differentiation and phenotypic changes. In this study, we examined the effect of CRC peptides with bioactive ligands from extracellular matrix proteins involved in differentiation and repair activities, fibronectin (RGDS) and laminin (LQVQ), on mesenchymal stromal cell (MSC) differentiation into osteoblasts.
Briefly, CRCs were covalently surface grafted onto collagen scaffolds via 1-ethyl-3(3-dimethylaminopropyl) carbodiimide hydrochloride (EDC) chemistry. Four peptide combinations tested were: P-CRC, P-CRC-RGDS/CRC, P-CRC-LQVQ/CRC and CRC-RGDS/CRC-LQVQ. They were examined for effects on proliferation and differentiation of MSCs in culture. No significant differences in proliferation rates were observed amongst samples. MSCs grown on CRC alone were unhealthy. All cells cultured on the peptide substrates, except for a combination of CRC-RGDS/CRC-LQVQ, had calcium deposits that were indicators of osteogenic differentiation. Cells grown on CRC/CRC-RGDS substrates showed most differentiation. The combination of RGDS/LQVQ peptides appeared to promote retention of an undifferentiated progenitor cell state.
We have therefore shown that modular, self-assembling peptides have the potential to be useful in modulating differentiation or retention of the stem cell phenotype. With further development, they could possibly be used to develop or enhance biomaterials scaffolds for use in modulating stem cell behaviour in potential therapeutic applications.
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Demir, Özlem. "Functional Characterization of Microtubule Associated Proteins in ES Cell Division and Neuronal Differentiation." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-163103.
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Microtubules are tubular polymers that are involved in a variety of cellular processes such as cell movement, mitosis and intracellular transport. The dynamic behavior of microtubules makes this possible because all of these processes require quick responses. Embryonic stem (ES) cells were first isolated from mouse embryos and they have two unique characteristics; they can be kept undifferentiated for many passages with a stable karyotype and they can be differentiated into any type of cells under appropriate conditions. The pluripotency of ES cells, their ease of manipulation in culture, and their ability to contribute to the mouse germ-line provides us a model of differentiation both in vitro and in vivo. In my thesis I focused on the cell division and neuronal differentiation of ES cells and developed two methods to understand the effects of microtubule dynamics in spindle assembly and chromosome segregation and to reveal the roles of different Microtubule Associated Proteins (MAPs) in the neuronal morphology formation.
In the first part, we developed a live-cell imaging method for ES cells to visualize, track and analyze the single cell behavior in a cell population over a time period. So far many techniques have been adapted and combined for imaging of cell lines, mainly for the cancer or immortalized ones. However, because ES cells are very prone to apoptosis, tend to form spheres and hard to stably label, it is quite tricky to image them in culture conditions. In our system, we combined the BAC-based gene expression with wide-field deconvolution microscopy for ES cells that are plated onto the laminin-511 coated surface and kept in CO2 independent culture conditions. This combined technique does not interfere with the growth of cells and keeps them healthy up to 24 hours on the microscope stage.
In the second part, we analyzed the effects of MAPs chTOG, EB1, Kif18A and MCAK in the overall spindle morphology and mitotic progression in mES cells. For this purpose, we utilized our stable TUBB-GFP and H2A-GFP cell lines along with our live-cell imaging set-up to reveal the effects of the above-mentioned proteins and the interplay among each other. By using RNAi method we either single or co-depleted the genes by siRNAs and measured the spindle length and width in RNAi conditions. We further analyzed the mitotic progression in H2A-GFP cell line in terms of the metaphase timing and the percentage of chromosome segregation errors. Our results showed that, EB1 depletion did not cause any significant changes in the overall spindle morphology or in the metaphase timing. However, the co-depletion of EB1 with chTOG partially rescued the sichTOG specific mini-spindle phenotype. siKif18A produced longer spindles without any change in the spindle width. Surprisingly, the co-depletion of antagonistic chTOG and Kif18A proteins had additive effects on the spindle dynamics and on mitotic progression in a way that spindle assembly was severely disrupted by the absence of these two proteins and as a result of this, both metaphase timing and chromosome missegregation levels increased significantly. These results overall indicate that MAPs have important roles in the regulation of dynamic instability and these proteins have an interplay among each other to be able to control the morphology of the spindle as well as the correct segregation of chromosomes into daughter cells.
