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Data publikacji: 6 września 2023

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1

Schwartz, Christine. "Muscle LIM protein and Nesprin-1 in Mechanotransduction". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066374/document.

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J’ai étudié trois protéines qui participent à deux vois différentes de méchano-transduction qui est la conversion des stimuli physiques en un signal biochimique.Dans une culture cellulaire en 2D, lorsque les cardiomyocytes sont étirés, MLP est transloqué vers le noyau. Sans translocation, les cellules ne parviennent pas à répondre à la stimulation. Les patients porteurs de mutations dans MLP développent une cardiomyopathie comme les souris MLP knock-out (MLP-/-). Mon objectif a été d’élucider le rôle de MLP dans ces cardiomyopathies en surexprimant des mutations de MLP dans les cardiomyocytes isolés des souris MLP-/- néonataux. Dans les cultures 2D mais pas 3D, MLP n’était pas transloqué vers le noyau après l’étirement des cellules. Bien que je n’aie pas pu résoudre ce problème, j’ai mis au point les expériences nécessaires à la poursuite de ce projet.Nesprins s’intègrent dans un complexe transmembranaire de l’enveloppe nucléaire (EN), le LINC complexe, qui connecte le cytosquelette à l’intérieur du noyau. Les myoblastes isolés des patients porteurs des mutations de Nesprin ou de Lamin, qui est associé au LINC complexe, ont présenté des noyaux déformés ainsi que des anomalies de réponses méchanosensibles : Si cultivées sur supports mous, les cellules affichaient un niveau élevé de fibres musculaires stressées et d’adhésions focales. Le knock-down de FHOD, une cible en aval de ROCK et SRC, qui également étaient actives dans ces myoblastes, a réduit ce phénotype. Bien que l’on ait émis l’hypothèse que les mutations dans Nesprins et Lamins conduisent à une instabilité mécanique de l’EN, ces résultats indiquent que les voies de signalisation par l’EN sont perturbées aussi
I 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
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2

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.

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LIM-homeodomain (LIM-HD) transcription factors act as key developmental regulators, through their ability to both bind DNA through homeodomain-DNA interactions, and to form larger complexes through protein-protein interactions. Many interactions that have been characterised are formed using their LIM domains, but likely also involve other regions, which have not yet been described for many LIM-HD proteins. The LIM-HD protein Isl1 has been implicated in the development of many tissues. However, relatively little detail is known about how Isl1 functions in these systems and the pathways in which it acts. The first part of this thesis aimed to identify and characterise novel binding partners for Isl1. An earlier project isolated ~180 potential binding partners through use of yeast two-hybrid mating screens; throughout this thesis further methodology was developed to identify additional proteins in a medium throughput manner. Validation protocols were then applied to determine which interactors were likely to represent biologically relevant interaction partners for Isl1. The second part of this thesis focussed on the mechanisms by which Isl1 and Lhx3 direct cell fate determination in the developing central nervous system. These proteins, along with Ldb1, interact via LIM:LID interactions to form cell-specific transcriptional complexes that target genes different to those targeted by either LIM-HD protein alone. It was not known if the homeodomains target these different sites solely because of the LIM:LID interactions or if the homeodomains themselves bind cooperatively to DNA. The DNA-binding behaviour of various iterations of the Lhx3/Isl1/Ldb1 complex are described, and structural characterisation of the Isl1/Lhx3 DNA-binding unit has been pursued. These data provide new insights into the mechanisms by which Isl1 and Lhx3 work together in regulating gene expression.
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3

Schwartz, Christine [Verfasser]. "Muscle LIM Protein and Nesprin-1 in Mechanotransduction / Christine Schwartz". Berlin : Freie Universität Berlin, 2017. http://d-nb.info/112815062X/34.

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4

Taniguchi, 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.

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5

Diefenbacher, 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.

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6

Robertson, 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.

