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Dissertations / Theses on the topic 'Connexin 26'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Meigh, Louise. "On the modulation of connexin 26 by CO2." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/61992/.

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The mechanism through which changes in PCO2 in the blood are detected is much disputed. Although many believe the stimulus for CO2 detection to be the associated increase in H+, increasing evidence supports a role for direct CO2 detection. In a recent development, Huckstepp et al demonstrated that connexin 26 hemichannels open in response to elevated CO2 in the absence of a pH change. This model however remained incomplete, with the mechanism of CO2 interaction with the channel being unknown. In this work I have employed site directed mutagenesis and dye loading studies to identify the CO2 bin

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2

Balandin, Taras [Verfasser]. "Expression and purification of human connexin 26 / Taras Balandin." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2016. http://d-nb.info/111776124X/34.

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3

Petersen, Lars. "Molekulargenetische Diagnostik von Connexin 26 bei genetisch bedingter, nicht-syndromaler, sensorineuraler Schwerhörigkeit." [S.l.] : [s.n.], 2001. http://archiv.ub.uni-marburg.de/diss/z2001/0302/.

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4

Sinnathuray, A. R. "Connexin 26 (GJB2) gene-related sensorineural deafness and outcomes after cochlear implantation." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446129.

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5

Whitehead, Caragh (Caragh Bryony). "Molecular analysis of GJB2 (connexin 26) and GJB6 (connexin 30) gene mutations in non-syndromic hereditary deafness in South Africa." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50028.

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Thesis (MSc)--University of Stellenbosch, 2004.<br>ENGLISH ABSTRACT: The most common inherited sensory disorder that affects I in 1 000 children is severe hearing loss. In developed countries, about a third of cases have a genetic origin, 80% of which are autosomal recessive forms (DFNB). Before 1993 few genes causing hearing loss had been identified, but since then a large number of genes related to this problem have been identified. Studies indicate that the DFNBI locus, located at position 13q11-12, contributes to 20% of all childhood deafness and may have a carrier rate as high as 2

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6

Donnelly, Steven. "Molecular mechanisms underlying mutations in Connexin 26 associated with genetically inherited skins disorders." Thesis, Glasgow Caledonian University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.688293.

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7

Iftoda, O. M. "Gender aspects of connexin 26 (GJB2) gene polymorphism in children with hearing loss." Thesis, БДМУ, 2022. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19712.

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8

Simpson, Charlotte Louise. "Molecular mechanisms regulating the epithelial barrier : key roles for Cx26 and ADAM17 during bacterial infection." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/9059.

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This study investigated how gastrointestinal and skin bacterial infections were affected by differential expression of connexin (Cx) 26 and a disintegrin and metalloprotease (ADAM) 17 in vitro. Cx26 is a component of gap junctions, which facilitate the transfer of small molecules between two cells. Recessive mutations in Cx26 cause non syndromic hearing loss (NSHL), and in certain populations, specific mutations account for the majority of Cx26 related NSHL. Their common occurrence suggests that they may provide a heterozygous, protective advantage to carriers. In this study adherence by the a

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9

Brockmeyer, Phillipp [Verfasser], Bernhard [Akademischer Betreuer] Hemmerlein, and Ralph [Akademischer Betreuer] Rödel. "Connexine als potenzielle Biomarker für den Progress oraler Plattenepithelkarzinome: Analyse der Expressionsmuster von Connexin 26, 43 und 45 und ihres Einflusses auf das Überleben / Phillipp Brockmeyer. Gutachter: Bernhard Hemmerlein ; Ralph Rödel. Betreuer: Bernhard Hemmerlein." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://d-nb.info/1053555377/34.

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10

Al-Hazza, Aseel [Verfasser], Wafaa [Gutachter] Shehata-Dieler, Kathleen [Gutachter] Wermke, and Thomas [Gutachter] Haaf. "Zu Grad, Konfiguration und Verlauf der Schallempfindungsschwerhörigkeit bei Kindern mit einer Connexin-26-Mutation / Aseel Al-Hazza ; Gutachter: Wafaa Shehata-Dieler, Kathleen Wermke, Thomas Haaf." Würzburg : Universität Würzburg, 2017. http://d-nb.info/1138196231/34.

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11

Fortunati, Nicola. "Molecular Dynamics Methods applied to flexible macromolecules." Doctoral thesis, Università degli studi di Padova, 2016. http://hdl.handle.net/11577/3424402.

