Дисертації з теми "LIM Protein"
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Schwartz, Christine. "Muscle LIM protein and Nesprin-1 in Mechanotransduction." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066374/document.
Повний текст джерелаI studied three striated muscle proteins that are participating in two different pathways of mechanotransduction, which is the translation of a physical stimulus into a biochemical signal.When isolated cardiomyocytes are stretched in 2D, MLP shuttles to the nucleus. Without shuttling MLP, these cells fail to respond to the stretch stimulus. Human patients with MLP-mutations develop cardiomyopathies, as well as mice with a knock-out of MLP (MLP-/-). By expressing mutated MLP in neonatal cardiomyocytes of MLP-/- mice, I wanted to elucidate the role of mutant MLP. Surprisingly, MLP did shuttle after stretching of 2D but not 3D cell cultures. Although I could not solve this issue, I prepared the setup for subsequent experiments.Nesprins are part of the nuclear envelope (NE) spanning LINC complex, which connects the cytoskeleton with the nucleus. Myoblasts from patients with mutations in Nesprins or LINC-associated Lamins displayed deformed nuclei and had defects in mechanosensitive responses with an elevated level of stress fibers and focal adhesions on soft surfaces. This phenotype could be rescued by knock-down of formin FHOD1, a downstream target of ROCK and SRC, which also were highly active in the mutant cells. While mutations in Nesprins and Lamins are thought to lead to mechanical instability of the NE, these results indicate that signaling pathways through the NE are disturbed as well
Smith, Ngaio Charlotte. "Investigating the role of protein-protein and protein-DNA interactions in the function of Isl1." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20655.
Повний текст джерелаSchwartz, Christine [Verfasser]. "Muscle LIM Protein and Nesprin-1 in Mechanotransduction / Christine Schwartz." Berlin : Freie Universität Berlin, 2017. http://d-nb.info/112815062X/34.
Повний текст джерелаTaniguchi, Yoshihito. "LIM protein KyoT2 negatively regulates transcription by association with the RBP-J DNA-binding protein." Kyoto University, 1998. http://hdl.handle.net/2433/182239.
Повний текст джерелаDiefenbacher, Markus Elmar. "The transcriptional co-activator function of the LIM-domain protein nTrip6." Eggenstein-Leopoldshafen Forschungszentrum Karlsruhe GmbH, 2010. http://d-nb.info/1002907535/34.
Повний текст джерелаRobertson, Neil. "Development and application of simple FRET-based methods for aggregation-prone LIM domain interactions." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/16912.
Повний текст джерелаHan, Li. "G protein coupled receptor signaling to phospholipase D1 mediated by G12 type G proteins, LIM kinase and cofilin." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968929923.
Повний текст джерелаLorenzen-Schmidt, Ilka. "The role of cytoskeletal LIM protein deficiency in the development of dilated cardiomyopathy /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3099547.
Повний текст джерелаKhurana, Bharat. "Characterization of DLIM1, a novel cytoskeleton-associated LIM domain containing protein of Dictyostelium discoideum." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961945737.
Повний текст джерелаDiefenbacher, Markus Elmar [Verfasser]. "The transcriptional co-activator function of the LIM-domain protein nTrip6 / Markus Elmar Diefenbacher." Eggenstein-Leopoldshafen : Forschungszentrum Karlsruhe GmbH, 2010. http://d-nb.info/1002907535/34.
Повний текст джерелаProeschel, Christoph Johann Wolfgang. "The cloning and characterisation of Lnk-1 : a novel LIM-domain containing protein kinase." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294778.
Повний текст джерелаLevin, Evgeny [Verfasser], Dietmar [Akademischer Betreuer] Fischer, and Hermann [Gutachter] Aberle. "Muscle Lim Protein in naïve and injured neurons / Evgeny Levin ; Gutachter: Hermann Aberle ; Betreuer: Dietmar Fischer." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/114137854X/34.
Повний текст джерелаBaron, Kyla Doreen. "The Role of LMO4 in the Regulation of SLK Localization & Activation within Migrating Cells and in Murine Mammary Tumorigenesis." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34195.