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LIM-only (LMO) and LIM-homeodomain (LIM-HD) proteins are important mediators of cell specification, proliferation and differentiation. These transcription factors all contain two tandem LIM domains (LIM1+2), which are non-classical zinc finger motifs that mediate protein-protein interactions. Many co-factors of these proteins contain LIM interacting domains (LIDs). The LID is a ~30-residue intrinsically disordered region (IDR) that folds upon binding to LIM1+2 domains. LID:LIM1+2 interactions and the competition established through different combinations of different binding partners play an important role in neural development and breast cancer. The ability to estimate affinities for these interactions would help provide mechanistic insight into LMO and LIM-HD complex formation and regulation. However, the propensity of LIM1+2 domains from LMO/LIM-HD proteins to aggregate and precipitate during recombinant protein production have made it difficult to measure binding affinities for LID:LIM1+2 interactions. This thesis outlines the design, optimisation and application of a series of Förster Resonance Energy Transfer (FRET)-based approaches to study LID:LIM1+2 interactions. LIM1+2 aggregation is prevented by tethering the domains to a LID using a flexible polypeptide linker. The interacting domains are in turn fused to fluorescent proteins that are optimised for FRET. Specific proteolytic cleavage of the linker allows equilibrium binding constants and dissociation rates to be determined using homologous competition and dilution-based approaches. Through the application of these simple FRET-based binding methods, this thesis reveals previously unappreciated and unknown properties of LMO and LIM-HD proteins. This work provides tools for studying other aggregation-prone proteins, as well as general implications for the activity of transcription factors and IDR interactions.
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7

Han, 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.

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8

Lorenzen-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.

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9

Khurana, 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.

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10

Diefenbacher, 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.

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11

Proeschel, 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.

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12

Levin, Evgeny [Verfasser], Dietmar [Akademischer Betreuer] Fischer i 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.

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13

Baron, 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.

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The Ste20-like kinase SLK plays a pivotal role in cell migration and focal adhesion turnover. SLK activity is regulated by the LIM domain-binding proteins Ldb1/2. In addition to playing role in tumor initiation and progression, these proteins have been demonstrated to interact with LMO4. Therefore, this project assessed the ability of LMO4 to interact and regulate SLK activity. Results show that LMO4 can directly bind to SLK and activate its kinase activity. LMO4 can be co-precipitated with SLK following the induction of cell migration by scratch wounding. Cre deletion of LMO4 inhibits cell migration and SLK activation, and impairs Ldb1 and SLK recruitment to the leading edge of migrating cells. Src/Yes/Fyn-deficient cells (SYF) express very low levels of LMO4 and do not recruit SLK to the leading edge. Src-family kinase inhibition impairs SLK recruitment to the leading edge, suggesting that both expression of LMO4 and the recruitment of SLK to the leading edge require c-Src activity. In conclusion, cell migration and activation of SLK requires its recruitment to the leading edge by LMO4 in a Src-dependent manner. This study also investigated whether LMO4 deletion through MMTV-Cre-driven excision would impair mammary tumorigenesis in a PyMT mouse model of breast cancer. No difference in Overall Survival was observed between animals with and without LMO4 expression. Western blot analysis and IHC showed that tumors expressed LMO4 protein in animals genotyped as Cre-positive. This result suggests that expression of LMO4 is required for tumor initiation in the PyMT model of murine mammary carcinoma. This project has established a novel cytosolic role for the transcriptional co-activator LMO4 and validated it’s involvement in the regulation of SLK and cell migration. This pathway may provide a novel therapeutic strategy as LMO4 appears to be critical to the initiation and progression of breast cancer.
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14

Diefenbacher, Markus Elmar [Verfasser], i 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.

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15

Wang, 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.

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16

Banthien, Nils [Verfasser]. "The four-and-a-half-LIM-domain Protein FHL2 is a novel regulator of pulmonary fibrosis / Nils Banthien". Gieߟen : Universitätsbibliothek, 2020. http://d-nb.info/1216142955/34.

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17

Gehmlich, 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/.

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Im Mittelpunkt dieser Arbeit standen Signaltransduktionsprozesse in den Strukturen der Kraftübertragung quergestreifter Muskelzellen, d. h. in den Costameren (Zell-Matrix-Kontakten) und den Glanzstreifen (Zell-Zell-Kontakten der Kardiomyozyten).

Es 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.
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18

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.

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Thesis (Ph. D.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed October 3, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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19

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.

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20

König, 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.

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21

Abdel, 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.

