Tesi: "Basic Helix loop Helix (bHLH)"

1

Zhang, Fan. "Cloning and characterization of genes encoding basic helix loop helix (bHLH) proteins in Arabidopsis /". Full text (PDF) from UMI/Dissertation Abstracts International, 2000. http://wwwlib.umi.com/cr/utexas/fullcit?p9992950.

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2

Saarikettu, Juha. "Calcium regulation and functions of basic Helix-Loop-Helix transcription factors". Doctoral thesis, Umeå : Department of Molecular Biology, Umeå University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-537.

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3

Zhou, Shengli. "ZNF451 is a novel binding partner of the bHLH transcription factor E₁₂". Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1225219996.

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Thesis (M.S.)--University of Toledo, 2008.
"In partial fulfillment of the requirements for the degree of Master of Science in Biomedical Sciences." Title from title page of PDF document. Bibliography: pages 49-62.

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4

Kele, Olovsson Julianna M. V. "Regulation of midbrain dopaminergic neuron development by Wnts, sFRPs and bHLH proteins/". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-242-2/.

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5

Brockop, Mia. "Twist1 and Tcf12 interaction is critical for the development of the coronal suture in human and mouse". Thesis, Paris 11, 2013. http://www.theses.fr/2013PA112195/document.

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Une craniosynostose est une pathologie caractérisée par la fusion prématurée d'une ou plusieurs sutures crâniennes. C'est un défaut de naissance assez fréquent (1/2500 naissances) qui résulte en une forme anormale du crâne et qui peut être accompagné d'une déficience mentale dans certains cas. Des mutations du gène TWIST1, qui encode un facteur de transcription basique Helix-Loop-Helix (bHLH) de classe II, causent le syndrome de Saethre-Chotzen qui est associé à une synostose de la suture coronale (El Ghouzzi et al. 1997; Howard et al. 1997). Un nouveau gène a récemment été découvert comme étant une nouvelle cause du syndrome Saethre-Chotzen ainsi que de synostose coronale asyndromique (Sharma, Fenwick, Brockop, et al., 2013): il s'agit du gène TCF12, qui encode un facteur de transcription bHLH de classe I.Nous démontrons qu'une reduction de l'expression génique de Twist1 et Tcf12 chez la souris cause une synostose coronale, et nous suggérons que les protéines bHLH Twist1 et Tcf12 forment des hétérodimères dont le dosage est critique pour le développement de la suture coronale.Nous nous concentrons aussi sur Twist1 et prouvons que son expression est requise dans les tissus dérivant du mésoderme ainsi que ceux dérivant des crêtes neurales pour le développement normal de la suture coronale.De plus, nous notons que dans la suture coronale, Twist1 exclut Notch2 afin de garder la suture ouverte, et beta-catenin joue un rôle dans la maintenance de l'ouverture de la suture en ciblant Jagged1 lors du développement de la suture coronale chez la souris.Enfin, nous mentionnons de nouveaux gènes qui pourraient avoir un impact sur le développement normal de la suture coronale: Aggrecan, Goosecoid, Gucy1a3 et Gucy1b3
Craniosynostosis, the premature fusion of one or more cranial sutures, is a common birth defect (1/2500 live births) that results in abnormalities in skull shape and sometimes in neurological deficiencies (Wilkie, 1997; Wilkie and Morriss-Kay, 2001). Mutations in TWIST1, which encodes a class II basic helix-loop-helix (bHLH) transcription factor, cause Saethre-Chotzen syndrome, associated with coronal synostosis (El Ghouzzi et al. 1997; Howard et al. 1997). We recently discovered a new craniosynostosis gene, TCF12, which encodes a class I bHLH transcription factor. Tcf12 causes.Saethre-Chotzen syndrome and asyndromic coronal synostosis. (Sharma, Fenwick, Brockop, et al., 2013). We show that a reduction in the dosage of Twist1 and Tcf12 in mouse causes coronal synostosis, and we suggest that the Twist1 and Tcf12 form heterodimers whose dosage is critical for coronal suture development. We also demonstrate that Twist1 is required in both neural-crest and mesoderm-derived tissues for the normal coronal suture development. Moreover, we show that in the coronal suture, Twist1 excludes Notch2 thus maintaining suture patency. and we show that beta-catenin also plays a role in the maintenance of suture patency by regulating Jagged1. Finally, we identified Aggrecan, Goosecoid, Gucy1a3 and Gucy1b3 as Twist1-regulated genes that could have an impact on the normal development of the coronal suture

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6

Rosenberg, Miriam Isaaca. "Diverse mechanisms employed by bHLH transcription factors to downregulate gene expression /". Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/5016.

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7

Grove, Christian A. "A Multiparameter Network Reveals Extensive Divergence Between C. elegans bHLH Transcription Factors: A Dissertation". eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/441.

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It has become increasingly clear that transcription factors (TFs) play crucial roles in the development and day-to-day homeostasis that all biological systems experience. TFs target particular genes in a genome, at the appropriate place and time, to regulate their expression so as to elicit the most appropriate biological response from a cell or multicellular organism. TFs can often be grouped into families based on the presence of similar DNA binding domains, and these families are believed to have expanded and diverged throughout evolution by several rounds of gene duplication and mutation. The extent to which TFs within a family have functionally diverged, however, has remained unclear. We propose that systematic analysis of multiple aspects, or parameters, of TF functionality for entire families of TFs could provide clues as to how divergent paralogous TFs really are. We present here a multiparameter integrated network of the activity of the basic helix-loop-helix (bHLH) TFs from the nematode Caenorhabditis elegans. Our data, and the resulting network, indicate that several parameters of bHLH function contribute to their divergence and that many bHLH TFs and their associated parameters exhibit a wide range of connectivity in the network, some being uniquely associated to one another, whereas others are highly connected to multiple parameter associations. We find that 34 bHLH proteins dimerize to form 30 bHLH dimers, which are expressed in a wide range of tissues and cell types, particularly during the development of the nematode. These dimers bind to E-Box DNA sequences and E-Box-like sequences with specificity for nucleotides central to and flanking those E-Boxes and related sequences. Our integrated network is the first such network for a multicellular organism, describing the dimerization specificity, spatiotemporal expression patterns, and DNA binding specificities of an entire family of TFs. The network elucidates the state of bHLH TF divergence in C. elegans with respect to multiple functional parameters and suggests that each bHLH TF, despite many molecular similarities, is distinct from its family members. This functional distinction may indeed explain how TFs from a single family can acquire different biological functions despite descending from common genetic ancestry.

