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1

BONCORAGLIO, GIORGIO BATTISTA. "Role of Ryanodine Receptor type 3 (RyR3) in ischemic stroke." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/317052.

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L'ictus è una delle principali cause di mortalità e disabilità acquisita in tutto il mondo. Il primo studio di associazione genome-wide in pazienti con ictus ischemico italiano ha trovato un'associazione significativa con il polimorfismo missenso a singolo nucleotide (SNP) rs4780144 nel gene del recettore della rianodina di tipo 3 (RyR3), che porta a una potenziale perdita di funzione. Molteplici evidenze hanno suggerito che una ridotta funzione di RyR3 potrebbe migliorare l'esito dell'ictus. Con questo studio abbiamo mirato a indagare il ruolo di RyR3 nell'ictus ischemico a livello funzionale
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2

Dabertrand, Fabrice. "Identification et rôle fonctionnels de variants d'épissage du récepteur de la ryanodine de type 3 (RyR3)." Bordeaux 2, 2006. http://www.theses.fr/2006BOR21351.

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La fonction du sous-type RYR 3 du récepteur de la ryanodine ne peut se comprendre qu'à travers l'étude de ses différents variants d'épissage. Dans les muscles lisses de souris, nous avons mis en évidence l'existence d'un variant court dominant négatif. En effet, dans le duodenum, celui-ci inhibe le sous-type RYR 2 responsable de la libération du calcium stocké dans le reticulum. L'isoforme complète de RYR3 n'interagit pas avec l'isoforme courte et code des oscillations calciques spontanées lors d'une surharge du contenu en calcium du reticulum. Enfin, cet épissage alternatif est modulé dans le
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3

Chameau, Pascal. "Le recepteur de la ryanodine de type 3 (ryr3) : localisation et role dans l'excitabilite neuronale et la transmission synaptique." Paris 6, 1999. http://www.theses.fr/1999PA066101.

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Le recepteur de la ryanodine de type 3 (ryr3), exprime dans les neurones, est l'isoforme la moins caracterisee de cette famille de recepteurs-canaux ca 2 + du reticulum endoplasmique. J'ai developpe un anticorps polyclonal dirige contre ryr3 qui m'a permis de determiner la localisation de cette isoforme dans la region proximale des dendrites apicaux des neurones pyramidaux de la region ca1 de l'hippocampe de souris. Cet anticorps s'est avere bloquant du mecanisme de calcium-induced calcium release (cicr) dans lequel ryr3 est implique. Dans les neurones ca1, l'injection de l'anticorps anti-ryr3
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4

Whiteley, Gareth. "Molecular architecture of Caveolin-3 and the investigation of an interaction with the ryanodine receptor." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/molecular-architecture-of-caveolin3-and-the-investigation-of-an-interaction-with-the-ryanodine-receptor(d5d4e1f1-88c5-4619-b208-7742d0cd81f5).html.

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The muscle-specific membrane protein, Caveolin-3, is a building block of caveolae a type of specialised lipid raft. Caveolin-3 is proposed to play a central role in variety of cellular functions both structural and functional, from cell signalling to cholesterol homeostasis. Caveolin-3 has also been implicated in processes involved in targeting membrane proteins to the plasma membrane, as well as mediating a host of cell signalling processes. Initial attempts were made to express full-length Caveolin-3 in E.coli. However, more success was achieved in expressing and purifying domains of Caveoli
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5

King, James Harmsworth. "Arrhythmogenic mechanisms in RYR2-P2328S murine hearts." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648837.

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6

Klipp, Robert Carl. "Novel Compound, 84F2, Inhibits Calmodulin Deficient RyR2." PDXScholar, 2017. https://pdxscholar.library.pdx.edu/open_access_etds/3484.

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The cardiac ryanodine receptor (RyR2) plays a key role in excitation-contraction coupling (ECC). Mutations in RyR2 are known to be linked to the arrhythmogenic disorder, catecholaminergic polymorphic ventricular tachycardia (CPVT), a deadly disease which is characterized by a leak of calcium from sarcoplasmic reticulum and a decrease in calmodulin (CaM) binding. A novel drug, 84F2, shown to inhibit arrhythmias in RyR2-R176Q heterozygous CPVT mouse hearts (2.5 µg/kg), decrease spark frequency in cells derived from CPVT mice (IC50 = 35 nM), and inhibit RyR2 single channel activity at low nanomol
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7

Wang, YueYi. "Ca2+ handling in a mice model of CPVT." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS156/document.