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Les douleurs neuropathiques ayant une origine à la suite de blessures traumatiques du SNC ou du SNP sont particulièrement difficiles à traiter en utilisant les moyens thérapeutiques actuellement disponibles. Il est donc nécessaire d'identifier de nouvelles stratégies thérapeutiques. Notre objectif était donc de définir les mécanismes impliqués dans ces douleurs neuropathiques. LIMK1 est l'un des acteurs possibles de la réorganisation épinière qui caractérise les lésions nerveuses. Une fonction très caractérisé de cette protéine, est la phosphorylation d'une famille de protéines appelées « cofilines ». Sa phosphorylation, ce qui induit la réorganisation du cytosquelette d'actine. Récemment, il a été montré qu’un microARN (miARNs) nomé miR-134 régule l'expression de LIMK1 en se liant au messager de LIMK1 (ARNm), inhibant sa traduction en protéine physiologiquement active. Notre hypothèse était que la régulation de LIMK1 par miR-134 pourrait jouer un rôle essentiel dans la sensibilisation à la douleur. Cette régulation pourrait ainsi être liée non seulement à la modulation neurochimique neuronale mais aussi à la plasticité fonctionnelle associée. Au cours de cette thèse, l’HIS a montré une diminution de miR-134 chez des rats SNL (neuropathique), cette sous-expression était concomitante à une augmentation de LIMK1 illustrée par l’IHC. Il est important de noter ici que l'ISH est une méthode de détection connue récemment et qui a été identifiée pour visualiser les miARNs. Des différents protocoles de l’HIS ont également été discutés dans le cadre de cette thèse. Ce résultat a été confirmé par Le qRT-PCR . Par la suite, afin de vérifier les changements comportementaux douloureux induits par miR-134 et LIMK1. Nous avons effectués des injections intrathécales de siRNA anti-LIMK1 pour inhiber l'expression endogène de LIMK1 chez les SNL. C’était intéressant de ne pas avoir trouvé aucun changement comportemenal chez les SNL après ce type d’injection. Une surexpression artificielle de miR-134 en utilisant un précurseur de miR-134 (premiR-134) chez les SNL a montré le même effet. Ensuite, nous avons essayé d'effectuer les mêmes injections chez les Sham (control), et c’était plus intéressant de trouver que ces injections (siRNA LIMK1 et premiR-134) ont provoqué une hypersensibilité douleureuse chez les sham. Cela a été illustré au moyen de deux tests de comportement; le Von Frey (VF) et la distribution pondérale dynamique (DWB). Pour etudier l'effet inverse, nous avons inhibé miR-134 en utilisant une sonde spécifique KD (Knock-Down); une diminution significative inattendue dans le seuil de retrait a été observée avec VF et DWB. qRT-PCR dans la plupart de ces cas, a confirmé la corrélation in vivo entre miR-134 et LIMK1. Enfin, nous avons cherché un mécanisme d'action possible qui pourrait réguler cette modulation. Des données récentes publiées ont montré une implication de l'ADF/cofiline sur le trafic des récepteurs AMPA (AMPAR). En accord avec les résultats mentionnés ci-dessus, la transfection du KD de miR-134 a montré une diminution dans AMPAR adressés à la membrane plasmique. Tout ensemble ces données suggèrent que l'effet antinociceptif de KD de miR-134 et la surexpression de LIMK1 sont indirectement régulé par l'insertion des AMPAR à la membrane plasmique.Il semble que miR-134 exerce un effet différent sur la douleur neuropathique que miR-103, discuté aussi dans le cadre de cette thèse. Il était demontré comme un régulateur de plusieurs cibles, les trois sous-unités formant les canaux calciques de type-L « Cav1.2 LTC ». MiR-103 a été trouvé également réprimés chez les SNL. La surexpression de miR-103 soulage la douleur neuropathique. Contrairement au miR-134, miR-103 exerce un rôle pronociceptive pendant la douleur neuropathique
Pains 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
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Braach, Martin [Verfasser], Harald [Akademischer Betreuer] Kögler, Gerd [Akademischer Betreuer] Hasenfuß, Ali [Akademischer Betreuer] El-Armouche i 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.

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23

Heilbock, 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.

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Du, 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.

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Beltrami, 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.

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Schnittger, 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.

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Alnajar, Abdulaleem [Verfasser], i 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.