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8

Mao, Weiming. "The role of bHLH gene ash1 in the developing chick eye". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/mao.pdf.

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9

Serre, Angéline. "Stratégies d'homogénéisation des populations de progéniteurs nerveux fœtaux humains dans une perspective de thérapie cellulaire du système nerveux central". Paris 6, 2007. https://tel.archives-ouvertes.fr/tel-00184239.

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Dans une perspective de médecine régénératrice, les cellules souches nerveuses et progénitrices fœtales humaines constituent indéniablement un des outils les plus adaptés au traitement des lésions du SNC et des maladies neurodégénératives. Jusqu’à présent, leur utilisation en thérapie cellulaire a eu recours à des populations hétérogènes composées à la fois de cellules immatures, de cellules en voie de différenciation et de cellules pleinement différenciées. Or des études récentes ont révélé l’intérêt de disposer de populations enrichies en un type cellulaire donné afin d’améliorer l’efficacité des greffes. Pour homogénéiser les populations et mieux cibler les pathologies, nous avons donc mis en œuvre deux stratégies. La première consiste à surexprimer, dans les cellules en culture, les gènes proneuraux à motif bHLH Ngn1, Ngn2, Ngn3 et Mash1 au travers de vecteurs lentiviraux dits « de différenciation ». Cette surexpression a permis d’orienter la différenciation des cellules majoritairement vers le lignage neuronal et également de spécifier des sous-types neuronaux. La seconde méthode utilise des vecteurs lentiviraux traceurs pour exprimer une protéine rapportrice sous le contrôle de promoteurs spécifiques des différents lignages du SNC en vue de leur sélection par tri cellulaire. Nous avons ainsi utilisé le promoteur Nestine pour les cellules immatures, le promoteur Synapsine pour les cellules neuronales et le promoteur GFAP pour les cellules astrocytaires. Si les promoteurs Synapsine et GFAP ont révélé une spécificité contestable, le promoteur Nestine, quant à lui, a permis de sélectionner une population enrichie à 81% en cellules nestine+. Ce travail s’inscrit dans un projet de plus grande envergure, qui a pour but d’évaluer les bénéfices de greffes de ces populations homogénéisées.

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10

Martin, Nathalie. "Studies on the regulation of the Napin napA promoter by ABI3, bZIP and bHLH transcription factors". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8713.

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11

Sieber, Martin Sieber Martin. "DNA binding reaction of basic-helix-loop-helix proteins /". [S.l.] : [s.n.], 2000. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=13578.

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12

Bloor, A. J. C. "Proteins for the basic helix-loop-helix transcription factor SCL". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596727.

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Members of the basic Helix-Loop-Helix (bHLH) family of transcription factors play critical roles in the control of development processes in species ranging from yeast to humans. The product of the SCL (Stem Cell Leukaemia) gene is a bHLH protein that was first identified by its ectopic expression in a case of childhood acute leukaemia and it has subsequently been characterised as a key player in the regulation of the development of blood and endothelium. The mechanism by which SCL functions are unclear, however it is likely that it regulates target genes by the formation of cell specific multiprotein complexes. A number of such complexes have been identified, however only in a small number of cell types. The aim of this project was to identify novel SCL partner proteins in order to better understand how it functions both normally and as an oncogene. Over 300 potential SCL interaction partners were identified in a yeast 2-hybrid screen of an embryonic cDNA library. Of these, the interaction between SCL and RFP (Ret Finger Protein) was characterised in the greatest detail. RFP is a ubiquitously expressed TRIM (Tripartite Motif) protein and little was previously known about its cellular function. RFP interacts with SCL in vitro and a stable complex of the two proteins was isolated in both COS cells and the haemopoietic progenitor cell line of 416B. RFP also interacts with a subset of other bHLH proteins via the bHLH domain but not with other classes of transcription factors and functions to repress their ability to transactivate reporter genes. The expression pattern of RFP was studied in a panel of haemopoietic cell lines. The subcellular location of RFP correlates with the lineage and development stage of the cell and also appears to be cell cycle regulated which suggests a number of novel mechanisms by which it could regulate SCL or other bHLH factors. Moreover, RFP is able to inhibit the ability of myogenic bHLH factors to convert multipotent fibroblasts into muscle indicating that its interaction with bHLH proteins is biologically significant.

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13

Imabayashi, Takeshi. "Expression of basic helix-loop-helix proteins in the glomeruli". Kyoto University, 2001. http://hdl.handle.net/2433/150563.

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14

Ma, Philip Chun-Ming. "Structural studies on the basic-helix-loop-helix region from MyoD". Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/28070.

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15

Sato, Tetsu. "The Basic Helix-Loop-Helix Gene hesr2 promotes gliogenesis in mouse retina". Kyoto University, 2004. http://hdl.handle.net/2433/148268.

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16

Hayward, Penelope Caroline. "The basic helix-loop-helix protein SCL and its role in haematopoietic development". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603895.

