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Relevant bibliographies by topics / DFNB16

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Journal articles
Dissertations / Theses
Book chapters
Conference papers

Academic literature on the topic 'DFNB16'

Author: Grafiati

Published: 7 September 2024

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Journal articles on the topic "DFNB16"

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Aldè, Mirko, Giovanna Cantarella, Diego Zanetti, et al. "Autosomal Dominant Non-Syndromic Hearing Loss (DFNA): A Comprehensive Narrative Review." Biomedicines 11, no. 6 (2023): 1616. http://dx.doi.org/10.3390/biomedicines11061616.

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Autosomal dominant non-syndromic hearing loss (HL) typically occurs when only one dominant allele within the disease gene is sufficient to express the phenotype. Therefore, most patients diagnosed with autosomal dominant non-syndromic HL have a hearing-impaired parent, although de novo mutations should be considered in all cases of negative family history. To date, more than 50 genes and 80 loci have been identified for autosomal dominant non-syndromic HL. DFNA22 (MYO6 gene), DFNA8/12 (TECTA gene), DFNA20/26 (ACTG1 gene), DFNA6/14/38 (WFS1 gene), DFNA15 (POU4F3 gene), DFNA2A (KCNQ4 gene), and

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Domínguez-Ruiz, María, Laura Ruiz-Palmero, Paula I. Buonfiglio, et al. "Novel Pathogenic Variants in the Gene Encoding Stereocilin (STRC) Causing Non-Syndromic Moderate Hearing Loss in Spanish and Argentinean Subjects." Biomedicines 11, no. 11 (2023): 2943. http://dx.doi.org/10.3390/biomedicines11112943.

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Non-syndromic hearing impairment (NSHI) is a very heterogeneous genetic condition, involving over 130 genes. Mutations in GJB2, encoding connexin-26, are a major cause of NSHI (the DFNB1 type), but few other genes have significant epidemiological contributions. Mutations in the STRC gene result in the DFNB16 type of autosomal recessive NSHI, a common cause of moderate hearing loss. STRC is located in a tandem duplicated region that includes the STRCP1 pseudogene, and so it is prone to rearrangements causing structural variations. Firstly, we screened a cohort of 122 Spanish familial cases of n

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Back, Daniela, Wafaa Shehata-Dieler, Barbara Vona, et al. "Phenotypic Characterization of DFNB16-associated Hearing Loss." Otology & Neurotology 40, no. 1 (2019): e48-e55. http://dx.doi.org/10.1097/mao.0000000000002059.

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Faridi, Rabia, Rizwan Yousaf, Sayaka Inagaki, et al. "Deafness DFNB128 Associated with a Recessive Variant of Human MAP3K1 Recapitulates Hearing Loss of Map3k1-Deficient Mice." Genes 15, no. 7 (2024): 845. http://dx.doi.org/10.3390/genes15070845.

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Deafness in vertebrates is associated with variants of hundreds of genes. Yet, many mutant genes causing rare forms of deafness remain to be discovered. A consanguineous Pakistani family segregating nonsyndromic deafness in two sibships were studied using microarrays and exome sequencing. A 1.2 Mb locus (DFNB128) on chromosome 5q11.2 encompassing six genes was identified. In one of the two sibships of this family, a novel homozygous recessive variant NM_005921.2:c.4460G>A p.(Arg1487His) in the kinase domain of MAP3K1 co-segregated with nonsyndromic deafness. There are two previously reporte

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Frykholm, Carina, Joakim Klar, Tatjana Tomanovic, Adam Ameur, and Niklas Dahl. "Stereocilin gene variants associated with episodic vertigo: expansion of the DFNB16 phenotype." European Journal of Human Genetics 26, no. 12 (2018): 1871–74. http://dx.doi.org/10.1038/s41431-018-0256-6.

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Avan, Paul, Sébastien Le Gal, Vincent Michel, et al. "Otogelin, otogelin-like, and stereocilin form links connecting outer hair cell stereocilia to each other and the tectorial membrane." Proceedings of the National Academy of Sciences 116, no. 51 (2019): 25948–57. http://dx.doi.org/10.1073/pnas.1902781116.