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Pašalić, 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/.

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Pasalic, 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.

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Heilbock, 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.

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Gupta, Shuchi [Verfasser], i 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.

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Nelson, Heather M. "Protein rich extruded snack foods using hydrolyzed proteins". Online version, 2003. http://www.uwstout.edu/lib/thesis/2003/2003nelsonh.pdf.

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Tuladhar, 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.

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The production of adult blood initiates from the haematopoietic stem cell (HSC). This clinically important cell has the capacity to maintain all blood lineages throughout the lifetime of an organism. HSCs emerge de novo from the haemogenic endothelium in the ventral wall of the embryonic dorsal aorta, from where they go on to seed adult sites of haematopoiesis. We have shown that Lmo4a is required for the emergence of HSCs in the zebrafish, and go on to demonstrate that Lmo4a regulates expression of the critical transcription factor, gata2a. Strikingly, both over- and under-expression of gata2a in the dorsal aorta severely diminishes HSC production. The LIM-only domain protein Lmo4 has previously been shown to interact with the known haematopoietic regulator, Ldb1. Together with our collaborators, we have identified novel binding partners of Lmo4 in mouse erythroleukaemic cells. Our functional analysis shows that many of these partners are also necessary for HSC emergence, thus revealing several new potential regulators of HSC formation. Given that these proteins were identified in an in vitro model of definitive erythropoiesis, it is remarkable that they also appear to act together in vivo at the level of HSC formation, and our data suggests that a transcriptional complex containing Lmo4 and these partners may directly repress gata2a. The related protein Lmo2 is also known to bind Ldb1. Together with Scl, Lmo2 is a master regulator of the haemangioblast programme. We have been utilising this activity, together with recent structural studies, to identify functionally important residues in the Lmo2 molecule. As a cell’s transcriptional programme drives both normal and pathological development, and misexpression of both Lmo2 and Lmo4 is involved in a variety of oncogenic states, the work presented in this thesis is likely to inform efforts to develop therapeutically relevant reagents.
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Hutchinson, 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.

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Thesis (Ph.D.)--University of Oregon, 2005.
Typescript. 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.
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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.

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Gu, 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.

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As some of the most important and widely utilised intercellular signalling molecules, transforming growth factor βs (TGFβs) play critical roles in normal development and in human disease. Establishing appropriate levels of signalling involves positive and negative feedback, driven by the same signal transduction components, but whether or how the two are distinguished has not previously been understood. Here we show that LIM domain binding proteins (Ldbs) drive the Smad6/7-mediated negative feedback of TGFβ signalling, but they are not required for the ligand-driven positive feedback or other downstream transcriptional activation. In Ldb-deficient zebrafish embryos, the homeostasis of TGFβ signalling is perturbed. As a consequence, signalling of TGFβ family members, Nodal and BMP, is stably enhanced, giving rise to excess mesoderm and endoderm, an effect that can be rescued by reducing Nodal and BMP. Later in development, conditional ldb2a knockdown causes defective vascular, angiogenic and haemogenic development, likely also by elevating TGFβ signalling. Thus, Ldbs control the homeostatic regulation of TGFβ signalling and therefore play critical roles in diverse developmental processes.
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Klaavuniemi, 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.