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The SCL gene encodes a basic helix-loop-helix protein that has a critical role in the normal development of all haematopoietic lineages, as well as an oncogenic role in T cell leukaemogenesis. SCL is suspected to function as a tissue specific transcription factor, but the mechanisms by which SCL mediates its functions are unclear. Identification and characterisation of protein-protein interactions SCL should begin to unravel the roles of this protein. As SCL is expressed in committed erythroid, mast and megakaryocytic cells as well as early haematopoietic progenitor cells, yeast-two-hybrid screens of haematopoietic cell line cDNA libraries were conducted to identify potential SCL interaction partner proteins. cDNA libraries were generated from an early haematopoietic progenitor cell line and a megakaryocytic cell line. These screens using both these libraries and a mouse E10.5 embryo cDNA library identified a range of potential interaction partners for the SCL protein. PolyA⁺ RNA was isolated from a wide range of haematopoietic cell lines, and embryonic tissues and Northern blot analysis was then used to investigate the expression patterns of these potential interaction partners. The combination of this expression data and data gathered from sequence analysis using bioinformatics programs was used to assess which of the proteins identified was the most promising candidate SCL interaction partner. The association between SCL and the IFNα inducible protein IFI60 was investigated.

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17

Hufnagel, Robert B. "The Role of Basic Helix-Loop-Helix Transcription Factors in Early Retinal Neurogenesis". University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1282932913.

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18

Bloor, Adrian John Clifton. "Identification of novel partner proteins for the basic helix-loop-helix transcription factor SCL". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619716.

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19

Jhas, Sumitpal. "Regulation of cortical neuron and astrocyte differentiation by the basic helix loop helix protein Hes6". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18671.

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During development of the mammalian cerebral cortex, pluripotent neural progenitor cells located in the ventricular zone lining the lateral ventricles give rise to neurons, astrocytes, and oligodendrocytes. Neurogenesis precedes astrocyte differentiation, followed by oligodendrocyte differentiation. The mechanisms regulating the transition of undifferentiated progenitor cells into the differentiated state are regulated in part by basic-helix-loop-helix (bHLH) transcription factors of the Hairy/Enhancer of split (Hes) family. A number of Hes proteins are induced in response to the activation of the Notch signaling pathway. Notch-activated Hes proteins, like Hes1 or Hes5, are transcriptional repressors that inhibit cortical neurogenesis and promote astrocyte differentiation. Another Hes family member, termed Hes6, is not activated in response to Notch signaling and promotes neurogenesis, in contrast to Notch-activated Hes1 and Hes5. The objectives of the present studies were a) to elucidate the molecular mechanisms underlying the pro-neuronal activity of Hes6, and b) to determine whether or not Hes6 is also involved in glial cell differentiation. To pursue these goals, a structure function analysis was performed in which mutated forms of Hes6 were examined for their ability to promote neurogenesis using primary cultures of cortical neural progenitor cells. Moreover, Hes6 and mutated forms thereof were tested to determine whether they would inhibit astrocyte differentiation. It is shown here that Hes6 inhibits astrogenesis in addition to inducing neuronal differentiation. These two activities require separate structural domains, suggesting that that they are mediated by different molecular mechanisms.
Durant le développement du cortex cérébral mammifère, des cellules souches neuronales situées dans la zone ventriculaire se différencient en neurones, astrocites, et oligodendrocites. Durant ce développement la neurogenèse prend place en premier, suivi par la différenciation des astrocites et celle des oligodendrocites. Les mécanismes régulateurs de la différenciation sont en parti sous le control des facteurs de transcriptions « basic-helix-loop-helix » (bHLH) appartenant au groupe « Hairy/Enhancer of split » (Hes). Plusieures protéines Hes sont activées par la signalisation de Notch. Ces protéines, tel Hes1 et Hes5, sont des inhibiteurs de transcription durant la neurogenèse corticale et promeuvent la différentiation des astrocites. Par contre Hes6, insensible aux signaux de Notch, promeut la neurogenèse. Les objectifs de cette étude consistent à: 1) mieux comprendre les mécanismes moléculaires de l'activité de Hes6 ; 2) étudier le rôle potentiel de Hes6 dans la différenciation des cellules glies. Nous avons analysé l'habileté de différents mutants de Hes6 à promouvoir la neurogenèse en employant un système de culture cellulaire primaire de cellules souches neuronales. De plus, ces différentes formes de Hes6 ont été testées pour leur effet sur l'inhibition de la différenciation des astrocites. Nous démontrons que Hes6 inhibe l'astrogenèse et promeut la différenciation neuronale. Ces deux activités requèrent différentes domaines structurelles, laissant présager différents mécanismes moléculaires.

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20

Narumi, Osamu. "OUT, a Novel Basic Helix-Loop-Helix Transcription Factor with an Id-like Inhibitory Activity". Kyoto University, 2000. http://hdl.handle.net/2433/180866.

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21

MacAlister, Cora Ann. "The role of the basic helix loop helix transcription factor speechless in the initiation of the stomatal lineage /". May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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22

Bergstrom, Donald Alan. "Orchestration of skeletal myogenesis by the myogenic bHLH family of transcription factors /". Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6358.

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23

Sakamoto, Masami. "The Basic Helix-Loop-Helix Genes Hesr1/Hey1 and Hesr2/Hey2 Regulate Maintenance of Neural Precursor Cells in the Brain". Kyoto University, 2004. http://hdl.handle.net/2433/147494.

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24

Qian, Yingjuan. "The role of DEC1 in P53-dependent cellular senescence". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/qian.pdf.

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25

Otsuka, Toshiyuki. "Regulated expression of neurogenic basic helix-loop-helix transcription factors during differentiation of the immortalized neuronal progenitor cell line HC2S2 into neurons". Kyoto University, 1998. http://hdl.handle.net/2433/182245.

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26

Simionato, Elena. "Evolution et diversification des protéines à basic Helix-Loop-Helix chez les métazoaires : apports pour la compréhension de l'évolution du système nerveux et de la neurogenèse". Paris 11, 2008. http://www.theses.fr/2008PA112213.