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The function of outer hair cells (OHCs), the mechanical actuators of the cochlea, involves the anchoring of their tallest stereocilia in the tectorial membrane (TM), an acellular structure overlying the sensory epithelium. Otogelin and otogelin-like are TM proteins related to secreted epithelial mucins. Defects in either cause the DFNB18B and DFNB84B genetic forms of deafness, respectively, both characterized by congenital mild-to-moderate hearing impairment. We show here that mutant mice lacking otogelin or otogelin-like have a marked OHC dysfunction, with almost no acoustic distortion produc

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Drury, Stacy S., and Bronya J. B. Keats. "Mouse Tales from Kresge: The Deafness Mouse." Journal of the American Academy of Audiology 14, no. 06 (2003): 296–301. http://dx.doi.org/10.1055/s-0040-1715745.

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Mouse models for human deafness have not only proven instrumental in the identification of genes for hereditary hearing loss, but are excellent model systems in which to examine gene function as well as the resulting pathophysiology. One mouse model for human nonsyndromic deafness is the deafness (dn) mouse, a spontaneous mutation in the curly-tail (ct) stock. The dn gene is on mouse Chromosome 19 and it was recently shown to be a novel gene called Tmc1. A mutation in Tmc1 is also found in Beethoven (Bth), which is another deaf mouse mutant. In humans, one autosomal dominant form of nonsyndrom

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Achard, S., F. Simon, F. Denoyelle, and S. Marlin. "Vertiges positionnels paroxystiques bénins récidivants chez deux enfants DFNB16 d’une même fratrie : cas clinique CARE." Annales françaises d'Oto-rhino-laryngologie et de Pathologie Cervico-faciale 140, no. 3 (2023): 129–32. http://dx.doi.org/10.1016/j.aforl.2022.10.008.

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Cosetti, Maura, David Culang, Sumankrishna Kotla, Peter O'Brien, Daniel F. Eberl, and Frances Hannan. "Unique Transgenic Animal Model for Hereditary Hearing Loss." Annals of Otology, Rhinology & Laryngology 117, no. 11 (2008): 827–33. http://dx.doi.org/10.1177/000348940811701106.

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Objectives: This study capitalizes on the unique molecular and developmental similarities between the auditory organs of Drosophila and mammals, to investigate genes implicated in human syndromic and nonsyndromic hearing loss in a genetically tractable experimental animal model, the fruit fly Drosophila. Methods: The Drosophila counterparts of 3 human deafness genes (DIAPH1/DFNA1, ESPN/DFNB36, and TMHS/DFNB67) were identified by sequence similarity. An electrophysiological assay was used to record sound-evoked potentials in response to an acoustic stimulus, the Drosophila courtship song. Resul

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Vona, B., M. A. H. Hofrichter, C. Neuner, et al. "DFNB16 is a frequent cause of congenital hearing impairment: implementation of STRC mutation analysis in routine diagnostics." Clinical Genetics 87, no. 1 (2014): 49–55. http://dx.doi.org/10.1111/cge.12332.

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Dissertations / Theses on the topic "DFNB16"

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Iranfar, Sepideh. "AAV-mediated gene therapy restores hearing and central auditory processing in a mouse model of human DFNB16 Deafness." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS127.pdf.

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La déficience auditive constitue un handicap fonctionnel majeur, affectant plus d'un demi-milliard de personnes dans le monde. Malgré sa prévalence élevée, aucun traitement curatif n'existe actuellement. Mon projet de thèse est translationnel et vise à établir la preuve de concept selon laquelle la thérapie génique virale peut restaurer l'audition dans le modèle préclinique de surdité DNFB16. La surdité DFNB16 est la deuxième cause de déficience auditive congénitale d'origine génétique. Elle est causée par des mutations du gène codant pour la stéréociline (STRC) et se caractérise par une surdi

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Delmaghani, Sedigheh. "Neuropathie auditive : identification du gène DFNB59 et physiopathologie." Paris 6, 2006. http://www.theses.fr/2006PA066164.

