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Relevant bibliographies by topics / TMEM16B

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Dissertations / Theses

Academic literature on the topic 'TMEM16B'

Author: Grafiati

Published: 14 March 2023

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Dissertations / Theses on the topic "TMEM16B"

1

Suzuki, Takayuki. "Functional Swapping between Transmembrane Proteins TMEM16A and TMEM16F." Kyoto University, 2014. http://hdl.handle.net/2433/188693.

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2

Ishihara, Kenji. "Role of Ca2+ in the Stability and Function of TMEM16F and 16K." Kyoto University, 2016. http://hdl.handle.net/2433/217141.

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3

Lancien, Mélanie. "Etude du rôle des gènes homologues Tmem176a et Tmem176b dans le système immunitaire : immunité de type 17 et biologie des cellules dendritiques." Thesis, Nantes, 2019. http://www.theses.fr/2019NANT1011.

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Notre système immunitaire assure la protection et régule l'homéostasie de l'organisme. Pour cela, il se compose d'une réponse immune innée et d'une réponse adaptative. Notre équipe a identifié TMEM176A et TMEM176B, deux protéines transmembranaires de structure et de fonction identiques. Ces protéines sont des canaux ioniques intracellulaires qui ont la particularité d'être fortement exprimés à la fois dans les cellules RORyt+ et dans les cellules dendritiques. La génération d'une souris déficiente pour ces deux gènes nous a permis d'étudier leur rôle. Nous avons mis en évidence que l'absence d

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4

Ubby, Ifeoma. "Regulation of TMEM16A altrenatice splincing." Doctoral thesis, Scuola Normale Superiore, 2012. http://hdl.handle.net/11384/85994.

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TMEM16A/Anoctamin1 is a novel calcium-‐activated chloride channel involved in neuronal and cardiac excitation, vascular tone, pain perception and olfactory and sensory signal transduction and GI tract motility. It is also associated to diverse type of cancer including breast cancer malignancy. Alternative splicing (AS) of exons 6b, 13 and 15 generates functionally distinct TMEM16A isoforms with different electrophysiological properties. To study their splicing regulation, I performed in minigene system a systematic analysis of exonic and intronic regulatory elements followed by co-‐transfect

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5

Adomaviciene, Aiste. "TMEM16A channels : molecular physiology and pharmacological regulation." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/tmem16a-channels-molecular-physiology-and-pharmacological-regulation(681d1c72-3207-41f5-bd78-c6af0a6ccdf3).html.

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Calcium-activated chloride channels (CaCCs) are a class of the ligand-gated channels involved in numerous cellular functions. In vascular smooth muscle, these ion channels couple agonist-induced calcium-release from the sarcoplasmic reticulum to membrane depolarisation and vasoconstriction. For this reason, CaCCs have been suggested as a potential molecular target to treat a range of vascular disorders. These ion channels, however, have not been yet explored as a drug target because their molecular identity has been elusive and their pharmacology has been restricted to compounds with low poten

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6

Meadows, Benjamin Roland Alexander. "Unravelling the cell adhesion defect in Meckel-Gruber syndrome." Thesis, University of Exeter, 2016. http://hdl.handle.net/10871/29380.

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Meckel-Gruber syndrome (MKS) is a universally lethal heritable human disease characterised by CNS malformations, cystic kidney, polydactyly, and liver fibrosis. MKS is classed as one of the ciliopathies due to its association with dysfunctional primary cilia, signalling organelles found on most cells in the human body. Some of the symptoms of MKS can be explained as a consequence of disrupted developmental signalling through the primary cilium, other defects are harder to explain, and evidence now exists for non-ciliary influences on ciliopathies. The nature of these influences, and the implic

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7

Brookfield, Rebecca. "The pharmacology and cardiovascular function of TMEM16A channels." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/the-pharmacology-and-cardiovascular-function-of-tmem16a-channels(bdc16466-cecd-4343-9d40-b20bc647d70f).html.

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Calcium-activated chloride channels (CaCCs) are ubiquitously expressed in a plethora of cell types and, consequently, are involved in numerous cellular processes as diverse as epithelial secretion, regulation of cardiac excitability and smooth muscle contraction. Current pharmacology of CaCCs is limited to compounds with low potency and poor selectivity. The lack of knowledge surrounding the molecular identity of the CaCC has greatly hindered the development of more specific drugs and has impaired our understanding of the channel physiology and biophysics. The recent discovery that the TMEM16A

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8

SCUDIERI, PAOLO. "Intermolecular Interactions in the TMEM16A Dimer Controlling Channel Activity." Doctoral thesis, Università degli studi di Genova, 2018. http://hdl.handle.net/11567/929402.

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TMEM16A e TMEM16B sono proteine di membrana con funzione di canali del cloruro attivati da calcio. Attraverso la generazione di canali chimerici, e in particolare, sostituendo la regione carbossi-terminale di TMEM16A con la regione equivalente di TMEM16B, sono stati ottenuti dei canali dotati di una maggiore attività. Il progressivo accorciamento della regione chimerica ha permesso di restringere il “dominio attivante” a una corta sequenza di 14 aminoacidi localizzata vicino all’ultimo dominio transmembrana e ha generato proteine-canale TMEM16A dotate di un’attività molto alta anche a c

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9

Gyobu, Sayuri. "A role of TMEM16E carrying a scrambling domain in sperm motility." Kyoto University, 2016. http://hdl.handle.net/2433/215460.

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論文1ページ目の下部に著作権を表示すること。（© 2016, American Society for Microbiology. ）<br>Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(医科学)<br>甲第19634号<br>医科博第72号<br>新制||医科||5(附属図書館)<br>32670<br>京都大学大学院医学研究科医科学専攻<br>(主査)教授近藤玄, 教授篠原隆司, 教授秋山芳展<br>学位規則第4条第1項該当

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10

Schwenk, Benjamin. "The FTLD risk factor TMEM106B controls lysosomal trafficking and dendrite outgrowth." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-181956.

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Frontotemporal dementia is the second most common neurodegenerative disease in people younger than 65 years. Patients suffer from behavioral changes, language deficits and speech impairment. Unfortunately, there is no effective treatment available at the moment. Cytoplasmic inclusions of the DNA/RNA-binding protein TDP-43 are the pathological hallmark in the majority of FTLD cases, which are accordingly classified as FTLD-TDP. Mutations in GRN, the gene coding for the trophic factor progranulin, are responsible for the majority of familiar FTLD-TDP cases. The first genome-wide association stud

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