In the last part, I will introduce you a new ES cell based differentiation and morphology model, which brings the advantages of high resolution imaging capacity, control over development and easy genetic manipulation and culturing. We have generated Tet-induced shRNA cell lines against chTOG, Kif18A and MCAK, which are also stably expressing TUBB-GFP. These labeled cells were mixed with unlabeled wild-type mES cells before differentiation at 1:1000 ratio and then they were differentiated into mouse cortical cells and spinal motor neurons. Our results showed that, all of the three genes could be successfully knocked-down by shRNA after 48 hours of Tet induction. After mixing the labeled and unlabeled cells, single neurons could be imaged at high resolution and their skeletons could be generated afterwards. The RNAi studies in shchTOG cell line showed that, the knock-down of this gene in early differentiation interferes with the neuronal differentiation.
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Bermeo, Serrato Sandra Milena. "Role of the Proteins of the Nuclear Envelope in Mesenchymal Stem Cell Differentiation." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14373.
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The nuclear envelope (NE) provides stiffness to the nucleus, protects the genome, and regulates the mechanotransduction process via its network of proteins. These roles govern gene transcription and cell survival and/or differentiation. Considering that these proteins transmit cytoplasmic signalling to the nucleus through interactions with transcription factors, the identification and control of these interactions could play an important role in the regulation of cell differentiation and survival. In mesenchymal stem cells (MSCs), it has been demonstrated that NE proteins are crucial to the differentiation process. Mutations in some of them are linked to envelopathies, in which mesenchymal tissues are differentially affected. In addition, during the ageing process, their level is decreased, which would explain in part some of the age-related changes in bone and muscle. Lamin A, emerin and MAN1 are the most studied NE proteins in terms of their involvement in the pathogenesis of envelopathies. In this thesis we hypothesized that these NE proteins are involved in the differentiation of MSCs into bone and fat, playing a role in the pathogenesis of age-related bone loss. Therefore, this research thesis reports new evidence on the role of these three proteins during osteoblastic and adipogenic differentiation of bone marrow-derived human MSCs.
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LA, MASTRA FEDERICA. "POLYCOMB GROUP PROTEINS RING1A/RING1B CONTROL PERIPHERAL B CELL HOMEOSTASIS AND TERMINAL DIFFERENTIATION." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/609574.
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Polycomb Repressive Complex 1 and 2 (PRC1 and PRC2) modulate chromatin accessibility through covalent histone modifications. The ubiquitous expression of PRC1 catalytic subunits throughout B cell development hypothesized roles for PRC1 in B cell physiology. This study aimed to dissect the contribution of PRC1 to peripheral B cell maturation, homeostasis and terminal differentiation. We analyzed mutant mice allowing conditional Cre-dependent inactivation of PRC1 catalytic function starting from late transitional B cells. In response to induced PRC1 inactivation, peripheral B cells in secondary lymphoid organs were reduced in number and displayed alterations in the surface phenotype, which reflected a major disturbance of their transcriptional profile. Reduced fitness of PRC1 mutant resting B cells was associated to heightened sensitivity to pro-apoptotic signals, consequent of the higher levels in these cells of the BIM protein and of the sub-optimal activation of the AKT kinase in response to either BAFF-R or BCR engagement. PRC1 mutant mice displayed major defects in the marginal zone (MZ) B cell subset, both in number and localization. This phenotype correlated with reduced expression of the Sphingosine-1-phosphate receptor-1 (S1pr1), which is crucial for B cell migration to the MZ, and the increased expression of the Polycomb target microRNA mir-125b, which targets S1pr1 transcript. Moreover, PRC1 mutant B cells displayed premature de-repression of Prdm1 gene and facilitated plasma cell differentiation upon lipopolysaccharide stimulation. Our work provides evidence for a crucial role played by PRC1 in peripheral B cell subset differentiation, B cell homeostasis and timing of terminal B cell differentiation.
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Bratt-Leal, Andrés Miguel. "Biomaterial integration within 3D stem cell aggregates for directed differentiation." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/45934.
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The derivation of embryonic stem cells (ESCs) has created an invaluable resource for scientific study and discovery. Further improvement in differentiation protocols is necessary to generate the large number of cells needed for clinical relevance. The goal of this work was to develop a method to incorporate biomaterial microparticles (MPs) within stem cell aggregates and to evaluate their use for local control of the cellular microenvironment for directed differentiation.