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Par une analyse de liaison génétique dans des grandes familles iraniennes atteintes de surdité prélinguale de transmission autosomique récessive, j’ai pu définir deux nouveaux loci de surdité isolée: DFNB40, sur le chromosome 22 (22q11. 21-12. 1) et DFNB59, sur le chromosome 2 (2q31. 1-31. 3). J’ai ensuite identifié le gène DFNB59. Il code pour une nouvelle protéine de 352 acides aminés, que j’ai nommée pejvakine. Afin de valider l’implication de ce gène dans la surdité DFNB59, j’ai produit un modèle de souris knock-in pour l’une des deux mutations humaines identifiées. Ces souris ont une neur

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Ceriani, Federico. "Quantitative estimate of biochemical and electrical intercellular coupling in the developing cochlea of wild type and DFNB1 mouse models." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423720.

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Hearing loss is the most common form of sensory impairment, with approximately one infant/1000 born with profound congenital deafness. Nonsyndromic hearing loss and deafness (DFNB1) is an inherited condition with a mild to severe deafness phenotype caused by mutations in GJB2 (which encodes the protein connexin26) and GJB6 (which encodes connexin30). Gap junction channels formed primarily by these two connexin protein subunits couple non-sensory cells (supporting and epithelial cells) of the mammalian cochlea, forming vast functional syncytia. Previous work has shown that electrical and metabo

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BERTO, Anna. "ACQUEDOTTO VESTIBOLARE ALLARGATO: S. DI PENDRED, DFNB4, SINDROME DELL’ACQUEDOTTO VESTIBOLARE ALLARGATO." Doctoral thesis, Università degli studi di Ferrara, 2010. http://hdl.handle.net/11392/2389300.

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L’acquedotto vestibolare è un canale osseo che si estende dalla parete mediale del vestibolo alla faccia cerebellare della piramide petrosa, contiene vasi e una componente del labirinto membranoso dell’orecchio interno, il dotto endolinfatico che si apre nel sacco endolinfatico. L’acquedotto vestibolare allargato (EVA) è la più comune malformazione congenita associata ad ipoacusia. Le mutazioni del gene SLC26A4 della pendrina sono considerate una delle più comuni cause di ipoacusia congenita ed EVA e sono coinvolte in circa il 10% di tutte le ipoacusie ereditate; due manifestazioni c

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Roux, Isabelle. "Physiopathologie de la surdité DFNB9 : identification de l'otoferline comme composant essentiel de l'exocytose des synapses à ruban des cellules sensorielles auditives." Paris 7, 2006. http://www.theses.fr/2006PA077153.

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Plusieurs mutations du gèneOTOF ont été identifiées comme responsables de la surdité autosomique récessive DFNB9. Ce gène code pour l'otoferline, une protéine transmembranaire à 6 domaines C2, domaines d'interaction potentielle avec le calcium et les phospholipides. Dans la cochlée adulte, l'otoferline est spécifiquement exprimée dans les cellules ciliées internes qui sont les véritables cellules sensorielles de la cochlée puisqu'elles transmettent le message auditif au système nerveux central. Dans ces cellules, l'otoferline est associée aux vésicules synaptiques entourant le ruban et à la me

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GRATI, M'HAMED. "Identification du gene otof, responsable de la surdite isolee recessive dfnb9 chez l'homme, et caracterisation de la proteine correspondante, l'otoferline, durant le developpement cochleaire chez la souris." Paris 7, 2001. http://www.theses.fr/2001PA077028.