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Pour tenter de comprendre l’évolution du système nerveux, j’ai étudié certaines protéines à basic Helix-Loop-Helix (bHLH) impliquées dans le développement neural et leur conservation ou divergence pendant l’évolution des animaux. D’abord, une recherche systématique des gènes à bHLH a été conduite dans les génomes des principales lignées de métazoaires y compris des non bilatériens, deux cnidaires et une éponge Amphimedon queenslandica. Les analyses phylogénétiques ont permis de proposer un modèle d’évolution et d’expansion de cette superfamille chez les métazoaires. Ensuite, j’ai étudié un gène à bHLH d’éponge AmqbHLH1, qui est un homologue des gènes proneuraux atonal/neurogenin de bilatériens. Les profils d’expression d’AmqbHLH1 et d’homologues des gènes Notch et Delta suggèrent qu’ils pourraient être impliqués dans la formation de cellules sensorielles chez l‘éponge. J’ai montré que AmqbHLH1 possède une activité proneurale qui est une combinaison des propriétés de neurogenin et atonal. Nous avons inféré que le mécanisme génétique comprenant les gènes proneuraux couplés à la voie de signalisation Notch/Delta, était déjà fonctionnel chez les métazoaires plus basaux pour former des cellules sensorielles. Enfin, pour comprendre quels aspects de la fonction des protéines à bHLH sont ancestraux aux bilatériens et quels sont des caractères dérivés spécifiques de certaines lignées, j’ai étudié des gènes à bHLH chez l’annélide Platynereis dumerilii. Tous les gènes identifiés sont exprimés pendant la formation du système nerveux de Platynereis et certains pourraient avoir des fonctions proneurales ou de spécification neuronale de manière similaire aux vertébrés
In order to understand the nervous system evolution, during my thesis I have studied some basic Helix-Loop-Helix (bHLH) proteins involved in neural development and their conservation or divergence during animal evolution. First, an extensive search for bHLH genes has been conducted in species representative of the main metazoan lineages, including three non-bilaterian species, two cnidarians and a sponge Amphimedon queenslandica. The phylogenetic analyses allowed us to propose an evolutionary scenario for the diversification of this superfamily in metazoans. Then, I have studied a sponge bHLH gene, AmqbHLH1, which is homolog to the bilaterian proneural genes, atonal and neurogenin. The expression of AmqbHLH1, as well as of homologs of Notch and Delta,in dicates that these genes may be involved in the formation of sensory cells in the sponge. I have also demonstrated that AmqbHLH1 has a proneural activity that is a combination of the properties of the neurogenin and atonal genes. We have inferred that the bilaterian neurogenic circuit, comprising proneural bHLH genes coupled with Notch/Delta signalling, was functional in the very first metazoans and was used to generate an ancient sensory cell type. Finally, to decipher which aspects of the function of bHLH genes are ancestral to bilaterians and which are derived characters specific of some lineages, I have studied the expression of several neural bHLH genes in an annelid, Platynereis dumerilii. All the identified genes are expressed during the formation of the Platynereis nervous system and some of these genes may have proneural or neural specification functions in a similar fashion to that observed in vertebrates

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27

Schmidt, Johanna Maria [Verfasser], e Magdalena [Akademischer Betreuer] Götz. "Temporal and cell-specific effects of the basic Helix-Loop-Helix Transcription factor Twist1 during breast cancer progression / Johanna Maria Schmidt ; Betreuer: Magdalena Götz". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1160876428/34.

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28

Oktay, Yavuz. "Defining a novel role for hypoxia inducible factor-2 alpha (HIF-2a)/EPAS1 : maintenance of mitochondrial and redox homeostasis". Access to abstract only; dissertation is embargoed until after 12/20/2006, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=134.

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29

Steen, Håkan. "Novel Interactors of X-linked Inhibitor of Apoptosis Protein : Expression and Effects on Tumor Cell Death". Doctoral thesis, Uppsala University, Neurobiology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8742.

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Abstract (sommario):

Programmed cell death, or apoptosis, has during the last decade received a lot of attention due to its involvement in a large number of pathological conditions. Since death is always irreversible, it is important for cells to fully control the initiation and execution of this process. One of many apoptosis-regulatory proteins is XIAP, which blocks the action of caspases, a family of proteases that are important during apoptosis. However, apoptosis inhibitors have to be tightly controlled since too little cell death can lead to the development of tumors and other diseases. This thesis is the result of an aspiration to fully understand the function and regulation of XIAP.

By using the yeast-2-hybrid system, we identified two novel binding partners of XIAP. The first, GPS2, was found to bind XIAP and inhibit its ability to block caspase-activity. In addition, GPS2 induced caspase-mediated cell death in two different tumour cell lines and XIAP inhibited this effect.

The second binding partner, Nulp1, preferentially bound XIAP in the presence of the apoptosis-inducer staurosporine. Nulp1 induced or sensitized cell lines to cell death when overexpressed, but this was not blocked by caspase-inhibitors or XIAP, suggesting a different reason for binding than apoptosis regulation. With the aim to understand the Nulp1-XIAP interaction, we continued to study Nulp1 in vivo and in vitro. We studied three different splice variants of Nulp1 and found that they were regulated by poly-ubiquitination and nuclear shuttling. Also, Nulp1 was expressed in embryonic mice, especially in the cortical plate, hippocampal neurons and cerebellar granular neurons. Expression of Nulp1 decreased with age but was still present in cerebellar deep nuclei and Purkinje cells of adult mice.

To summarize, we have identified GPS2 as an apoptosis-inducing factor and an inhibitor of XIAP in vitro, and Nulp1 as a XIAP-interacting protein during staurosporine-induced apoptosis.