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Le canal calcique de libération du Ca2+, appelé récepteur à la ryanodine (RyR) est localisé dans la membrane du réticulum sarcoplasmique des cardiomyocytes, en incluant ceux du pacemaker, et a un rôle important dans le couplage excitation contraction et la génération du rythme cardiaque. Des mutations dans leur gène sont responsables de la tachycardie catécholergique (CPVT), qui est une maladie létale, manifestée par des syncopes ou mort subite lors de stress émotionnel ou physique. Au repos, ces patients ont un électrocardiogramme normal, mais une tendance plus importante à la bradycardie.Nos
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8

Yin, Liheng. "Impact of the catecholaminergic polymorphic ventricular tachycardia (CPVT) mutation RyR2R420Q in cell function." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASS068.

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La tachycardie ventriculaire polymorphe catécholergique (CPVT) est une arythmie génétique létale qui se manifeste par une syncope ou une mort subite chez les enfants et les jeunes adultes dans des conditions de stress sans anomalie structurelle cardiaque évidente. Plusieurs mécanismes ont été proposés pour expliquer les altérations fonctionnelles sous-jacentes de la libération de Ca2+ dues aux mutations de RyR2 ou de ses protéines accessoires. Une nouvelle mutation CPVT située sur la partie N terminale de RyR2 a été identifiée dans une famille espagnole (RyR2R420Q). Ici, nous avons utilisé un
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9

Kathirvel, Paramasivam. "Mapping and manipulation of the murine ryanodine receptor gene (Ryr1)." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/12330.

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In this present study, experiments were carried out a) to characterise the mouse skeletal muscle ryanodine receptor (<i>Ryr1)</i> gene cDNA, b) to construct a contiguous map of the murine Ryr1 gene and c) to evaluate the phenotype of the <i>Ryr1</i> knockout transgenic mice and to develop a mouse model, which carries a homologue of the C1843T mutation, associated with MH in pigs and some humans. The murine <i>Ryrl</i> cDNA has been characterised by cDNA cloning and sequence analysis. Murine <i>Ryrl</i> exon-specific RT-PCR primers were designed and used to generate <i>Ryrl</i> cDNA fragments f
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10

Nicoll, Baines Katie Mhairi. "Muscle energetics and ageing in the context of RYR1 variants." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/17288/.

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In aged muscle, from humans and mice, the ryanodine receptor (RyR1) is leaky, leading to increased levels of resting Ca2+ in the myoplasm. This is also a feature of skeletal muscle disorders caused by variants in RyR1 such as malignant hyperthermia (MH), central core disease (CCD), exertional heat illness (EHI) and late-onset axial myopathy (LOAM). Elevated Ca2+ is damaging to mitochondria, leading to production of reactive oxygen and nitrogen species associated with MH susceptibility to inhalational anaesthetics. Mice with Ryr1 variants show premature muscle ageing and highlight the cycle of
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11

Bround, Michael J. "The effects of RYR2 gene deletion on cardiac function and metabolism." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/57589.

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The cardiac ryanodine receptor 2 (RYR2) is a sarcoplasmic reticulum Ca²⁺ release channel central to cardiomyocyte biology. RYR2 Ca²⁺ release has a well-established role in activating cardiomyocyte motor proteins during excitation-contraction coupling and is therefore critical for heart function. RYR2 is also poised to have other important cardiac functions such as setting heart rate, stimulating ATP metabolism, regulating cardiac hypertrophy, and controlling cardiomyocyte survival. In addition, there is evidence that RYR2 dysfunction occurs during heart disease, suggesting that RYR2 may be a d
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12

Ginta, Daniela Laura. "Genetic and molecular characterization of l(3)ry93 in Drosophila melanogaster." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ61558.pdf.

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13

Anthony, Diana Francesca. "CaMK118 interaction with the RyR2 complex in normal and failing rabbit hearts." Thesis, University of Strathclyde, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488532.