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Abstract The Z-disk is a sophisticated structure that connects adjacent sarcomeres in striated muscle myofibrils. α-Actinin provides strength to the Z-disks by crosslinking the actin filaments of adjacent sarcomeres. α-Actinin is an antiparallel homodimer, composed of an N-terminal actin binding domain (ABD), the central rod domain, and two pairs of C-terminal EF-hands. The PDZ-LIM domain proteins interact with α-actinin at the Z-disk. Of these proteins, only the actinin-associated LIM protein (ALP), Z-band alternatively spliced PDZ-containing protein (ZASP/Cypher) and C-terminal LIM protein (CLP36) have a ZASP/Cypher-like (ZM) motif consisting of 26-27 conserved residues in the internal region between the PDZ and LIM domains. The aim of this work was to understand the molecular interplay between the ZM-motif containing members of the PDZ-LIM proteins and α-actinin. To unveil the biological relevance of the interaction between the PDZ-LIM proteins and α-actinin, naturally occurring human ZASP/Cypher mutations were analyzed. Two interaction sites were found between ALP, CLP36 and α-actinin using recombinant purified proteins in surface plasmon resonance (SPR) analysis. The PDZ domain of ALP and CLP36 recognized the C-terminus of α-actinin, whereas the internal regions bound to the rod domain. Further characterization showed that the ALP internal region adopts and extended conformation when interacting with α-actinin and that the ZM-motif partly mediated the interaction, but did not define the entire interaction area. ZASP/Cypher also interacted and competed with ALP in binding to the rod domain. The internal fragments containing the ZM-motif were important for co-localization of ALP and ZASP/Cypher with α-actinin at the Z-disks and on stress fibers. The absence of ALP and ZASP/Cypher in focal contacts indicates that other interacting molecules, for instance vinculin and integrin, may compete in binding to the rod in these areas or additional proteins are required in targeting to these locations. The co-localization of the ZASP/Cypher with α-actinin could be released by disrupting the stress fibers leading to an accumulation of α-actinin in the cell periphery, whereas ZASP/Cypher was not in these areas. This suggests that an intact cytoskeleton is important for ZASP/Cypher interaction with α-actinin. Earlier studies have shown that mutations in the ZASP/Cypher internal region are associated with muscular diseases. These mutations, however, did not affect ZASP/Cypher co-localization with α-actinin or the stability of ZASP/Cypher proteins. The Z-disk possesses a stretch sensor, which is involved in triggering hypertrophic growth as a compensatory mechanism to increased workloads. α-Actinin is a docking site of molecules that are involved in hypertrophic signaling cascades mediated by calsarcin-calcineurin and protein kinase C (PKC) isoforms. The internal interaction site may be involved in targeting PKCs, which bind to the LIM domains of ZASP/Cypher, to the Z-disks. The similar location of the internal interaction site with calsarcin on the rod suggests that ZASP/Cypher, ALP and CLP36 may regulate calsarcin-mediated hypertrophic signaling.
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Yang, 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.

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MUNDEL, 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.

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Les proteines lim sont caracterisees par la presence d'un domaine en double doigt de zinc particulier : le domaine lim. Elles sont impliquees dans des phenomenes de differenciation cellulaire, morphogenese et developpement. Wlim-1 est une proteine a domaines lim dont l'adnc a ete isole a partir d'une banque d'adnc de tournesol helianthus annuus l. Elle comporte deux domaines lim separes par un long domaine interlim et presente des homologies de structure et de sequence avec les proteines lim animales mlp et crp, des proteines lim impliquees dans l'organisation du cytosquelette a actine. Le gene wlim-1 correspondant a ete isole et sequence. Des experiences d'immunodetection indiquent que la proteine est presente dans de nombreux organes de la plante sous au moins deux formes. Des immunolocalisations realisees sur les feuilles, tiges, ovaires et racines montrent que wlim-1 est presente dans de nombreux tissus au sein de chaque organe avec trois localisations : nucleaire, cytoplasmique ou au niveau des plastes. Lors de ces experiences, nous avons remarque que wlim-1 semble se concentrer entre les deux lots de chromosomes dans des cellules en division (anaphase et telophase). Cette localisation nous ammene a postuler un role de wlim-1 dans la division cellulaire.
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Liu, 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.

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Forbes-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.

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Breyer, 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.

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Papuga, Jessica. "Role of the Arabidopsis LIM proteins in the regulation of the actin cytoskeleton organisation and dynamics". Strasbourg, 2011. http://www.theses.fr/2011STRA6022.

