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Academic literature on the topic 'Ryanodine receptor type 2'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Ryanodine receptor type 2"

1

Kawai, Ryo, Tetsuro Horikoshi, and Manabu Sakakibara. "Involvement of the Ryanodine Receptor in Morphologic Modification of Hermissenda Type B Photoreceptors After In Vitro Conditioning." Journal of Neurophysiology 91, no. 2 (February 2004): 728–35. http://dx.doi.org/10.1152/jn.00757.2003.

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We examined whether Ca2+ induced Ca2+ release through ryanodine receptors is involved in the conditioning of specific morphologic changes at the axon terminals of type B photoreceptors in the isolated circumesophageal ganglion of Hermissenda. Calcium chelation by bis(2-aminophenoxy) ethane- N,N,N′, N′-tetraacetic acid prevented the conformational change at the terminals after five paired presentations of light and vibration, which produce terminal branch contraction of B photoreceptors. Two ryanodine receptor blockers, dantrolene and micromolar concentrations of ryanodine, depressed the increase in excitability due to in vitro conditioning and the increase in intracellular Ca2+ in response to membrane depolarization. Although the ability to increase intracellular Ca2+ was depressed, synaptic transmission was preserved in the normal state from hair cells under dantrolene and ryanodine incubation. Ryanodine receptor blockers also prevented contraction at the B photoreceptor axon terminals. These results suggest that the ryanodine receptor has a crucial role in inducing the in vitro conditioning specific changes both physiologically and morphologically, including “focusing” at the B photoreceptor axon terminal.
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Chugun, Akihito, Osamu Sato, Hiroshi Takeshima, and Yasuo Ogawa. "Mg2+ activates the ryanodine receptor type 2 (RyR2) at intermediate Ca2+ concentrations." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C535—C544. http://dx.doi.org/10.1152/ajpcell.00275.2006.

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To clarify whether activity of the ryanodine receptor type 2 (RyR2) is reduced in the sarcoplasmic reticulum (SR) of cardiac muscle, as is the case with the ryanodine receptor type 1 (RyR1), Ca2+-dependent [3H]ryanodine binding, a biochemical measure of Ca2+-induced Ca2+ release (CICR), was determined using SR vesicle fractions isolated from rabbit and rat cardiac muscles. In the absence of an adenine nucleotide or caffeine, the rat SR showed a complicated Ca2+ dependence, instead of the well-documented biphasic dependence of the rabbit SR. In the rat SR, [3H]ryanodine binding initially increased as [Ca2+] increased, with a plateau in the range of 10–100 μM Ca2+, and thereafter further increased to an apparent peak around 1 mM Ca2+, followed by a decrease. In the presence of these modulators, this complicated dependence prevailed, irrespective of the source. Addition of 0.3–1 mM Mg2+ unexpectedly increased the binding two- to threefold and enhanced the affinity for [3H]ryanodine at 10–100 μM Ca2+, resulting in the well-known biphasic dependence. In other words, the partial suppression of RyR2 is relieved by Mg2+. Ca2+ could be a substitute for Mg2+. Mg2+ also amplifies the responses of RyR2 to inhibitory and stimulatory modulators. This stimulating effect of Mg2+ on RyR2 is entirely new, and is referred to as the third effect, in addition to the well-known dual inhibitory effects. This effect is critical to describe the role of RyR2 in excitation-contraction coupling of cardiac muscle, in view of the intracellular Mg2+ concentration.
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Takasawa, Shin, Michio Kuroki, Koji Nata, Naoya Noguchi, Takayuki Ikeda, Akiyo Yamauchi, Hiroyo Ota, et al. "A novel ryanodine receptor expressed in pancreatic islets by alternative splicing from type 2 ryanodine receptor gene." Biochemical and Biophysical Research Communications 397, no. 2 (June 2010): 140–45. http://dx.doi.org/10.1016/j.bbrc.2010.05.051.

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4

Ayabe, T., G. S. Kopf, and R. M. Schultz. "Regulation of mouse egg activation: presence of ryanodine receptors and effects of microinjected ryanodine and cyclic ADP ribose on uninseminated and inseminated eggs." Development 121, no. 7 (July 1, 1995): 2233–44. http://dx.doi.org/10.1242/dev.121.7.2233.