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Cardiac Ca2+ cycling consist of a series of tightly controlled events, regulated by a number of key proteins that release and sequester Ca2+ both at the cell surface and via intracellular stores. RyR2 is the main SR Ca2+ release channel. Direct regulation of RyR2 by CaMKIId, an important Ca -dependent enzyme, has previously been demonstrated.
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14

Lobo, Joshua J. "3D RECONSTRUCTION OF RyR1 AND STRUCTURAL VALIDATION UNDER DIFFERENT LEVELS OF NOISE." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3633.

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Ryanodine receptors (RyR) are intracellular channels that are intricately involved in Ca2+ release. These channels large membrane proteins~2.26MDa in size. In this multi-goal project firstly we successfully studied the gating mechanics of the RyR1 in the presence of Mg2+. We used single particle reconstruction and image processing techniques to obtain the 3D structure of the RyR1 with Mg2+. The 3D structure in the presence of Mg2+ and an ATP analog is the closest representation of human physiological conditions. The open and closed state structures of RyR1 are known. However, the physiological
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15

Bertan, Fabio [Verfasser]. "Ryanodine Receptor 2 (RyR2) underlies maintenance and remodeling of dendritic spines / Fabio Bertan." Bonn : Universitäts- und Landesbibliothek Bonn, 2020. http://d-nb.info/1229989161/34.

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16

Lüpken, Thomas [Verfasser]. "Hochauflösende Kartierung der Virusresistenzgene rym11 und Ryd3 der Gerste (Hordeum vulgare L.) / Thomas Lüpken." Gießen : Universitätsbibliothek, 2015. http://d-nb.info/1073119084/34.

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17

Fry, Debra L. "Modulating intracellular Ca2+ signalling using recombinant fragments of the human cardiac ryanodine receptor (RyR2)." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/54780/.

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Interaction between discrete domains of the cardiac ryanodine receptor (RyR2) has emerged as a pivotal mechanism regulating channel function. RyR2 mutations perturb conformational intra-molecular constraints that are linked to dysregulated Ca2+ release. Previous work from this laboratory identified an interacting- or I-domain of human RyR2 that mediates interaction between the large cytoplasmic assembly and the transmembrane (TM) domain of RyR2. Bioinformatic approaches revealed striking structural homology between sub-fragments of the RyR2 I-domain and I-domain-like regions of inositol 1,4,5-
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18

Bogucka, Joanna. "Mikrostruktura mięśnia najdłuższego grzbietu świń kilku ras z uwzględnieniem genotypu odporności na stres (RYR1)." Rozprawa doktorska, [Nakł.aut.], 2004. http://dlibra.utp.edu.pl/Content/116.

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Celem pracy było porównanie mikrostruktury m. longissimus lumborum świń czystorasowych (pbz, pietrain, złotnicka pstra) i mieszańców P x (wbp x pbz) z uwzględnieniem genotypu odporności na stres RYR1 oraz wykazanie powiązań między typami włókien mięśniowych a niektórymi cechami jakości mięsa
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19

Milbradt, Anita [Verfasser], and Andreas [Akademischer Betreuer] Ludwig. "Konditionelle Gendeletion des Ryanodinrezeptors RyR2 im Herzen der Maus / Anita Milbradt. Betreuer: Andreas Ludwig." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2011. http://d-nb.info/1018309039/34.

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20

Dornan, Thomas J. "Antioxidant Anthocyanidins and Calcium Transport Modulation of the Ryanodine Receptor of Skeletal Muscle (RyR1)." PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/319.

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Cardiovascular disease (CVD) claims more lives than any other disease in the world. Although numerous biological pathways share the blame, ventricular tachyarrhythmia (VT) is estimated to account for ~25% of all CVD deaths. A complete understanding of the molecular mechanisms underlying VT is unknown but recent studies have linked VT to improper calcium handling in the heart (canine). The principle calcium regulator in the muscle cell is the calcium ion release channel (aka RyR). Numerous endogenous and exogenous compounds can affect the way the RyR regulates calcium. In particular, abnormal l
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21

Zhou, Xinyu. "Modulation of Ca2+ Signaling by Trimeric Intracellular Cation Channels in the Heart." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1546600975458309.