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30

Chen, Tingting [Verfasser], Brigitte [Akademischer Betreuer] Poppenberger-Sieberer, Ralph [Gutachter] Hückelhoven e Brigitte [Gutachter] Poppenberger-Sieberer. "Characterization of factors that may modulate function of the basic helix-loop-helix protein CESTA / Tingting Chen ; Gutachter: Ralph Hückelhoven, Brigitte Poppenberger-Sieberer ; Betreuer: Brigitte Poppenberger-Sieberer". München : Universitätsbibliothek der TU München, 2017. http://d-nb.info/1149824166/34.

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31

Ravanpay, Ali Cyrus. "Insights into the molecular interactions of the neurogenic basic helix-loop-helix transcription factor, neuroD2, and the mechanism of regulation of a key target, RE-1 silencing transcription factor /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10628.

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32

Chao, Christina Seng. "The roles of Nkx2.2 in determination of mouse islet cell fates /". Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Abstract (sommario):

Thesis (Ph.D. in Cell & Developmental Biology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 144-158). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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33

Wikström, Ingela. "Molecular genetics of B- and T-lymphocyte development /". Umeå : Department of Medical Biosciences, Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-802.

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34

Ruan, Xuan 1974. "Differential circadian regulation of Bmal1 transcription by orphan nuclear receptors". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112358.

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In mammals, circadian rhythms are generated by transcriptional-translational feedback loops consisting of a set of clock genes and their protein products. Among them, Bmal1 is a critical clock gene in generating and maintaining circadian rhythms. Moreover, orphan nuclear receptors REV-ERBs and RORs were known to respectively repress and activate Bmal1 transcription. In our study, we further demonstrated that: (1) REV-ERBalpha might be the main regulator in maintaining Bmal1 oscillation in thymus. (2) Rorgamma mRNA is constant in muscle and testis, and rhythmic in liver, while Rorgammat mRNA is only expressed in thymus, at constant levels. Moreover, the expressions of these two Rorgamma isoforms are affected in Clock mutant mice in a distinct way. (3) RORgamma and RORgammat can activate Bmal1 transcription at a similar level. (4) Rorgamma is a clock-controlled gene. Altogether, our results suggest that the crucial role of REV-ERBs and RORs in peripheral clocks. Furthermore, our work highlights functional differences among mammalian peripheral clocks, which provides important insights into the complexity of the circadian system.

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Glasgow, Stacey Marie. "The role of PTF1A in spinal cord development". Access to abstract only; dissertation is embargoed until after 5/15/2007, 2006. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=155.

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Johansson, Térèse A. "Pancreatic Endocrine Tumourigenesis : Genes of potential importance /". Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9294.

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37

Yu, Elizabeth A. "Investigating Age-Dependent Arthropathy in a Circadian Mutant Mouse Model: A Dissertation". eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/544.

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Ectopic calcification can cause pain and limit mobility. Studies suggest that circadian genes may play a role in the calcification process. Core circadian genes Clock, Npas2, and Bmal1 are transcription factors that form CLOCK:BMAL1 or NPAS2:BMAL1 transactivator complexes that drive the rhythmic expression of circadian oscillator genes and output genes. Circadian oscillator genes Period1-3 and Cryptochrome1-2 encode proteins that form transcription repressor complexes that feedback to inhibit CLOCK/NPAS2:BMAL1 activity, thus completing the feedback loop that is the basis of the molecular circadian clockwork. Arrhythmic Bmal1-/- mice exhibit site-specific, age-dependent arthropathy. While studying the circadian phenotype of Clock-/-;Npas2m/m double mutant mice, we discovered that these double mutant mice develop site-specific arthropathy similar to the arthropathy described in Bmal1-/- mice. Based on the circadian clockwork mechanism, we hypothesized that CLOCK/NPAS2:BMAL1 transactivator complexes drive the expression of a gene (or genes) that prevents age-dependent arthropathy. To investigate Clock-/-;Npas2m/m double mutant mouse arthropathy, we evaluated mutant mice using X-ray, micro-computed tomography, and histology, and found that Clock-/-;Npas2m/m double mutant mice exhibit age-dependent, site-specific arthropathy that phenocopies that of Bmal1-/- mice. The costosternal junction and calcaneal tendon are most prominently affected, in that calcification of those tissues is detectable as early as 4-5 weeks and 11-12 weeks, respectively. The arthropathic lesions in these tissues consist of calcium phosphate vii deposits, and in Bmal1-/- costosternal junction calcifications, the deposits contain calcium pyrophosphate dihydrate crystals. Mechanical stress, disregulation of centrally-regulated circadian rhythms, and systemic serum mineral imbalances likely do not contribute to this pathology. In vitro micromass cultures generated from Clock-/-;Npas2m/m double mutant mouse embryonic fibroblasts do not exhibit irregular chondrocyte differentiation compared to wild-type cultures, suggesting that chondrocyte cell-autonomous mechanisms are insufficient to induce this arthropathy. Analysis of Clock-/-;Npas2m/m double mutant intersternebral tissue RNA did not reveal significant changes in chondrocyte or calcification-related gene expression. Histological stains showed an absence of osteoblasts and osteoclasts around costosternal junction calcifications, suggesting that these cell types are not contributing to this pathology. Instead, chondrocytes are localized to the costosternal junction but there were no significant changes in the distribution of chondrocyte markers in this tissue, as evaluated by immunohistochemistry. These findings suggest that Clock or Npas2, and Bmal1, regulate ectopic calcification through a combination of systemic and local factors, and that the cells affected by Clock and Npas2, or Bmal1, disruption are a subset of the cells distributed in specific tissues that develop age-dependent arthropathy. The significance of these findings is that “circadian genes” play a role in the regulation of ectopic calcification in a non-oscillator capacity. Understanding this new mechanism by which ectopic calcification is controlled could lead to novel approaches for the treatment of some human calcification diseases.