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Sperm-induced activation of mammalian eggs is associated with a transient increase in Ca2+ concentrations thought to be derived from inositol 1,4,5-trisphosphate-sensitive and -insensitive intracellular stores. Whereas the importance of inositol 1,4,5-trisphosphate-sensitive Ca2+ stores has been evaluated, the identity and role of inositol 1,4,5-trisphosphate-insensitive stores are poorly understood. To explore the role of the ryanodine-sensitive Ca2+ store, we first used reverse transcription-polymerase chain reaction to identify transcripts of the ryanodine receptor in eggs and determined that transcripts for the type 2 and 3 receptor were present. Immunoprecipitation of radioiodinated egg extracts with an antibody that recognizes both type 2 and 3 receptors detected specifically a band of Mr = 520,000. Immunolocalization of the receptor(s) using laser-scanning confocal microscopy revealed that the receptor(s) was uniformly distributed in the cortex of the germinal vesicle-intact oocyte, but became asymmetrically localized to the cortex in a region apposed to the meiotic spindle in the metaphase II-arrested egg; this asymmetrical localization developed by metaphase I. The role of the ryanodine receptor in mouse egg activation was examined by determining the effects of microinjected ryanodine or cyclic ADP ribose on endpoints of egg activation in either uninseminated or inseminated eggs. Ryanodine induced the conversion of the zona pellucida glycoprotein ZP2 to its postfertilization form ZP2f in a biphasic concentration-dependent manner; nanomolar concentrations stimulated this conversion, whereas micromolar concentrations had no stimulatory effect. Cyclic ADP ribose also promoted the ZP2 conversion, but with a hyperbolic concentration dependence. Neither of these compounds induced cell cycle resumption. Inhibiting the inositol 1,4,5-trisphosphate-sensitive Ca2+ store did not inhibit the ryanodine-induced ZP2 conversion and, reciprocally, inhibiting the ryanodine-sensitive Ca2+ store did not inhibit the inositol 1,4,5-trisphosphate-induced ZP2 conversion. Last, treatment of eggs under conditions that would block the release of Ca2+ from the ryanodine-sensitive store had no effect on any event of egg activation following fertilization. Results of these experiments suggest that although ryanodine receptors are present and functional, release of Ca2+ from this store is not essential for sperm-induced egg activation.
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Saeki, Kazuhiko, Ichiro Obi, Noriko Ogiku, Munekazu Shigekawa, Toshiaki Imagawa, and Takeshi Matsumoto. "Doxorubicin directly binds to the cardiac-type ryanodine receptor." Life Sciences 70, no. 20 (April 2002): 2377–89. http://dx.doi.org/10.1016/s0024-3205(02)01524-2.

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Coronado, R., J. Morrissette, M. Sukhareva, and D. M. Vaughan. "Structure and function of ryanodine receptors." American Journal of Physiology-Cell Physiology 266, no. 6 (June 1, 1994): C1485—C1504. http://dx.doi.org/10.1152/ajpcell.1994.266.6.c1485.

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Membrane depolarization, neurotransmitters, and hormones evoke a release of Ca2+ from intracellular Ca(2+)-storing organelles like the endoplasmic reticulum and, in muscle, the sarcoplasmic reticulum (SR). In turn, the released Ca2+ serves to trigger a variety of cellular responses. The presence of Ca2+ pumps to replenish intracellular stores was described more than 20 years ago. The presence of Ca2+ channels, like the ryanodine receptor, which suddenly release the organelle-stored Ca2+, is a more recent finding. This review describes the progress made in the last five years on the structure, function, and regulation of the ryanodine receptor. Numerous reports have described the response of ryanodine receptors to cellular ions and metabolites, kinases and other proteins, and pharmacological agents. In many cases, comparative measurements have been made using Ca2+ fluxes in SR vesicles, single-channel recordings in planar bilayers, and radioligand binding assays using [3H]ryanodine. These techniques have helped to relate the activity of single ryanodine receptors to global changes in the SR Ca2+ permeability. Molecular information on functional domains within the primary structure of the ryanodine receptor is also available. There are at least three ryanodine receptor isoforms in various tissues. Some cells, such as amphibian muscle cells, express more than a single isoform. The diversity of ligands known to modulate gating and the diversity of tissues known to express the protein suggest that the ryanodine receptor has the potential to participate in many types of cell stimulus-Ca(2+)-release coupling mechanisms.
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Chiang, David Y., Satadru Lahiri, Guoliang Wang, Jason Karch, Meng C. Wang, Sung Y. Jung, Albert J. R. Heck, Arjen Scholten, and Xander H. T. Wehrens. "Phosphorylation-Dependent Interactome of Ryanodine Receptor Type 2 in the Heart." Proteomes 9, no. 2 (June 7, 2021): 27. http://dx.doi.org/10.3390/proteomes9020027.