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L’organisation et la dynamique du cytosquelette d’actine sont régulées par de nombreuses protéines de fixation à l’actine (« actin-binding proteins »). Récemment, les protéines à deux domaines LIM (LIMs) ont été caractérisées comme de nouvelles protéines impliquées dans le pontage (« crosslinking ») des filaments d’actine chez les animaux et les végétaux. Chez ces derniers, les protéines LIMs peuvent être classées en deux sous-familles dont les profils d’expression diffèrent. Les membres de la sous-famille WLIM sont largement exprimés dans les tissus végétatifs alors que les membres de la sous-famille PLIM sont abondamment et quasi exclusivement exprimés dans le pollen. Une question centrale était de savoir pourquoi les plantes possèdent plusieurs protéines LIMs et si les différents membres d’une même famille possèdent ou non les mêmes fonctions. Afin d’aborder cette question, nous avons caractérisé et comparé les activités régulatrices du cytosquelette d’actine des six membres de la famille des protéines LIMs d’Arabidopsis. L’analyse par microscopie confocale de plantes d’Arabidopsis exprimant chacune des protéines LIMs fusionnée à la « Green Fluorescent Protein » (GFP-LIM) ainsi que des analyses biochimiques in vitro démontrent que les protéines LIMs d’Arabidopsis sont toutes de véritables « actin-binding proteins » capables d’interagir directement avec le cytosquelette d’actine. De plus, les six protéines LIMs d’Arabidopsis stabilisent les filaments d’actine et induisent la formation d’épais câbles d’actine in vitro ainsi que dans les plantes exprimant les GFP-LIMs. Par ailleurs, des investigations in vitro ont suggéré que les membres des sous-familles WLIM et PLIM sont régulés de façon différente. Ainsi, seules les protéines PLIMs sont inactivées pas des valeurs de pH et/ou de [Ca2+] élevées. Ces résultats ont pu être confirmés par des expériences dans des cellules d’Arabidopsis dont le pH et la [Ca2+] cytoplasmiques ont été artificiellement modifiés. Enfin, le domaine C-terminal a été identifié comme le domaine régulateur conférant aux protéines PLIMs une sensibilité au pH et au Ca2+
Actin 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+
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44

Zhang, Xiyuan. "The expression of human leukemia inhibitory factor in Pichia pastoris". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29919.

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Background: Leukemia inhibitory factor (LIF) is an interleukin 6 class cytokine that inhibits cell differentiation during cell development. LIF is widely used as an important component in stem cell culture medium for cell therapy and tissue engineering applications, to inhibit spontaneous cell differentiation. However, commercially available recombinant LIF proteins are expensive, unstable, and prone to degradation in prolonged tissue culture, which has limited its applications. Purpose: We aim to develop a lab-scale method, using a yeast cell, namely, P. pastoris, to produce recombinant hLIF (rhLIF), with novel recombinant protein expression techniques. Methods: We first designed the structure of plasmid and generated the plasmid using the service of an external supplier. The plasmid was amplified in E. coli using a heat shock method. The amplified plasmid was then linearized and transcribed in the P. pastoris. Methanol was used in the medium to induce the expression of rhLIF in P. pastoris. The resultant rhLIF was tested verified by sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS-PAGE) Results: The plasmids were successfully amplified in E. coli. The generation of rhLIF in P. pastoris was verified by the SDS-PAGE results. To our knowledge, it is the first study to express rhLIF using lower eukaryotic yeast. Future direction: In the future studies, we will study the glycosylation sites of rhLIF using liquid chromatography–mass spectrometry (LC–MS). In addition, the function and stability of the rhLIF will be compared with commercial products.
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45

Pinto, 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.

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46

Pinto, Belinda Sophia. "Understanding the role of LEM domain proteins in Drosophila development". Diss., University of Iowa, 2009. https://ir.uiowa.edu/etd/421.

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The nuclear lamina is a filamentous network that underlies the nuclear envelope. Lamina components include the family of LEM domain (LEM-D) proteins, named for LAP2, emerin and MAN1. Mutations in genes encoding LEM-D proteins cause tissue-restricted human disease, even though these genes are globally expressed. To understand the contributions of the LEM-D proteins to nuclear lamina function, investigations of the Drosophila LEM-D proteins was undertaken. The Drosophila genome encodes four LEM-D proteins and this thesis describes work done on the Drosophila homologues of MAN1 and emerin, Drosophila MAN1 (dMAN1) and Otefin (Ote). Chapter 2 describes the generation and phenotypic analyses of dMAN1 mutants. These mutants display a range of tissue-specific defects associated with an increase in BMP/Dpp signaling. This suggests that dMAN1 downregulates BMP/Dpp signaling at the nuclear periphery. Chapter 3 describes the identification and phenotypic analyses of ote mutants. Loss of Ote is associated with a tissue-specific defect of the female germline where ote mutant females display defects in germline stem cell (GSC) maintenance. Loss of Ote causes defects in the germline cells, the cap cells of GSC niche and an increased sensitivity to Dpp signaling in both germline and somatic cells. These findings support models suggesting that laminopathies arise from dysfunction of the homeostasis in stem cell populations. Taken together, these studies suggest that the nuclear lamina may play tissue-specific roles through regulation of signal transduction pathways. Our data also support the use of Drosophila as a system to elucidate the mechanistic basis of diseases associated with defects in the nuclear lamina.
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Crompton, 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.