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L'audition joue un role majeur dans la communication entre individus dans la societe puisqu'elle permet la perception de la parole, vehicule du langage. Par une approche de clonage positionnel et de gene candidat, nous avons identifie le gene otof dont les mutations sont responsables de la surdite isolee autosomique recessive humaine dfnb9. Il coderait pour deux proteines, l'une de 140 et l'autre de 257 kda contenant respectivement 3 et 6 domaines c2, et un domaine transmembranaire cooh-terminal. Le gene otof et son orthologue murin otof comprennent 48 exons. Ils codent pour plusieurs transcri

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Fasquelle, Lydie. "TMPRSS3 dont les mutations sont responsables des surdités humaines DFNB8/10, joue un rôle crucial dans la survie des cellules sensorielles lors de l'entrée en fonction cochléaire : caractérisation du modèle animal et identification des voies de signalisation impliquées." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T026.

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TMPRSS3 est une sérine protéase mutée dans les surdités humaines DFNB8/10. Pour déterminer le rôle de cette protéine dans la physiologie cochléaire, nous avons généré puis caractérisé le phénotype auditif d'un modèle murin mimant la pathologie humaine. Les souris mutantes homozygotes sont profondément sourdes, due à une perte rapide et complète des cellules sensorielles cochléaires au moment de leur entrée en fonction. Afin de caractériser les mécanismes moléculaires responsables de la perte de ces cellules, nous avons comparé le protéome de souris sauvages et mutantes par des gels en 2-dimens

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Correia, Bárbara Isabel de Carvalho. "Analysis of DFNB1 locus in presbycusis." Master's thesis, 2017. http://hdl.handle.net/10451/30529.

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Tese de mestrado, Biologia Molecular e Genética, Universidade de Lisboa, Faculdade de Ciências, 2017<br>Introdução: O ouvido é um órgão sensorial que tem como função a transmissão e a tradução de sons para o cérebro assegurando assim a audição essencial a uma comunicação oral eficaz. A surdez é considerada a deficiência sensorial mais comum na população humana, comprometendo a integração social do indivíduo afetado e envolve a perda total ou parcial da capacidade de um indivíduo detetar sons. Aproximadamente 1/1000 recém-nascidos apresentam surdez, bem como cerca de 1/3 dos indivíduos com idad

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Jorge, Catarina de Jesus dos Santos. "DFNB1 : surdez hereditária neurosensorial associada a mutações nos genes das conexinas." Master's thesis, 2019. http://hdl.handle.net/10451/42888.

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Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2019<br>A surdez é a deficiência sensorial mais comum e afecta cerca de 466 milhões de pessoas em todo o mundo, das quais 34 milhões são crianças. Apesar de a surdez hereditária poder estar associada a causas adquiridas, estima-se que, de todos os casos de surdez, mais de 50% tenha uma causa genética, tendo já sido identificados mais de 100 genes em humanos associados a esta patologia. A surdez não sindrómica, corresponde a cerca de 70% dos casos congénitos e destes, cerca de 80% está asso

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Banghová, Karolína. "Pendrin v patogenezi vrozené nedostatečnosti štítné žlázy." Doctoral thesis, 2009. http://www.nusl.cz/ntk/nusl-273887.

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Pendrin is an anion transporter that is expressed in several organs. In the thyroid gland, pendrin is localized at the apical pole of thyrocytes and it is responsible for the iodide efflux from thyrocytes into the colloid in the follicular lumen where iodide is organificated. The extrathyroidal expression was shown in the inner ear, kidney, placenta and mammary gland. Carriers of mutations in the pendrin gene (PDS, SLC26A4) display variable phenotypical features following the autosomal recessive manner of the inheritance: combined thyroid and hearing affection (Pendred syndrome - OMIM274600),

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Book chapters on the topic "DFNB16"

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Yasunaga, S., M. Grati, and C. Petit. "DFNB9 and DFNB12." In Advances in Oto-Rhino-Laryngology. KARGER, 2000. http://dx.doi.org/10.1159/000059097.

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Scott, D. A., and V. C. Sheffield. "DFNB11." In Advances in Oto-Rhino-Laryngology. KARGER, 2000. http://dx.doi.org/10.1159/000059095.

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Denoyelle, F., M. Mustapha, and C. Petit. "DFNB21." In Advances in Oto-Rhino-Laryngology. KARGER, 2002. http://dx.doi.org/10.1159/000066827.