Повний текст джерелаDiefenbacher, Markus Elmar [Verfasser], and A. [Akademischer Betreuer] Cato. "The transcriptional co-activator function of the LIM-domain protein nTrip6 / Markus Elmar Diefenbacher. Betreuer: A. Cato." Karlsruhe : KIT-Bibliothek, 2009. http://d-nb.info/1014222877/34.
Повний текст джерелаWang, Hui. "The Roles of a LIM Domain Protein, Hic-5/ARA55, in TGF-β Signaling in Prostate Cancer Cells". Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1220931692.
Повний текст джерелаBanthien, Nils [Verfasser]. "The four-and-a-half-LIM-domain Protein FHL2 is a novel regulator of pulmonary fibrosis / Nils Banthien." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1216142955/34.
Повний текст джерелаGehmlich, Katja. "Strukturen der Kraftübertragung im quergestreiften Muskel : Protein-Protein-Wechselwirkungen und Regulationsmechanismen." Phd thesis, Universität Potsdam, 2004. http://opus.kobv.de/ubp/volltexte/2005/257/.
Повний текст джерелаEs ließ sich zeigen, dass sich die Morphologie der Zell-Matrix-Kontakte während der Differenzierung von Skelettmuskelzellen dramatisch ändert, was mit einer veränderten Proteinzusammensetzung einhergeht. Immunfluoreszenz-Analysen von Skelettmuskelzellen verschiedener Differenzierungsstadien implizieren, dass die Signalwege, welche die Dynamik der Fokalkontakte in Nichtmuskelzellen bestimmen, nur für frühe Stadien der Muskeldifferenzierung Relevanz haben können. Ausgehend von diesem Befund wurde begonnen, noch unbekannte Signalwege zu identifizieren, welche die Ausbildung von Costameren kontrollieren: In den Vorläuferstrukturen der Costamere gelang es, eine transiente Interaktion der Proteine Paxillin und Ponsin zu identifizieren. Biochemische Untersuchungen legen nahe, dass Ponsin über eine Skelettmuskel-spezifische Insertion im Carboxyterminus das Adapterprotein Nck2 in diesen Komplex rekrutiert. Es wird vorgeschlagen, dass die drei Proteine einen ternären Signalkomplex bilden, der die Umbauvorgänge der Zell-Matrix-Kontakte kontrolliert und dessen Aktivität von mitogen activated protein kinases (MAPK) reguliert wird.
Die Anpassungsvorgänge der Strukturen der Kraftübertragung an pathologische Situtation (Kardiomyopathien) in der adulten quergestreiften Muskulatur wurden ausgehend von einem zweiten Protein, dem muscle LIM protein (MLP), untersucht. Es konnte gezeigt werden, dass ein mutiertes MLP-Protein, das im Menschen eine hypertrophe Kardiomyopathie (HCM) auslöst, strukturelle Defekte aufweist und weniger stabil ist. Weiterhin zeigte dieses mutierte Protein eine verringerte Bindungsfähigkeit an die beiden Liganden N-RAP und alpha-Actinin. Die molekulare Grundlage der HCM-verursachenden Mutationen im MLP-Gen könnte folglich eine Veränderung der Homöostase im ternären Komplex MLP – N-RAP – alpha-Actinin sein. Die Expressionsdaten eines neu generierten monoklonalen MLP-Antikörpers deuten darauf hin, dass die Funktionen des MLP nicht nur für die Integrität des Myokards, sondern auch für die der Skelettmuskulatur notwendig sind.
The cell-matrix-contacts (costameres) and cell-cell-contacts (intercalated discs of cardiomyocytes) of cross-striated muscle cells transmit mechanical forces to the exterior. On top of this mechanical function, both structures have been implied to be involved in signal transduction processes.