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22

Caldwell, Patricia Theresa. "Investigations into the Molecular Mechanisms of Trichloroethylene Cardiotoxicity in vivo and in vitro." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195364.

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Trichloroethylene (TCE) is among the most common water contaminant in the United States and around the world. It is estimated that between 9% and 34% of all drinking water sources contain some TCE. The EPA set a drinking water standard for TCE at 5 parts per billion (ppb) in 1989, however since this date, many studies have shown TCE is dangerous to the health of adults and unborn children, even at low-level exposures. These studies reveal exposure to TCE can cause multi-organ damage, especially for the kidney, liver, reproductive and development systems. We investigated how TCE can effect
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23

Brulé, Cédric. "Vieillissement musculaire : impact de la protéolyse intracellulaire calcium-dépendante." Thesis, Bordeaux 1, 2009. http://www.theses.fr/2009BOR13899/document.

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La sarcopénie ou perte involontaire progressive de la masse musculaire chez le sujet âgé s’accompagne de l’altération de nombreux phénomènes physiologiques comparables à ceux observés chez les myopathes. Le processus de régénération musculaire est très ralenti, les activités protéolytiques intracellulaires sont modifiées et de nombreuses fonctions cellulaires sont perturbées en raison d’un stress oxydatif incontrôlé. L’intervention des calpaïnes, protéases neutres calcium-dépendantes, dans les processus associés au développement, à la régénération et à l’intégrité du tissu musculaire est incon
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Bosson, Caroline. "Caractérisation génétique des hyperthermies déclenchées." Thesis, Université Grenoble Alpes, 2020. https://thares.univ-grenoble-alpes.fr/2020GRALV015.pdf.

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L’Hyperthermie d’Effort (HE) et l’Hyperthermie Maligne (HM) sont deux pathologies potentiellement fatales déclenchées par un exercice physique intense pour la première, et par l’administration d’anesthésiques halogénés pour la seconde. A ce jour, seule l’HM est bien caractérisée sur le plan génétique car elle est causée en majorité par des mutations dans le gène RYR1, responsables d’une anomalie de l’homéostasie calcique dans le muscle squelettique. L’HM et l’HE partageant de nombreuses similarités cliniques et physiopathologiques, une origine génétique commune a été suggérée. Dans ce contexte
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Krempler, Andrea. "Analyse der RyREF2-Bindungsstelle im Promotor des porcinen RyR1-Gens und Charakterisierung des porcinen FHL1-Gens." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=963553518.

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Clack, Aaron Ian. "Investigating the functional consequences of cardiac ryanodine receptor (RyR2) polymorphisms on arrhythmia-linked Ca2+ release dysfunction." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54155/.

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This data provides compelling evidence that mutation-linked RyR2 channel dysfunction is modulated by common sequence polymorphisms and predicts that a more severe clinical phenotype results from the in cis inheritance of G1885E / L433P. Our studies also show that co-expression of L433P and G1885E subunits partially restores the functionality of the resultant heterotetrameric channels. The potential therapeutic benefits of positively modulating RyR2 mutant channel dysfunction via such a trans-complementation approach remain to be explored.
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Anttila, K. (Katja). "Swimming muscles of wild, trained and reared fish:aspects of contraction machinery and energy metabolism." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514290770.

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Abstract Billions of reared fish are released to the wild to compensate e.g. for the loss of natural populations. However, the efficiency of the releases is low. It has been proposed that one of the factors affecting the low survival rate of reared fish is their low swimming capacity. The molecular, metabolic and structural characters of muscle fiber define the swimming capacity of fish. Swimming capacity is related to the ecological competence of the fish, including the ability to complete long migrations and catch pray. One of the aims of the current study is to compare the properties of mus
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28

Krieger, Thorsten. "Pathophysiologie der malignen Hyperthermie und des Human-Stress-Syndroms Nachweis von drei neuen Mutationen im Ryanodinrezeptorgen (RYR1)." Saarbrücken VDM Verlag Dr. Müller, 2007. http://d-nb.info/989322130/04.