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48

Shanmugasundaram, Mathura. "Gene and protein interactions in limb development : the case of Msx and Gli3". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066279/document.

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Le bourgeon de membre est, dès son émergence dans le flanc de l'embryon, divisé en deux domaines distincts, l'un antérieur, l'autre postérieur. Nous analysons le rôle des gènes Msx dans cette polarisation. Chez la souris, les gènes Msx constituent une petite famille multigénique comprenant Msx1 et Msx2: ces gènes codent pour des facteurs de transcriptions à homéodomaine. Les souris mutantes pour Msx1 et Msx2 présentent également une surcroissance de la région antérieure du bourgeon de membre, associée à la perte d'un domaine apoptotique, qui conduit à des polydactylies antérieures. La projet vise à élucider les mécanismes par lesquels les Msx agissent sur la morphogenèse de cette région du membre. Au cours de cette investigation, nous avons fait d'intéressantes observations qui indiquent que les Msx interagissent avec Gli3, et nous avons obtenu d'intéressants résultats expérimentaux par co-immunoprécipitation des Msx et de Gli3 (co-IP) dans des cellules en culture transfectées, et par test de ligation de proximité (PLA) sur le bourgeon de membre in situ. La stratégie repose aussi sur l'analyse différentielle des transcriptome d'embryons doubles mutants pour Msx1 et Msx2 et d'embryons normaux, de façon à identifier les cibles qu'ils peuvent avoir en commun avec Gli3, ces dernières étant déjà décrites. Ces modèles devraient permettre de corréler le niveau d'apoptose avec la surcroissance du bourgeon et la polydactylie qui en résulte, apportant une importante contribution aux mécanismes de la morphogenèse qui sont encore très mal compris
The 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
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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.

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50

Bridge, 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.

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In order to survive in a given environment, adequate levels of oxygen are required throughout cells and tissues, as defined by cellular function and tissue type. Rapid reaction and adaption of a cell or tissue to low p02 (hypoxia) can enable it to remain viable, thus reducing potential damage to the organism. The hypoxic response signalling pathway is activated by hypoxia inducible factors (HIFs); these transcription factors activate genes whose products enable the cell to adapt to hypoxic conditions, including vascular endothelial growth factor (VEGF) and erythropoietin (EPO) . Under normal oxygen conditions (normoxia), the HIF-la subunit is rapidly degraded as a result of hydroxylation by the prolyl hydroxylase domain proteins (PHDl-3) and subsequent binding of the von Hippel-Lindau protein (VHL), which induces ubiquitination and degradation of HIF-la by the 265 proteasome. Data presented in this thesis identify the LlM domains-containing tumour suppressor gene product LlMD1, as well as other members of the ZYX class of LlM domain proteins, as regulators of HIF-l and the hypoxic response. LlMDl interacts with the PHDs and VHL at distinct sites to facilitate efficient HIF-la degradation by bringing the hydroxylase and ubiquitinase enzymes into close proximity. LlMDl enhances HIF-la degradation via the oxygen dependent degradation (ODD) domain and represses HIF-l transcriptional activity; these effects are dependent upon the ability of LlMDl to engage PHD2/VHL. In addition to LlMD1, ZYX class members Ajuba and WTIP also interact with PHD1/3 and VHL, and Ajuba confers enhanced HIF-la protein degradation. Preliminary evidence suggests Zyxin, TRIP6 and LPP, also members of the ZYX class, act as positive regulators of HIF-l, enhancing HIF-la protein stability and HIF-l transcriptional activity. This thesis therefore identifies LlMDl and implicates the ZYX class of LlM domain proteins as a unique family of protein regulators of HIF-l and the hypoxic response.
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