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Hyperphosphorylation of the calcium release channel/ryanodine receptor type 2 (RyR2) at serine 2814 (S2814) is associated with multiple cardiac diseases including atrial fibrillation and heart failure. Despite recent advances, the molecular mechanisms driving pathological changes associated with RyR2 S2814 phosphorylation are still not well understood. Methods: Using affinity-purification coupled to mass spectrometry (AP-MS), we investigated the RyR2 interactome in ventricles from wild-type (WT) mice and two S2814 knock-in mutants: the unphosphorylated alanine mutant (S2814A) and hyperphosphorylated mimic aspartic acid mutant (S2814D). Western blots were used for validation. Results: In WT mouse ventricular lysates, we identified 22 proteins which were enriched with RyR2 pull-down relative to both IgG control and no antibody (beads-only) pull-downs. Parallel AP-MS using WT, S2814A, and S2814D mouse ventricles identified 72 proteins, with 20 being high confidence RyR2 interactors. Of these, 14 had an increase in their binding to RyR2 S2814A but a decrease in their binding to RyR2 S2814D. We independently validated three protein hits, Idh3b, Aifm1, and Cpt1b, as RyR2 interactors by western blots and showed that Aifm1 and Idh3b had significantly decreased binding to RyR2 S2814D compared to WT and S2814A, consistent with MS findings. Conclusion: By applying state-of-the-art proteomic approaches, we discovered a number of novel RyR2 interactors in the mouse heart. In addition, we found and defined specific alterations in the RyR2 interactome that were dependent on the phosphorylation status of RyR2 at S2814. These findings yield mechanistic insights into RyR2 regulation which may guide future drug designs.
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Kada, Gerald, Lynda Blayney, Anneliese Raab, Sidney Fleischer, Hansgeorg Schindler, F. Anthony Lai, and Peter Hinterdorfer. "Recognition Force Microscospy of Single Ryanodine Receptor Type 1 (RyR1)." Single Molecules 1, no. 2 (June 2000): 174. http://dx.doi.org/10.1002/1438-5171(200006)1:2<174::aid-simo174>3.0.co;2-g.

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9

Bare, Dan J., Claudia S. Kettlun, Mei Liang, Donald M. Bers, and Gregory A. Mignery. "Cardiac Type 2 Inositol 1,4,5-Trisphosphate Receptor." Journal of Biological Chemistry 280, no. 16 (February 13, 2005): 15912–20. http://dx.doi.org/10.1074/jbc.m414212200.