The effects of unloaded MPs on ESC differentiation were first determined by controlled incorporation of poly(lactic-co-glycolic acid) (PLGA), agarose and gelatin MPs. Embryoid body (EB) formation, cell viability, and gross morphology were not affected by the presence of the MPs. Further analysis of gene expression and patterns of phenotypic marker expression revealed alterations in the differentiation profile in response to material incorporation. The ability of MPs to direct ESC differentiation was investigated by incorporation of growth factor loaded MPs within EBs. MPs were loaded with bone morphogenetic protein-4 (BMP-4). BMP-4 loaded MPs incorporated within EBs induced mesoderm gene expression while inhibiting expression of an ectoderm marker compared to untreated EBs.
Finally, magnetic MPs (magMPs) were incorporated within EBs to induce magnetic sensitivity. The responsiveness of EBs to applied magnetic fields was controlled by the number of magMPs incorporated within the aggregates. Magnetic guidance was then used to control the precise location of single EBs or populations of EBs for bioreactor culture and for construction of heterogeneous cell constructs. Overall, the results indicated that PSC differentiation within spheroids is sensitive to various types of biomaterials. Incorporation of MPs within EBs can be used to direct ESC differentiation by control of the cellular environment from microscale interactions, by delivery of soluble factors, to macroscale interactions, by control of EB position in static and suspension cultures.
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Gibb, Natalie L. "sfrp 1 promotes myocardial differentiation in Xenopus laevis by inhibiting canonical wnt6 signalling." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=196016.
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Wnt signalling is a key regulator of vertebrate heart development yet the exact requirements of the Wnt signalling components remains unclear. The endogenous Wnt ligand Wnt6 has been identified as a regulator of cardiogenesis required for controlling heart muscle differentiation via canonical Wnt/β-catenin signalling. We show for the first time a requirement for an endogenous Wnt signalling inhibitor for normal heart muscle differentiation. Expression of sfrp1 is strongly induced in differentiating heart muscle. We show that sfrp1 is not only able to promote heart muscle differentiation but is also required for the formation of a normal sized heart muscle in the developing embryo. sfrp1 is functionally able to inhibit Wnt6 signalling and its requirement during heart development relates to relieving the cardiogenesis-restricting function of endogenous wnt6. In turn, we discover that sfrp1 gene expression in the heart is regulated by wnt6 signalling, which for the first time indicates that sfrp genes can function as part of a negative Wnt feedback regulatory loop. Our experiments indicate that sfrp1 controls the size of the differentiating heart muscle primarily by regulating cell fate within the cardiac mesoderm between muscular and non-muscular cell lineages. The cardiac mesoderm is therefore not passively patterned by signals from the surrounding tissue, but regulates its differentiation into muscular and non-muscular tissue using positional information from the surrounding tissue. This regulatory network may ensure that Wnt activation enables expansion and migration of cardiac progenitors, followed by Wnt inhibition permitting cardiomyocyte differentiation.
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Yang, Zhongfa. "The role of GA binding protein (GABP) transcription factor in myeloid differentiation and cell cycle progression /." View online version; access limited to Brown University users, 2005. http://wwwlib.umi.com/dissertations/fullcit/3174701.
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Luong, Mai X. "Involvement of CDP/Cux in the Regulation of Histone H4 Gene Expression, Proliferation and Differentiation: a Dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/34.
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Proliferation and differentiation are essential processes for the growth and development of higher eukaryotic organisms. Regulation of gene expression is essential for control of cell division and differentiation. Normal eukaryotic cells have a limited proliferative capacity, and ultimately undergo cellular senescence and apoptosis. Terminal differentiation of cells is associated with loss of proliferative capacity and acquisition of specialized functions. Proliferation and differentiation are processes required for the creation and maintenance of diverse tissues both during embryonic development and postnatal life. The cell cycle is the process by which cells reproduce, and requires duplication and segregation of hereditary material. Loss of cell cycle control leads to genetic instability and cancer.
Expression of replication-dependent histone genes is tightly coupled to DNA synthesis, thus making histone genes a good model for studying cell cycle regulation. The HiNF-D complex interacts with all five classes (H1, H2A, H2B, H3 and H4) of histone genes in a cell cycle-dependent manner. The CCAAT displacement protein (CDP)/Cux and the tumor suppressor pRB are key components of the HiNF-D complex. However, the molecular interactions that enable CDP/Cux and pRB to form a complex and thus convey cell growth regulatory information onto histone gene promoters are poorly understood. Transient transfection assays show that CDP/Cux represses the histone H4 promoter and that the pRB large pocket domain functions with CDP/Cux as a co-repressor. Direct interaction between CDP/Cux C-terminus and the pRB pocket domain was observed in GST pull-down assays. Furthermore, co-immunoprecipitation assays and immunofluorescence microscopy established that CDP/Cux and pRB form complexes in vivo and associate in situ. pRB interaction and co-repression with CDP/Cux is independent of pRB phosphosphorylation sites, as revealed by GST pull-down assays and transient transfection assays using a series of pRB mutant proteins. Thus, several converging lines of evidence indicate that complexes between CDP/Cux and pRB repress cell cycle-regulated histone gene promoters.