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Zugl.: Hamburg, Univ., Diss., 2007 u.d.T.: Krieger, Thorsten: Nachweis von drei neuen Mutationen im Ryanodinrezeptorgen (RYR1) bei Patienten mit maligner Hyperthermie und Human-Stress-Syndrom<br>Hergestellt on demand
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Georgeon, Chartier Carole. "Evaluation des effets du vieillissement sur la signalisation calcique des cellules musculaires lisses des artères cérébrales dans les modèles murins C57BL6/J, SAMR1 et SAMP8 dans des conditions normales et sous restriction calorique." Thesis, Bordeaux 1, 2012. http://www.theses.fr/2012BOR14692/document.

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Au cours du vieillissement, les artères cérébrales subissent des modifications structurelles et fonctionnelles, notamment au niveau des cellules musculaires lisses (CML). La CML a pour rôle de maintenir la réactivité vasculaire via une signalisation calcique qui fait intervenir différents acteurs pouvant ainsi réguler deux phénomènes : la contraction et la relaxation. Ces acteurs rassemblent, au sein d’une même cellule, des canaux (CCVD, RYR, IP3R), des pompes calciques (SERCA, PMCA, NCX, STIM/ORAI) et leurs régulateurs (PLB, FKBP12.6, TRPP2, SARAF, TRIC). La restriction calorique (RC), appara
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Phillips, Michael Sean. "The structural organization of the human skeletal muscle ryanodine receptor gene (RYR1) and its involvement in malignant hyperthermia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0015/NQ45648.pdf.

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Robin, Gaëlle. "Caractérisation de l'efflux calcique du réticulum sarcoplasmique du muscle squelettique normal et dystrophique." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10138.

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La contraction du muscle squelettique est initiée par une libération de Ca2+ du réticulum sarcoplasmique (RS) en réponse à une dépolarisation du sarcolemme. Celle-ci induit un changement de conformation du récepteur des dihydropyridines (DHPR) localisé dans les tubules T entraînant l'ouverture du récepteur de la ryanodine de type 1 (RyR1), canal calcique du RS, et la libération du Ca2+ accumulé dans le RS. Au repos, RyR1 serait maintenu fermé par une action répressive du DHPR. Néanmoins, un efflux de Ca2+ continu se développe à travers la membrane du RS, constamment compensé par l'activité des
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Jiang, Jie. "Tuning Calcium Bindging Affinities with Related Biological Functions of Calmodulin and Designing Protein Based Contrast Agent." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/chemistry_diss/60.

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Calmodulin (CaM) is a ubiquitous intracellular protein that regulates biological activities of numerous enzymes and ion channels. Upon responding Ca2+ concentration change, Ca2+- dependent CaM activates the hydrolyzation of cGMP by PDE and Ca2+ releasing channel activity of ryanodine receptor. In this dissertation, a series of CaM variants were engineered to enhance Ca2+ binding affinities by increasing the number of negative charged residues in individual EF-hand. The capability of shifting the biphasic Ca2+-activation profile of RyR1 is significantly altered by changing Ca2+ binding affinity
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飯田, 綱規. "小胞体膜タンパク質TRICチャネルの分子機能解析". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225529.

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陶, 晟辰. "循環器における小胞体タンパク質TRICに関する研究". 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/188726.

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35

Yehya, Mohamad. "Implication des voies du stress oxydant dans le remodelage du récepteur de la Ryanodine au cours de la Dysfonction Diaphragmatique induite par la Ventilation Mécanique." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONT4001.

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La ventilation mécanique en réanimation (VM) est une mesure de sauvetage pour les patients qui présentent une incapacité temporaire à assurer par leur fonction ventilatoire une oxygénation tissulaire adéquate. Elle peut pourtant être à l’origine d’une dysfonction diaphragmatique induite par la ventilation (DDIV), augmentant la dépendance du patient à son ventilateur et la durée de son séjour en réanimation. La mise au repos brutale du diaphragme induite par la ventilation peut engendrer un stress énergétique ainsi qu’un stress mécanique participant à l’initiation d’un stress oxydant à la base
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Polster, Alexander [Verfasser]. "FRET reveals substantial reorientation of the cytoplasmic interface of the skeletal muscle DHPR in the presence of RyR1 / Alexander Polster." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover, 2011. http://d-nb.info/1011397404/34.