Dramatic morphological changes in the overall structure of cell-matrix-contacts of skeletal muscle cells were revealed during differentiation. Moreover, this reorganisation was accompanied by alterations in protein composition. Immunofluorescence microscopy indicated that signalling pathways which control the dynamics of focal contacts in non-muscle cells seem to be important only for early differentiation stages of skeletal muscle cells. To explore novel signalling pathways involved in regulating the formation of costameres, signalling molecules engaged were identified. Thus, paxillin and ponsin transiently interact at the precursors of costameres during muscle development. In addition, biochemical data indicate that a skeletal muscle specific module in the carboxyterminal part of ponsin can recruit the adapter protein Nck2 to this complex. Hence, the three proteins might form a ternary signalling complex involved in controlling the reorganisation of cell-matrix-contacts. Apparently, the activity of this signalling complex is regulated by mitogen activated protein kinases (MAPK).
A second approach has focussed on adaptational processes of the same structures observed in pathological situations. In particular, the role of muscle LIM protein (MLP) in hypertrophic cardiomyopathy (HCM) was investigated. It was shown that a HCM-causing mutant MLP protein fails to fold properly and that the consequent loss of stability is reflected in altered binding properties: the mutant MLP protein shows decreased binding to both N-RAP and alpha-actinin. Hence, the molecular basis for HCM-causing mutations in the MLP gene might be an altered homeostasis of the ternary complex MLP – N-RAP – alpha-actinin. Increasing evidence indicates that the functions of MLP are required not only for the integrity of the myocardium. In addition, MLP seems to have regulatory functions in skeletal muscle tissues.
Raskin, Anna Maria. "Four and half LIM Domain-1 protein and its role in passive mechanics and hypertrophic signaling of the heart." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3320727.
Повний текст джерелаTitle from first page of PDF file (viewed October 3, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Klingberg, Rebecca [Verfasser]. "Quantitative Proteomanalyse der Bindeproteine von Histon H3 und dem Four-and-a-Half-LIM-3-(FHL3)-Protein / Rebecca Klingberg." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1027151531/34.
Повний текст джерелаKönig, Katharina [Verfasser]. "The role of Four-and-a-half LIM domain protein 2 in dendritic cell migration / Katharina König. Mathematisch-Naturwissenschaftliche Fakultät." Bonn : Universitäts- und Landesbibliothek Bonn, 2011. http://d-nb.info/1018829962/34.
Повний текст джерелаAbdel, Salam Ibrahim Mohamed Sherine. "A duo implication of miR-134 microRNA and LIM Kinase1 protein in neuropathic pain modulation of the rat spinal cord." Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR21932/document.
Повний текст джерелаPains having a neuropathic origin following CNS or PNS traumatic injury are particularly difficult to treat using the actually available therapeutic means. It is thus necessary to identify new therapeutic strategies. Hence, our aim was to define the mechanisms implicated in these neuropathic pains. Nervous lesions are characterised by an anatomical reorganization of the neuronal network of the dorsal horn. Neurochemical alterations are also involved. Some of the molecular mechanisms underlying the neuronal plasticity (a main feature of neuropathic pain) have been emphasized here by a variety of complementary technical approaches. LIMK1 is one of the possible actors of this reorganization. Among this protein’s known functions, and the most characterized is the phosphorylation of a family of proteins known as cofilins. Their phosphorylation induces the reorganization of actin cytoskeleton. Recently, it has been shown that a miR-134 miRNA regulates LIMK1 expression by binding to the LIMK1 messenger, inhibiting its translation into physiologically active protein. Our hypothesis is that LIMK1 regulation by miR-134 might play an essential role in pain sensitization by modulating neuron neurochemical reorganization and the associated functional neuronal plasticity. Firstly, by means of IHC and ISH, we studied miR-134/LIMK1 distribution within the dorsal horn of the spinal cord in sham animal (control group) and in neuropathic pain model (SNL model). Important to note here that ISH is a known detection method recently identified to visualize miRNA. Different