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Cement-based materials, such as concrete or mortars, are usually considered materials with low technological level. Although they are the most employed human made materials in the world, others such as wood, plastics, metals and even stones are usually more valued in the everyday life: probably the fact that cement is cheap, readily available, common, and has been employed successfully for centuries, contributes to its low technology perception. However, this vision is far from the reality: the cement paste is a complex multicomponent and heterogeneous composite system, with different structu

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12

Martins, Ana Maria Cristina Rabello Pinto da Fonseca. "Estudo retrospectivo-sistemático e análise quantitativa da proliferação celular e apoptose; identificação da proteína conexina 43 e 26 aberrante em glândula perianal normal, hiperplásica e neoplásica em cães." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-11012007-153552/.

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Duzentos e quarenta e cinco neoplasias de glândula perianal de cães dos arquivos do Departamento de Patologia da FMVZ/ USP, de 1984 à 2004, foram revisadas histologicamente. A grande maioria dos casos (34%) foi classificada como adenoma moderadamente diferenciado, grupo II, em machos com mais de oito anos de idade o que reflete a dependência androgênica dessas neoplasias. A análise quantitativa da proliferação celular e apoptose nos diferentes tipos histológicos de neoplasias, hiperplasia e tecido normal dessas glândulas determinou um padrão paralelo de aumento de ambas as quantificações. Com

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13

PITTS, STACIE A. "SURVEY OF NEWBORN HEARING SCREENING AND GENETIC TESTING PRACTICES IN STATES AND HOSPITALS IN THE UNITED STATES." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1115987400.

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14

Eubanks, James L. "Connexins 26 and 32 in the developing neocortex /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/10648.

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15

Denoyelle, Françoise. "Prevalence et caracterisation clinique des surdites dues a une atteinte du gene de la connexine 26." Paris 6, 1999. http://www.theses.fr/1999PA066148.

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La surdite de perception atteint un enfant sur 1000 a la naissance. On estimait jusqu'a ces dernieres annees qu'environ un tiers des surdites de l'enfant etait de cause environnementale, un tiers etait de cause genetique cliniquement reconnue, et un tiers etaient des cas sporadiques sans cause retrouvee. Les formes genetiques etaient reconnues soit par l'integration de la surdite dans un syndrome polypathologique genetique (30% de ces formes), soit par l'existence d'une surdite familiale non syndromique (70%) se transmettant alors majoritairement (80%) sur un mode autosomique recessif (formes

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16

Heeb, Cornelia. "Immunhistochemische und molekularbiologische Untersuchung der räumlichen und zeitlichen Expression der Connexine 26, 32 und 43 im Plazentom des Rindes." Wettenberg : VVB Laufersweiler, 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968397948.

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17

Heeb, Cornelia [Verfasser]. "Immunhistochemische und molekularbiologische Untersuchung der räumlichen und zeitlichen Expression der Connexine 26, 32 und 43 im Plazentom des Rindes / von Cornelia Heeb." Wettenberg : VVB Laufersweiler, 2003. http://d-nb.info/968397948/34.

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18

Lahlou, Hicham. "Mécanismes moléculaires du signal anti-prolifératif transmis par le récepteur de somatostatine sst2 : implication des connexines 26 et 43." Toulouse 3, 2004. http://www.theses.fr/2004TOU30130.

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Le récepteur de somatostatine sst2 est un facteur déterminant dans le contrôle négatif de la prolifération des cellules normales et tumorales. Son expression est perdue dans 90% des adénocarcinomes pancréatiques. La correction de son déficit par transfert de gène dans les cellules cancéreuses pancréatiques humaines BxPC-3 conduit à l'inhibition de leur prolifération. Nous avons identifié les connexines 26 et 43 comme étant impliquées dans cet effet. Nos études montrent que l'induction de l'expression de ces connexines par sst2 résulte essentiellement d'une régulation au niveau de l'initiation

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19

Piatto, Vânia Belintani. "Análise molecular do gene da conexina 26 em pacientes com deficiênica auditiva sensorioneural não-sindrômica." Faculdade de Medicina de São José do Rio Preto, 2003. http://bdtd.famerp.br/handle/tede/245.