CDP/Cux is regulated by phosphorylation and acetylation at the C-terminus, which contains two repressor domains and interacts with histone deacetylase HDAC1. In vivo function of the CDP/Cux C-terminus in development and gene regulation was assessed in genetically targeted mice (Cutl1tm2Ejn, referred to as Cutl1ΔC). The mice express a mutant CDP/Cux protein with a deletion of the C-terminus including the homeodomain. Indirect immunofluorescence microscopy showed that the mutant protein exhibited significantly reduced nuclear localization in comparison to the wildtype protein. Consistent with these data, DNA binding activity of HiNF-D was lost in nuclear extracts derived from mouse embryonic fibroblasts (MEFs) or adult tissues of homozygous mutant (Cutl1 ΔC -/-) mice, indicating the functional loss of CDP/Cux in the nucleus. No significant difference in growth characteristics or total histone H4 mRNA levels was observed between wildtype and Cutl1 ΔC -/- MEFs in culture. However, the histone H4.1 (murine FO108) gene containing CDP/Cux binding sites have reduced expression levels in homozygous mutant MEFs. Stringent control of growth and differentiation appears to be compromised in vivo. Homozygous mutant mice exhibit stunted growth (20-50% weight reduction), a high postnatal death rate of 60-70%, sparse abnormal coat hair and severely reduced fertility. Hair follicle deformities and severely diminished fertility in Cutl1 ΔC -/- mice suggest that CDP/Cux is required for normal development of dermal tissues and reproductive functions. Together the data presented in this dissertation provide new insight into the in vivo functions of CDP/Cux in the regulation of histone gene expression, growth control and differentiation.
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Squillace, Rachel Marguerite. "Inhibition of muscle differentiation by the novel muscleblind-related protein CHCR /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/15468.
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Fernandez, Cristina Carmen. "Biochemical analysis of the role of the truncated HOXA1 transcript in cell differentiation /." Access full-text from WCMC:, 2008. http://proquest.umi.com/pqdweb?did=1432806151&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Young, Teresa Marie. "Statistical thermodynamics of cluster formation in dilute colloidal and coarse-grained protein solutions." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 206 p, 2010. http://proquest.umi.com/pqdweb?did=1997524011&sid=2&Fmt=2&clientId=8331&RQT=309&VName=PQD.
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Paquette, Benoit F. "SMN is required for dynamic relocalization of methylated nucleolar proteins during skeletal muscle differentiation." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/28012.
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Deletions or loss-of-function mutations in the Survival of Motor Neuron 1 (Smn1) gene in humans is responsible for Spinal Muscular Atrophy (SMA), one of the leading genetic causes of infant mortality. The pathological hallmarks of this disease include the degeneration of lower motor neurons in the anterior horn of the spinal cord, weakness, paralysis and atrophy of the associated skeletal muscles and eventually of the entire trunk, often times causing respiratory failure and early death during disease progression. Although current knowledge supports the notion that this disease arises from the massive motoneuron loss early in development, mounting evidence suggests that intrinsic muscle defects may also contribute to the pathology. Arginine methylation is also known to be important for normal skeletal muscle differentiation. Since SMN can serve as an adaptor module for arginine methylated proteins, we speculated that SMN will perform its function in skeletal muscle by promoting methyl-dependent interactions.
This study has documented a dynamic profile of proteins containing methylated arginines during myoblast differentiation, and that this dynamic profile is dependent on the presence of SMN. Furthermore, I have identified Fibrillarin, a snoRNP component, as one of the methylated proteins that is misregulated in the absence of SMN. Finally, I have also shown that the profile of arginine methylated proteins differs between skeletal muscles from wild type mice and a mouse model of SMA. Taken together, these results represent a novel defect in SMA and provide evidence for the importance of skeletal muscle tissue in this disease.
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Pollett, Jonathan Barclay. "The role of the PAR proteins, HLF and DBP, in transactivation and liver differentiation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28247.pdf.
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