protocols of ISH were discussed in a part of this thesis. ISH showed a decrease in miR-134 expression in SNL rats concomitantly with an increase in LIMK1 illustrated by IHC. This finding has been confirmed by qRT-PCR techniques. Afterward, in order to check for the possible behavioural-induced changes of miR-134 and LIMK1. We intrathecally injected an anti-LIMK1 siRNA to inhibit endogenous LIMK1 expression in SNL rats. Interestingly no significant changes in pain behaviour have been observed. Artificial overexpression of miR-134 using a PremiR-134, showed the same effect. Then we tried to perform the same injections on sham rats, and more interestingly, siRNA LIMK1 and premiR-134 evoked pain hypersensitivity in shams rats. This was illustrated by means of two behaviour tests; Von Frey (VF) and the Dynamic Weight bearing (DWB). To explore the reverse effect, we inhibited miR-134 using a specific KD probe in SNL rats; unexpectedly a significant decrease in pain withdrawal threshold was observed with VF and DWB. qRT-PCR in most cases confirmed the in vivo correlation between miR-134 and LIMK1. Finally, we searched for the possible mechanism of action that could regulate this modulation. Recent published data showed an involvement of ADF/cofilin on AMPAR trafficking. In line with the above mentioned findings, miR-134 KD transfection showed a decrease in AMPAR addressed to the plasma membrane. Altogether suggest that the antinociceptive effect of miR-134 KD and LIMK1 overexpression are mediated by AMPAR insertion at the plasma membrane. It seems that miR-134 exerts a different effect on neuropathic pain than miR-103 another miRNA discussed within the frame of this thesis. MiR-103 has been proved to regulate multiple targets, the three subunits forming Cav1.2 LTC. Pain sensitization involves Cav1.2 activation which consequently alters gene expression during this form of plasticity. MiR-103 was found downregulated also in the SNL model. Conversely to miR-134, overexpression of miR-103 partially alleviates pain. It decreases pain withdrawal threshold of the Von Frey test. Unlike miR-134, miR-103 exerts a pronociceptive role during neuropathic pain
Braach, Martin [Verfasser], Harald [Akademischer Betreuer] Kögler, Gerd [Akademischer Betreuer] Hasenfuß, Ali [Akademischer Betreuer] El-Armouche, and Martin [Akademischer Betreuer] Oppermann. "Modifikation des Hypertrophie-Phänotyps der Myosin-Bindungs-Protein-C defizienten Maus durch Muscle-LIM-Protein / Martin Braach. Gutachter: Gerd Hasenfuß ; Ali El-Armouche ; Martin Oppermann. Betreuer: Harald Kögler." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/104399680X/34.
Повний текст джерелаHeilbock, Christine. "Das Lim-Domänen-Protein Trip6 ist essentiell für den Crosstalk der Transkriptionsfaktoren GR, AP-1 und NF-kB [NF-kappa-B]." Karlsruhe : FZKA, 2005. http://bibliothek.fzk.de/zb/berichte/FZKA7108.pdf.
Повний текст джерелаDu, Xiaojuan. "A four-and-a-half LIM protein FHL2 acts as a coactivator for the Wilms' tumor suppressor WT1 during gonadal differentiation." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963843095.
Повний текст джерелаBeltrami, Alessandra [Verfasser]. "Structural and functional analysis of cGMP dependent protein kinase I (cGKI) and LIM kinase 1 (LIMK1) engaged in BMP signaling crosstalk / Alessandra Beltrami." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/102781607X/34.
Повний текст джерелаSchnittger, Josef [Verfasser]. "Characterization of a novel interaction between four-and-a-half-LIM domains 2 and cardiomyopathy-associated protein 5 in cardiac myocytes / Josef Schnittger." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2019. http://nbn-resolving.de/urn:nbn:de:gbv:18-ediss-87981.
Повний текст джерелаAlnajar, Abdulaleem [Verfasser], and Viktor [Akademischer Betreuer] Wixler. "The role of the Four and a half LIM only protein 2 (FHL2) in bleomycin induced lung fibrosis / Abdulaleem Alnajar ; Betreuer: Viktor Wixler." Münster : Universitäts- und Landesbibliothek Münster, 2013. http://d-nb.info/1141383721/34.
Повний текст джерелаPašalić, Zlatana. "The four and a half LIM domain protein 2 (FHL2) interacts with CALM and is highly expressed in acute myeloid leukemia (AML) with complex aberrant karyotypes." kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/10582/.
Повний текст джерелаPasalic, Zlatana. "The four and a half LIM domain protein 2 (FHL2) interacts with CALM and is highly expressed in acute myeloid leukemia (AML) with complex aberrant karyotypes." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-105825.