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Made available in DSpace on 2016-01-26T12:51:55Z (GMT). No. of bitstreams: 1 vaniapiatto_tese.pdf: 1479841 bytes, checksum: 96e04c84851d635167398b1a4196d2fe (MD5) Previous issue date: 2003-11-28<br>Mutações no gene que codifica a proteína conexina 26 têm contribuído para a maioria das deficiências auditivas pré-lingual, sensorioneural não-sindrômicas recessivas. Uma mutação específica, a 35delG, é a mais freqüente das mutações detectadas no gene GJB2 nos vários grupos étnicos estudados. O objetivo foi determinar a prevalência de mutações no gene GJB2 em pacientes com deficiência auditiva sen

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20

HENTATI, KSIBI OLFA. "Comparaison des permeabilites pour une serie de molecules fluorescentes des canaux jonctionnels homotypiques constitues des connexines 43, 32 et 26 de rat induites par transfection de leurs genes dans des lignees cellulaires non communicantes." Poitiers, 1999. http://www.theses.fr/1999POIT2376.

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Des canaux jonctionnels formes par les connexines (cx) de rat 43, 32 ou 26 induites apres transfection de leurs genes dans des lignees cellulaires deficientes en cx ont montre des permeabilites selectives differentes liees a la taille et a la charge de molecules fluorescentes. Les souches sauvages, les trois clones hela/cx43, 32 ou 26 et le clone skhep/cx43 ont ete fournis par deux laboratoires dans le cadre d'un contrat de recherche des communautes europeennes. L'immunomarquage des clones hela/cx43, 32 et 26 revele des connexines associees aux contacts cellulaires. Les permeabilites sont quan

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21

Brodmann, Tobias. ""Eine vergleichende Genexpressionsanalyse von Gap- Junction- Strukturproteinen in oralen Plattenepithelkarzinomen und gesunder Schleimhaut"." Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-0006-B31D-1.

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22

Al-Hazza, Aseel. "Zu Grad, Konfiguration und Verlauf der Schallempfindungsschwerhörigkeit bei Kindern mit einer Connexin-26-Mutation." Doctoral thesis, 2017. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-150966.

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Verschiedene Forschungsergebnisse der letzten zehn Jahre ergaben, dass die weitaus häufigeren, nicht-syndromalen Schwerhörigkeiten durch Mutation eines Gens (GJB2-Gen) entstehen, welches im Cortischen Organ des Innenohrs exprimiert wird. Das GJB2-Gen (Connexin-26-Gen), dessen Veränderung etwa 50 % der Fälle von autosomal rezessiver Schwerhörigkeit ausmacht, liegt im Chromosomenbereich 13q11–12. Aktuell identifiziert sind mehr als 70 weitere Loki, die in Verbindung mit nicht-syndromalen Formen von Schwerhörigkeit stehen. Die Prävalenz von NSHL beträgt nach neusten Studien ca. 1,33 pro 1000 Neug

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23

Brockmeyer, Phillipp. "Connexine als potenzielle Biomarker für den Progress oraler Plattenepithelkarzinome: Analyse der Expressionsmuster von Connexin 26, 43 und 45 und ihres Einflusses auf das Überleben." Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0022-5EE8-5.

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24

Petersen, Lars [Verfasser]. "Molekulargenetische Diagnostik von Connexin 26 bei genetisch bedingter, nicht-syndromaler, sensorineuraler Schwerhörigkeit / von Lars Petersen." 2001. http://d-nb.info/971997470/34.

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25

Schmalisch, Kathrin Helene [Verfasser]. "Funktionelle Charakterisierung von Connexin-26-Mutationen bei Patienten mit autosomal-rezessiver Schwerhörigkeit / vorgelegt von Kathrin Helene Schmalisch." 2008. http://d-nb.info/99135981X/34.

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26

Kabahuma, Rosemary I. "Genetic aspects of hearing loss in the Limpopo Province of South Africa." Thesis, 2010. http://hdl.handle.net/10539/8566.

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The aetiological diagnosis of recessive non-syndromic hearing loss poses a challenge owing to marked heterogeneity and the lack of identifying clinical features. The finding that up to 50% of recessive non-syndromal genetic hearing loss among Caucasians was due to mutations in GJB2, the gene encoding Connexin 26 (Cx26) was a breakthrough, whose value as a diagnostic tool has been limited by the significant variation in the prevalence of deafness genes and loci among population groups. The significant association of the GJB6-D13S1830 deletion among individuals with one mutant GJB2 allele

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