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Otto, Aline Pedrosa. "Análise molecular do gene HES1 em pacientes portadores de hipopituitarismo congênito". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-27082014-112356/.

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Estudos em modelos animais transgênicos possibilitaram o conhecimento de parte dos genes envolvidos na embriogênese hipofisária e da etiologia genética do hipopituitarismo em humanos. Entretanto, a etiologia da maior parte dos casos de hipopituitarismo congênito, principalmente os associados à neuro-hipófise ectópica (NE), ainda é pouco definida. Mutações no gene PROP1 são a causa genética mais comum de hipopituitarismo descritas até o momento, mas estão sempre associadas à neuro-hipófise tópica. Estudos destinados a esclarecer o mecanismo molecular da mutação do gene Prop1 em camundongos demonstraram a participação da via de sinalização Notch e de seus componentes, dentre eles, o gene Hes1. O HES1 é um gene que codifica um fator de transcrição que participa de estágios precoces do desenvolvimento hipofisário e está envolvido com a morfogênese da neuro-hipófise. A avaliação do camundongo com nocaute em homozigose deste gene acarreta uma hipoplasia da adeno-hipófise e ausência da neuro-hipófise; e sua expressão constitutiva está associada ao hipopituitarismo. Como a NE é um achado comum no hipopituitarismo congênito e o gene HES1 pode estar relacionado a sua fisiopatologia, a região codificadora do gene HES1 foi avaliada em 192 pacientes com hipopituitarismo congênito. A variante alélica c.578G > A (p.G193D) em heterozigose foi encontrada em um paciente com hipopituitarismo congênito associado à NE. A avaliação da predição in silico do efeito funcional da variante pela ferramenta MutationTaster sugere que a troca do aminoácido glicina, altamente conservado entre os mamíferos, por ácido aspártico, seja deletéria. No estudo da segregação familiar, quatro irmãos aparentemente normais apresentam a mesma variante, sendo que dois deles possuem alterações discretas na imagem da hipófise. Em conclusão, esta é uma nova variante alélica descrita no gene HES1, ausente em grandes bancos de dados e controles saudáveis da população brasileira, mas presente em irmãos não afetados. Estudos funcionais in vitro são necessários para esclarecer o efeito biológico desta variante. Um padrão de herança complexo com penetrância incompleta é possível e já descrito em outros genes associados ao hipopituitarismo. Na tentativa de elucidar a causa genética do hipopituitarismo neste caso, o material genético deste paciente e de seus familiares foram submetidos ao sequenciamento do exoma, mas os resultados estão inconclusivos até o momento
Studies of transgenic animal models have allowed for the discovery of genes involved in human pituitary embryogenesis and the genetic etiology of hypopituitarism. However, the genetic causes of most cases of congenital hypopituitarism, especially those associated with an ectopic posterior pituitary, remain poorly defined. Mutations in the gene PROP1 are the most common genetic causes of hypopituitarism described to date, and are always associated with an ectopic posterior pituitary. Studies to elucidate the molecular mechanisms of Prop1 mutations in mice have demonstrated the involvement of the Notch signaling pathway, including its downstream target Hes1. The HES1 gene encodes a transcription factor that participates in early stages of pituitary development and is involved in posterior pituitary morphogenesis. Hes1 knockout mice exhibit a hypoplastic anterior pituitary and absence of a posterior pituitary. Conversely, constitutive expression of Hes1 is associated with hypopituitarism. Since an ectopic posterior pituitary is commonly found in congenital hypopituitarism and the HES1 gene may be related to its pathophysiology, the coding region of gene HES1 was screened in 192 patients with congenital hypopituitarism. A heterozygous allelic variant c.578G >A (p.G193D) was identified in a patient with congenital hypopituitarism associated with an ectopic posterior pituitary. Assessment by MutationTaster, a bioinformatic tool for in silico prediction of functional effect of missense variants, suggests that substitution of glycine (a highly conserved amino acid in this position among mammals) for aspartic acid is deleterious. In the genetic study of family members, we identified four apparently normal siblings with the same variant, two of which have discrete changes in their pituitary MRI. In conclusion, we described a new allelic variant in the gene HES1, absent in large databases and healthy Brazilian controls, but present in the unaffected siblings. In vitro functional studies are needed to clarify the biological effect of this variant. A complex pattern of inheritance with incomplete penetrance is possible in this case, as it has already been described in other genes associated with hypopituitarism. In an attempt to elucidate the genetic cause of hypopituitarism in the family described, DNA samples of this patient and his family were submitted to exome sequencing, but results are inconclusive at this time

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Varshney, Gaurav. "Identification of downstream targets of ALK signaling in Drosophila melanogaster /". Doctoral thesis, Umeå : Umeå universitet, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1894.

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Johnston, Brian T. "Serotonin-Expressing Cells in the Corpus of the Stomach Originate from Bone Marrow: A Master’s Thesis". eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/639.

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Neurogenin 3 and its downstream target NeuroD are basic helix-loop-helix transcription factors which promote endocrine differentiation in the gastrointestinal tract. However, mice lacking Ngn3 still produce several hormones in the stomach. Lineage tracing mouse models demonstrated that a majority of hormone cells in the corpus region of the stomach did not express Ngn3 or NeuroD during differentiation. Serotonin and histamine cells were entirely NeuroD-independently derived, and serotonin cells were additionally entirely Ngn3-independently derived. In this study, we isolated serotonin and histamine cells from the gastric corpus of transgenic mice expressing the fluorescent marker CFP. Serotonin cells expressed multiple mast cell markers by RT-PCR, and were found to be nearly absent in a mast cell-deficient mouse model. Labeled bone marrow transplant mice showed all serotonin cells derived from bone marrow. Histamine-expressing ECL cells, while lacking NeuroD, did not appear to express granulocyte or mast cell markers by analytical flow cytometry and RT-PCR, and resemble other enteroendocrine cell populations. Mouse gastric corpus serotonin cells, but not antral serotonin cells, are bone marrow-derived mast cells.