Повний текст джерелаHeilbock, Christine [Verfasser]. "Das Lim-Domänen-Protein Trip6 ist essentiell für den Crosstalk der Transkriptionsfaktoren GR, AP-1 und NF-κB [NF-kappa-B] / Forschungszentrum Karlsruhe GmbH, Karlsruhe. Christine Heilbock". Karlsruhe : FZKA, 2005. http://d-nb.info/976406365/34.
Повний текст джерелаGupta, Shuchi [Verfasser], and Bernhard [Akademischer Betreuer] Nieswandt. "The role of the Canonical transient receptor potential 6 (TRPC6) channel and the C terminal LIM domain protein of 36 kDa (CLP36) for platelet function / Shuchi Gupta. Betreuer: Bernhard Nieswandt." Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://d-nb.info/1043906622/34.
Повний текст джерелаNelson, Heather M. "Protein rich extruded snack foods using hydrolyzed proteins." Online version, 2003. http://www.uwstout.edu/lib/thesis/2003/2003nelsonh.pdf.
Повний текст джерелаTuladhar, Kapil. "Lim-only domain proteins in developmental haematopoiesis." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:d6b73e89-7095-402f-9d9f-4d7837a4db00.
Повний текст джерелаHutchinson, Sarah Ann. "The role of LIM homeodomain proteins in zebrafish motoneuron development /." view abstract or download file of text, 2005. http://wwwlib.umi.com/cr/uoregon/fullcit?p3201682.
Повний текст джерелаTypescript. Includes vita and abstract. Includes bibliographical references (leaves 96-103). Also available for download via the World Wide Web; free to University of Oregon users.
Bauer, Kristin. "Zellbiologische Charakterisierung des PDZ- und LIM-Domäne Proteins CLP-36." Diss., lmu, 2000. http://nbn-resolving.de/urn:nbn:de:bvb:19-1932.
Повний текст джерелаGu, Wenchao. "Exploring the roles of LIM domain binding proteins in zebrafish development." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:54f520f6-170a-480a-a195-1a0739055031.
Повний текст джерелаKlaavuniemi, T. (Tuula). "PDZ-LIM domain proteins and α-actinin at the muscle Z-disk". Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514282647.
Повний текст джерелаYang, Chih-Chin. "Identification and characterization of proteins that interact with myocyte enhancer factor 2, E12, and smooth muscle LIM proteins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0023/NQ49928.pdf.
Повний текст джерелаMUNDEL, CHRISTOPHE. "Etude de wlim-1, une proteine a domaines lim de tournesol (helianthus annuus l. )." Université Louis Pasteur (Strasbourg) (1971-2008), 1999. http://www.theses.fr/1999STR13024.
Повний текст джерелаLiu, Sunbin. "Investigation of protein-protein interactions within the human spliceosomal U4/U6.U5 tri-snRNP particle." Doctoral thesis, [S.l.] : [s.n.], 2005. http://webdoc.sub.gwdg.de/diss/2005/liu/liu.pdf.
Повний текст джерелаForbes-Robertson, Sarah Anne Natasha. "Structure and expression of the chicken bone morphogenetic protein-2 gene." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244093.
Повний текст джерелаBreyer, Tobias. "Untersuchung des kardialen LIM-Domänen-Proteins FHL2 im menschlichen Myokard Rolle von FHL2 bei der Herzinsuffizienz /." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961237643.
Повний текст джерелаPapuga, Jessica. "Role of the Arabidopsis LIM proteins in the regulation of the actin cytoskeleton organisation and dynamics." Strasbourg, 2011. http://www.theses.fr/2011STRA6022.