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Ziober, Iris Lamberti. "Carnes PSE (pale, soft, exudative) de frangos : análise dos transcritos do gene codificador da proteína ?RyR." Universidade Estadual de Londrina. Centro de Ciências Agrárias. Programa de Pós-Graduação em Ciência de Alimentos, 2009. http://www.bibliotecadigital.uel.br/document/?code=vtls000151534.

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Carnes PSE (pálida, flácida e exsudativa) ocorrem por fatores múltiplos, e o estresse e causas genéticas tem papeis cruciais. Em suínos, uma mutação no gene RYR1 (receptor de rianodina tipo 1) leva à PSS (Síndrome do Estresse Suíno) e às carnes PSE. A RyR1 é uma proteína formadora do canal de liberação de Ca2+ no retículo sarcoplasmático de células musculares. Em suínos com a mutação neste gene o estresse desencadeia um acúmulo intracelular de Ca2+, e consequentemente à uma contração muscular permanente, fazendo com que a célula dispenda mais glicogênio tentando relaxar o músculo, produzindo a
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Bosch, Calero Cristina. "Determinants moleculars de la mort sobtada cardíaca en una gran família de les Illes Canàries." Doctoral thesis, Universitat de Girona, 2016. http://hdl.handle.net/10803/406951.

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Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a sudden cardiac death (SCD) associated disease characterized by the presence of polymorphic or bidirectional ventricular tachycardia during emotional or physical stress. Most cases of CPVT are caused by mutations in the RyR2 gene. This thesis starts with the identification of a large family in the Canary Islands, with a long history of SCD due to CPVT. The genetic study revealed the presence of a mutation in the RyR2 gene in affected patients. The functional and proteomic studies of the channel has shown that the mutation
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Owen, Laura Jean. "Calcium and Redox Control of the Calcium Release Mechanism of Skeletal and Cardiac Muscle Sarcoplasmic Reticulum." PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/430.

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The sarcoplasmic reticulum is an internal membrane system that controls the Ca²⁺ concentration inside muscle cells, and hence the contractile state of both skeletal and cardiac muscle. A key protein that that regulates the Ca²⁺ concentration in this membrane is known as the calcium release channel (CRC). The effects on Ca²⁺ dependent activation is of major importance in the study of CRC since other channel modifiers cannot effect the channel in the absence of Ca²⁺, or they require Ca²⁺ for maximum results. In this study of the high-affinity Ca²⁺ binding site, expected increases in total bindin
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Filipova, Dilyana [Verfasser], Niels [Gutachter] Gehring, and Stefan [Gutachter] Herzig. "From excitation-contraction coupling to gene expression: Roles of RYR1 and Cav1.1 in myogenesis / Dilyana Filipova ; Gutachter: Niels Gehring, Stefan Herzig." Köln : Universitäts- und Stadtbibliothek Köln, 2018. http://d-nb.info/1165772779/34.

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Dornan, Thomas Joseph. "Calcium Transport Inhibition, Stimulation, and Light Dependent Modulation of the Skeletal Calcium Release Channel (RyR1) by the Prototropic Forms of Pelargonidin." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1931.

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The principle calcium regulator in the muscle cell is the calcium ion release channel (RyR). Improper calcium homeostasis in the muscle cell is the foundation of many pathological states and has been targeted as a contributing factor to ventricular tachycardia, which is known to precede sudden cardiac arrest. Numerous endogenous and exogenous compounds can affect the way RyR regulates calcium. In this study the anthocyanidin Pelargonidin (Pg), an important natural colorant and dietary antioxidant, is evaluated for its effect on regulating the transport of calcium through the RyR1 of skeletal m
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Panella-Riera, Núria. "Estratègies prèvies al sacrifici que poden afectar el benestar animal i la qualitat de la carn de porcs de diferent genotip RYRI." Doctoral thesis, Universitat de Girona, 2011. http://hdl.handle.net/10803/37381.