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Avraham, K. B. "DFNA15." In Advances in Oto-Rhino-Laryngology. KARGER, 2000. http://dx.doi.org/10.1159/000059091.

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McGuirt, W. T., S. D. Prasad, R. A. Cucci, G. F. Green, and R. J. H. Smith. "Clinical Presentation of DFNB1." In Advances in Oto-Rhino-Laryngology. KARGER, 2002. http://dx.doi.org/10.1159/000066821.

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Denoyelle, F., and C. Petit. "DFNB9." In Advances in Oto-Rhino-Laryngology. KARGER, 2002. http://dx.doi.org/10.1159/000066822.

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Mueller, R. F., and N. J. Lench. "Mapping of the DFNB1 Locus." In Advances in Oto-Rhino-Laryngology. KARGER, 2000. http://dx.doi.org/10.1159/000059090.

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Lalwani, A. K., J. A. Goldstein, and A. N. Mhatre. "Auditory Phenotype of DFNA17." In Advances in Oto-Rhino-Laryngology. KARGER, 2002. http://dx.doi.org/10.1159/000066818.

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Govaerts, P. J., G. De Ceulaer, K. Daemers, et al. "Clinical Presentation of DFNA8-DFNA12." In Advances in Oto-Rhino-Laryngology. KARGER, 2002. http://dx.doi.org/10.1159/000066805.

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Tamagawa, Y., K. Ishikawa, K. Ishikawa, et al. "Clinical Presentation of DFNA11 (MYO7A)." In Advances in Oto-Rhino-Laryngology. KARGER, 2002. http://dx.doi.org/10.1159/000066808.

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Conference papers on the topic "DFNB16"

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Back, D., S. Schraven, B. Vona, et al. "Phänotyp-Charakterisierung von 9 Patienten mit DFNB16-Gendefekt." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640738.

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Back, D., S. Schraven, B. Vona, et al. "Phenotype characterization of 9 patients with mutations in DFNB16-gene." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640739.

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Pangrsic, T., MM Picher, V. Rankovic, and T. Moser. "Towards future gene therapy for DFNB93-associated hearing loss." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686470.

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Strenzke, N., M. Pelgrim, M. Jeschke, and E. Reisinger. "Mechanisms and consequences of auditory fatigue in auditory synaptopathy DFNB9." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686516.

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Strenzke, N., M. Pelgrim, M. Jeschke, and E. Reisinger. "Mechanismen und Konsequenzen der pathologischen Hörermüdung bei der auditorischen Synaptopathie DFNB9." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686287.

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Oestreicher, David, Shashank Chepurwar, Vladan Rankovic, Dirk Beutner, Nicola Strenzke, and Tina Pangrsic. "Ein Mausmodell für DFNB93 bestätigt eine nutzungsabhängige Verschlechterung der synaptischen übertragung und der Hörnervenfaseraktivität als zugrunde liegenden Krankheitsmechanismus." In 94. Jahresversammlung Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1766813.

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Reisinger, E., H. Al-Moyed, A. Cepeda, S. Kügler, S. Jung, and T. Moser. "Gentherapie gegen Taubheit: eine Machbarkeitsstudie zeigt die teilweise Wiederherstellung des Hörvermögens in einem Mausmodell für DFNB9." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686252.

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Oestreicher, David, Shashank Chepurwar, Vladan Rankovic, Dirk Beutner, Nicola Strenzke, and Tina Pangrsic. "A mouse model for DFNB93 corroborates use-dependent deterioration of Synaptic Transmission and Auditory Nerve Fiber Spiking as the underlying disease mechanism." In 94th Annual Meeting German Society of Oto-Rhino-Laryngology, Head and Neck Surgery e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1767446.

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Reisinger, E., H. Al-Moyed, A. Cepeda, S. Kügler, S. Jung, and T. Moser. "Gene therapy against deafness: a proof of concept study demonstrates partial rescue of hearing in a mouse model for deafness DFNB9." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686481.

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