Повний текст джерелаActin cytoskeleton organisation and dynamics are regulated by different types of actin-binding proteins. Recently, novel actin filament crosslinkers involved in the formation of parallel bundles have been characterized in both plants and animals: the two LIM domain-containing (LIM) proteins. In plants, these proteins can be divided into two sub-families whose members differ in their expression pattern. The WLIM sub-family members are widely expressed in vegetative tissues (WLIMs) whereas the PLIM subfamily members (PLIMs) are highly and almost exclusively expressed in pollen grains. An important question that remained to be answered is: why do plants have several proteins of this family and are the different members functionally distinct, or do they share one or several functions? To address these issues, we characterised and compared the actin regulatory activities of all six LIM proteins from Arabidopsis. Confocal analyses of transgenic Arabidopsis plants expressing individual GFP- fused LIM proteins and in vitro biochemical assays demonstrate that all the Arabidopsis LIM proteins are “true” actin-binding proteins able to directly interact with the actin cytoskeleton. In addition, all six Arabidopsis LIM proteins retain the ability to stabilize actin filaments and to trigger the formation of thick actin bundles in vitro as well as in transgenic LIM-expressing plants. Interestingly, in vitro investigations suggest that the members of WLIM and PLIM subfamilies are differentially regulated. Indeed, only PLIM respond to changes in pH and [Ca2+]. Whereas the modification of these parameters has no significant effects on WLIM activities, an increase of pH or [Ca2+] markedly inhibits PLIM activities. These data are strongly supported by live cell experiments in which we artificially modulated the cytoplasmic pH and [Ca2+] of cells derived from the transgenic LIM-overexpressing plants. The C-terminal domain of PLIMs has been identified as necessary for their regulation by pH and Ca2+
Zhang, Xiyuan. "The expression of human leukemia inhibitory factor in Pichia pastoris." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29919.
Повний текст джерелаPinto, Belinda Sophia Geyer Pamela Kent. "Understanding the role of LEM domain proteins in Drosophila development." [Iowa City, Iowa] : University of Iowa, 2009. http://ir.uiowa.edu/etd/421.
Повний текст джерелаPinto, Belinda Sophia. "Understanding the role of LEM domain proteins in Drosophila development." Diss., University of Iowa, 2009. https://ir.uiowa.edu/etd/421.
Повний текст джерелаCrompton, Leslie Alan. "Acute nutritional signals in the control of hind-limb protein turnover in lambs in vivo." Thesis, University of Reading, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281367.
Повний текст джерелаShanmugasundaram, Mathura. "Gene and protein interactions in limb development : the case of Msx and Gli3." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066279/document.
Повний текст джерелаThe vertebrate limb is a paradigmatic model for morphogenesis. The anteroposterior (AP) growth and patterning of the limb bud rely on an intricate regulatory genetic network involving many genetic players such Shh and Gli3. Shh is produced in the posterior region of the limb mesoderm and acts as a morphogen along the AP axis. It regulates both digit number and identity of different AP positions. As the main function of Shh is to prevent proteolysis of Gli3FL into Gli3R, Gli3R concentrates anteriorly which is also where apoptosis takes place. In the mouse, paradoxically, despite a quasi-symmetrical expression profile, Msx1/2 null mutants show systematic anterior defects with an overgrowth in the anterior limb domain, resulting in anterior polydactyly. Both Gli3 and Msx mutant limb defects are concentrated anteriorly in a similar fashion suggesting an interaction between these genes and a possible role of this interaction in AP patterning in the limb bud as well as dysregulation of apoptosis. Indeed, we demonstrate interactions between Msx and Gli3 genes and even proteins. Mutations of Msx and Gli3 result in anterior polydactylous phenotypes and a similar loss of anterior apoptosis. This morphological analysis is associated with a search for common Gli3 and Msx transcriptional targets and partners in an attempt to link gene activity with changes in cell physiology that underlie morphogenesis. We have performed a differential transcriptome (RNA-Seq) on whole limb buds of Msx1-/-Msx2 narrowing down on a number of potential common targets of Gli3 and Msx. We demonstrate that Msx and Gli3 work together in regulating the AP axis of limb development, independent of Shh
Haines, Bryan Peter. "Alternate transcription and translation of the LIF gene produces a novel intracellular protein /." Title page, contents and summary only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phh1518.pdf.
Повний текст джерелаBridge, Katherine S. "Regulation of HIF-l and the hypoxic response by the tumour suppressor LIMDl and LIM domains-containing proteins." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606229.
Повний текст джерела