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Kumar, Meenakshi Swaminathan. "Regulation of smooth muscle differentiation by E-boxes, basic helix-loop-helix (bHLH) proteins, and bHLH-interacting factors /". 2003. http://wwwlib.umi.com/dissertations/fullcit/3077320.

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42

Bertulat, Bianca. "Identifizierung und Charakterisierug von basic Helix-Loop-Helix (bHLH)- Transkriptionsfaktoren im Zusammenhang mit dem interstitiellen Stammzell-System des Süßwasserpolypen Hydra". Phd thesis, 2008. https://tuprints.ulb.tu-darmstadt.de/980/1/bertulat_2008_Teil1.pdf.

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Meine Arbeit befasst sich mit der Superfamilie der basic Helix-Loop-Helix (bHLH)-Transkriptionsfaktoren, im Zusammenhang mit Differenzierungs-mechanismen interstitieller Stammzellen (I-Zellen) im Süßwasserpolypen Hydra. Da bHLH-Dimere konservierte Funktionen bei der Auswahl von Vorläuferzellen und deren Differenzierung und Subspezifizierung zu einzelnen Zelltypen übernehmen, interessierte mich, welche bHLH-Faktoren an der Spezifizierung des I-Zell-Systems beteiligt sind, das in Hydra neben Gameten und Drüsenzellen alle neuronalen Zelltypen hervorbringt. Mein Fokus richtete sich dabei speziell auf die beiden neuronalen Differenzierungswege in Hydra (Nervenzell- und Nematocyten-differenzierungsweg) und die neuronalen bHLH-Familien des Achaete/Scute-Complexes (AS-C) und der Atonal Related Proteine (ARP). Vor dem Hintergrund, dass bislang nur ein AS-C-Homolog (Cnidarian Achaete/Scute-Homolog, Cnash) in Hydra beschrieben werden konnte (Grens et al., 1995) gelang es mir vier ARP- und zwei AS-C-Homolge zu isolieren, von denen das AS-C-Homolog hyLiAS (Hydra Like Achaete/Scute) weiter charakterisiert werden konnte (Stenotelen und Desmonemen). Zusätzlich gelang es LiAS eine Interaktion mit der cytoplasmatischen Hydra Cadherin-Domäne nachzuweisen, wodurch sich eine duale Funktion dieses neuen AS-C-Homologs mit Aufgaben außerhalb des Zellkerns andeutet. Meine Arbeit zeigt, dass bereits in den Anfängen der Nervensystem-Evolution vor etwa 650 Millionen Jahren ein complexes Netzwerk von bHLH-faktoren der AS-C- und ARP-Familie vorlag und unterstreicht den Wert der Cnidarier als Modellorganismen für die Evolution von Differenzierungsmechanismen und Signalwegen.

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Bertulat, Bianca [Verfasser]. "Identifizierung und Charakterisierug von basic Helix-Loop-Helix (bHLH)-Transkriptionsfaktoren im Zusammenhang mit dem interstitiellen Stammzell-System des Süßwasserpolypen Hydra / von Bianca Bertulat". 2008. http://d-nb.info/988983281/34.

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Bersten, David Christopher. "Regulation of expression and activity of the bHLH-PAS transcription factor NPAS4". Thesis, 2014. http://hdl.handle.net/2440/96833.

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Development of the Central Nervous System (CNS) relies on complex transcriptional programs to specify distinct neuronal areas/cell types, and guide the formation of neuronal networks. Synaptic activity during post-natal brain development dictates the number and strength of synapses as well as promoting neuronal cell survival through activation of transcriptional programs. The establishment of synapses during this “critical period” of post-natal neuronal development and the local rearrangement, fine tuning and maintenance of synaptic connections into adulthood contributes to synaptic plasticity, memory, learning and cognitive function, while dysfunction in these processes is thought to contribute to a number of neuropsychiatric diseases. Studying transcription which underlies these events and disease states has been technically challenging due to the lack of gain and loss of gene expression systems to interrogate complex biological questions in primary neurons or the developing nervous system of rodents. As a result, despite clinical and anatomical data, the molecular mechanisms underlying neuropsychiatric disease or memory and learning remain poorly understood. The basic-Helix-Loop-Helix (bHLH) – Per/Arnt/Sim (PAS) (bHLH-PAS) homology domain transcription factor Neuronal PAS factor 4 (NPAS4) is tightly coupled to neuron function by homeostatically regulating neuronal activity via stimulating formation of inhibitory synapses. NPAS4 expression is brain restricted and highly induced following neuronal depolarisation, paradigms of learning, seizure or ischemia. NPAS4 null mice are prone to seizures, hyperactivity, have defects in memory formation, social interaction, cognitive impairments, as well as age related neurodegeneration. This thesis shows that NPAS4 expression is highly restricted to the CNS, in particular the cortex, by repressive activity of RE-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor (REST/NRSF) in non-neuronal cells and stem cells. In addition, we also provide evidence that microRNA-224 targets the NPAS4 3’UTR, which may contribute to regionalised NPAS4 expression in the brain. We identify human variants within NPAS4 and ARNT2 which disrupt NPAS4 function, which may have implications for neuropsychiatric disease. Using structural modelling and biochemical experiments we show that one of these variants disrupts dimerisation, providing insight into bHLH-PAS dimerisation mechanisms. We also describe a new system for knockdown and ectopic expression which is broadly applicable for reliable, flexible and temporal control of gene expression to facilitate investigating gene function. This system incorporates single gateway compatible vector systems for lentiviral infection and Recombination Mediated Cassette Exchance (RMCE), the latter targeting the Collagen 1a1 (Col1a1) locus in germline competent embryonic stem cells. Using an optimised reverse tetracycline transactivator (rtTA) system with reduced background expression and increased sensitivity to doxycycline, we have shown that we can rapidly generate inducible overexpression and short hairpin RNA (shRNA) mediated knockdown cell lines with homogenous, inducible expression. The work encompassed within this thesis investigates the molecular mechanisms underlying the restricted expression pattern of NPAS4, the contribution of human non-synonymous variants to NPAS4/ARNT2 transcription factor function, and the development of flexible, inducible and reversible gene expression systems for studying NPAS4 function in vitro and in vivo.
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2014

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Whelan, Fiona. "The aryl hydrocarbon receptor: structural analysis and activation mechanisms". Thesis, 2010. http://hdl.handle.net/2440/95877.