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The main objective of this thesis was to study (i) the effect of the fasting and lairage on carcass and technological meat quality and (ii) the inclusion of magnesium (MgCO3 and MgSO4) and/or tryptophan during 5 days before slaughtering pigs as a strategy to decrease stress levels and improve meat quality, with two different porcine RYR1 genotypes (NN and nn). An adequate combination of fasting and lairage period is recommended. A supplement of MgCO3 or Trp did not improve meat quality under minimal stressful ante mortem conditions; and MgSO4 had a laxative effect on pigs supplemented with it.
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Palahniuk, Chris G. "Evidence for a luminal, calcium-mediated cross talk between SERCA1 pumps and RyR1 calcium release channels in heavy sarcoplasmic reticulum, HSR, membranes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0015/MQ53201.pdf.

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Tang, Lifei. "Effects of Neuronal Nitric Oxide Synthase Signaling on Myocyte Contraction during Beta-Adrenergic Stimulation." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385336408.

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Pacini, Federico. "Sviluppo di Metodologie Molecolari per la Qualità dei Prodotti di Origine Animale." Doctoral thesis, Università degli studi di Padova, 2007. http://hdl.handle.net/11577/3425519.

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The objectives of this study were to develop and optimize molecular techniques based on the DNA melting analysis for the detection of allele variants or SNPs in genes involved in the quality of animal products. For the dairy industry the detection of the cow k-casein B allele (CSN3*B) is very important for the role of its codifying protein during the cheese making. It is known that the k-casein B allele plays a major role in cheese technology with great effects in the quality and quantity of cow milk. The availability of accurate and reliable protocols for the identification of the most comm
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Ye, Yanping. "Designing New Drugs to Treat Cardiac Arrhythmia." PDXScholar, 2012. https://pdxscholar.library.pdx.edu/open_access_etds/638.

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Heart failure resulting from different forms of cardiomyopathy is defined as the inability of the heart to pump sufficient blood to meet the body's metabolic demands. It is a major disease burden worldwide and the statistics show that 50% of the people who have the heart failure will eventually die from sudden cardiac death (SCD) associated with an arrhythmia. The central cause of disability and SCD is because of ventricular arrhythmias. Genetic mutations and acquired modifications to RyR2, the calcium release channel from sarcoplasmic reticulum, can increase the pathologic SR Ca2+ leak during
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Färber, Sandra [Verfasser]. "High resolution mapping and identification of candidate genes for the BaMMV/BaYMV-resistance gene rym13 and Ryd3 involved in BYDV-tolerance of barley / Sandra Färber." Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1188563688/34.

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Dalton, Desire Lee. "Screening of the RYR1 gene in malignant hyperthermia probands from South Africa indicates towards a novel epigenetic eatiology in this population / by Desiré Lee Dalton." Thesis, North-West University, 2007. http://hdl.handle.net/10394/717.

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Malignant hyperthermia (MH) is an autosomal dominant, potentially lethal pharmacogenetic disorder of skeletal muscle, which is elicited by exposure to volatile anaesthetics and depolarising muscle relaxants. Susceptible individuals appear clinically normal, but may present with a hypermetabolic crisis and muscle contracture when exposed to triggering substances that elicit excessive release of calcium ions from the sarcoplasmic reticulum. Diagnosis of MH susceptibility is currently made via the in vitro contracture test. Genetically, in more than 50% of the affected families, MH occurs due to
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Chen, Wenbo [Verfasser], Misha [Gutachter] Kudryashev, and Klaas Martinus [Gutachter] Pos. "Structure and function of integral and peripheral membrane proteins by cryo-EM: RyR1 and SidE family proteins / Wenbo Chen ; Gutachter: Misha Kudryashev, Klaas Martinus Pos." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2020. http://d-nb.info/1221184938/34.

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Blancard, Malorie. "Identification de nouveaux variants responsables d'arythmies cardiaques avec risque de mort subite." Electronic Thesis or Diss., Sorbonne université, 2018. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2018SORUS406.pdf.

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La mort subite cardiaque est initiée par une tachycardie ventriculaire - ou une extrasystole ventriculaire - dégénérant en fibrillation ventriculaire. Les morts subites sont le plus souvent associées à des anomalies structurales du cœur ou d’origine ischémique. Cependant, certaines arythmies ventriculaires surviennent dans un contexte de cœur structurellement normal avec un ECG basal normal telles que les tachycardies ventriculaires polymorphes catécholaminergiques (CPVT) ou les torsades de pointes à couplage court (TdPcc). Le premier objectif de ma thèse a été d’étudier l’origine génétique de
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