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The Aryl-hydrocarbon Receptor (AhR) is a basic Helix-Loop-Helix Per-ARNT-Sim (bHLH.PAS) transcription factor (TF) which binds partner protein Aryl hydrocarbon Receptor Nuclear Translocator (ARNT), in order to activate target genes in response to environmental or endogenous stimuli. The PAS region of these TFs consists of two adjacent repeats of the PAS domain, where the PAS repeat defines dimerization specificity and also serves as a primary sensor in exogenous ligand activation of AhR. Active AhR/ARNT heterodimer binds specific DNA sequences, termed Xenobiotic Response Elements (XRE). The molecular detail of interactions that dictate dimerization and DNA binding specificity are unknown for this TF family. In addition, active AhR has recently been shown to function as a recognition component of an E3 ubiquitin ligase. Reports that AhR null mice have poor fertility and defects in liver vasculature are indicative of the potential for a number of endogenous roles. Research into activation of AhR has highlighted that post-translational modifications may affect function by regulating subcellular localization. The complex regulatory outcomes of AhR expression and activation require a number of approaches to elucidate mechanistic information. In this thesis, a structural investigation of heterodimerization and DNA binding has been used to propose a molecular mechanism for target gene recognition and activation following XRE binding. Crystallographic approaches have yielded crystals of bHLH.PAS-A regions of AhR/ARNT heterodimer bound to DNA. Atomic force microscopy and small angle x-ray scattering analyses have illustrated an XRE binding mechanism whereby the DNA is bent, and the PASA region of the dimer flattens around the DNA. A targeted mutagenesis screen of the AhR ligand binding domain (LBD) was performed to investigate polycyclic aromatic hydrocarbon (PAH) and atypical ligand binding specificity. In parallel, mutant AhR proteins were assessed for inducibility by nonexogenous ligand modes of activation, including cell suspension and application of shear stressed serum. This process identified an LBD mutant selectively activated by novel ligand YH439, and completely inactive following PAH, cell suspension and shear stressed serum treatments, inferring the potential for differential ligand binding pocket access by YH439. Finally, given the complex output following expression and activation of AhR, regulation by post-translational modification was investigated as a potential means of subtle regulation of signalling fate. A thorough analysis of untreated AhR has revealed a concert of modifications occurring on functionally relevant regions of the protein that are implicated in regulating subcellular localization, protein: protein interactions, and potentially, protein stability. Preliminary analyses of YH439 and cell suspension treated AhR has additionally indicated the possibility of activation state specific modification patterns. In summary, this thesis describes: Novel approaches to structural characterisation of a bHLH.PAS protein dimer bound to DNA; atypical ligand binding to a novel site of AhR; and an analysis of a proposed AhR PTM code.
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Sciences, Discipline of Biochemistry, 2009

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Espira, Leon Masunde. "The basic helix-loop-helix transcription factor scleraxis regulates cardiac fibroblast collagen gene expression". 2009. http://hdl.handle.net/1993/21353.

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Huang, Kai-min, e 黃凱民. "Myogenic basic helix-loop-helix transcription factors regulate PGC-1α during terminal myogenic differentiation". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/22729909948641516355.

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碩士
國立中央大學
生命科學研究所
95
Skeletal muscle are generally classified as two types – type I (slow - twitch) and type II (fast - twitch). The former is rich in mitchondria and thus provides constant ATP through oxidative metabolism. The latter depends on the glycolytic metabolism as the energy source. PGC-1α is a transcriptional coactivator mainly expressed in the slow-twitch fibers. Previous studies indicated that over-expression of PGC-1α promotes the conversion from fast-twitch fibers to slow-twitch fibers. According to previous observations, we know that the E2-box on the PGC-1α promoter is essential for MyoD-mediated transactivation. In this study, we found that Stra13, a putative E1-box binding transcriptional repressor, repressed the MyoD mediated PGC-1α promoter activation. The interaction between MyoD and Stra13 was almost undetectable by GST-Pull down assay and EMSA. In addition, over-expression of P/CAF, but not CBP, can rescue the Stra13-mediated repression. These data suggest that Stra13 represses MyoD-mediated PGC-1 activation by sequestering P/CAF from MyoD.

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Brzózka, Magdalena Marta. "Untersuchungen zur Funktion des basischen Helix-Loop-Helix (bHLH)-Transkriptionsfaktors ME2 bei Lern- und Gedächtnisprozessen in der Maus". Doctoral thesis, 2008. http://hdl.handle.net/11858/00-1735-0000-0006-AD69-F.

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Brzózka, Magdalena Marta [Verfasser]. "Untersuchungen zur Funktion des basischen Helix-Loop-Helix (bHLH)-Transkriptionsfaktors ME2 bei Lern- und Gedächtnisprozessen in der Maus / vorgelegt von Magdalena Marta Brzózka". 2008. http://d-nb.info/996829318/34.

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Holder, Jimmy Lloyd Jr. "The bHLH/PAS transcription factor SIM1 is a novel obesity gene". 2005. http://edissertations.library.swmed.edu/pdf/HolderJ050305/HolderJimmy.pdf.

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