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The type 2 inositol 1,4,5-trisphosphate receptor (InsP3R2) was identified previously as the predominant isoform in cardiac ventricular myocytes. Here we reported the subcellular localization of InsP3R2 to the cardiomyocyte nuclear envelope (NE). The other major known endo/sarcoplasmic reticulum calcium-release channel (ryanodine receptor) was not localized to the NE, indicating functional segregation of these channels and possibly a unique role for InsP3R2 in regulating nuclear calcium dynamics. Immunoprecipitation experiments revealed that the NE InsP3R2 associates with Ca2+/calmodulin-dependent protein kinase IIδ (CaMKIIδ), the major isoform expressed in cardiac myocytes. Recombinant InsP3R2 and CaMKIIδBalso co-immunoprecipitated after co-expression in COS-1 cells. Additionally, the amino-terminal 1078 amino acids of the InsP3R2 were sufficient for interaction with CaMKIIδBand associated upon mixing following separate expression. CaMKII can also phosphorylate InsP3R2, as demonstrated by32P labeling. Incorporation of CaMKII-treated InsP3R2 into planar lipid bilayers revealed that InsP3-mediated channel open probability is significantly reduced (∼11 times) by phosphorylation via CaMKII. We concluded that the InsP3R2 and CaMKIIδ likely represent two central components of a multiprotein signaling complex, and this raises the possibility that calcium release via InsP3R2 in the myocyte NE may activate local CaMKII signaling, which may feedback on InsP3R2 function.
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Costa, Roberta Ribeiro, Wamberto Antonio Varanda, and Celso Rodrigues Franci. "A calcium-induced calcium release mechanism supports luteinizing hormone-induced testosterone secretion in mouse Leydig cells." American Journal of Physiology-Cell Physiology 299, no. 2 (August 2010): C316—C323. http://dx.doi.org/10.1152/ajpcell.00521.2009.

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Leydig cells are responsible for the synthesis and secretion of testosterone, processes controlled by luteinizing hormone (LH). Binding of LH to a G protein-coupled receptor in the plasma membrane results in an increase in cAMP and in intracellular Ca2+ concentration ([Ca2+]i). Here we show, using immunofluorescence, that Leydig cells express ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs). Measurements of intracellular calcium changes using the fluorescent calcium-sensitive dye fluo-3 and confocal microscopy show that both types of receptors are involved in a calcium-induced calcium release (CICR) mechanism, which amplifies the initial Ca2+ influx through plasma membrane T-type calcium channels (CaV3). The RyRs and IP3Rs are functional, as judged from both their activation by caffeine and IP3 and block by ryanodine and 2-aminoethoxydiphenyl borate (2-APB), respectively. RyRs are the principal players involved in the release of Ca2+ from the endoplasmic reticulum, as evidenced by the fact that global Ca2+ changes evoked by LH are readily blocked by 100 μM ryanodine but not by 2-APB or xestospongin C. Finally, steroid production by Leydig cells is inhibited by ryanodine but not by 2-APB. These results not only broaden our understanding of the role played by calcium in Leydig cells but also show, for the first time, that RyRs have an important role in determining testosterone secretion by the testis.
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Dissertations / Theses on the topic "Ryanodine receptor type 2"

1

Walker, Micaela. "Biochemical characterisation of the type 3 ryanodine receptor." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286791.

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Bertocchini, Federica. "Expression and functional analysis of murine ryanodine receptor type 3." Thesis, Open University, 1998. http://oro.open.ac.uk/57732/.

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Ryanodine receptors (RyRs) are intracellular homotetrameric Ca2+-release channels constituting a family of three different isoforms, named RyRl, RyR2 and RyR3. RyRl and RyR2 are highly expressed in skeletal and cardiac muscles respectively, where they localize in the terminal cisternae of the sarcoplasmic reticulum (SR). Although RyRl and RyR2 have been found to be expressed in several other tissues at much lower level than in striated muscles, their major functional role is related to Ca2+-release from the SR following electrical depolarization of the plasma membrane, a process referred to as excitation-contraction (e-c) coupling and known to regulate striated muscle contraction. The third isoform, RyR3, is characterized by a wide pattern of expression, without any specific association to a tissue or a cell-type. The finding that RyR3 is also expressed in mammalian skeletal muscles parallels the presence of two distinct isoforms, o- and P-RyR, in non-mammalian vertebrate skeletal muscles, and suggests that two functionally distinct RyRs may be involved in the regulation of skeletal muscle contraction. The expression of RyR3 was analyzed in murine skeletal muscle from late foetal stages to adult, throughout neonatal phases of development. RyR3 was expressed widely during skeletal muscle post-natal development, disappearing in all muscles analyzed except diaphragm and soleus. RyR3 knockout mice were generated, and contractile properties of skeletal muscles were analyzed. Skeletal muscle contraction in RyR3-/- mice was impaired during the neonatal phase of development. In skeletal muscles isolated from RyR3-1- mice, the twitch elicited by electrical stimulation was strongly depressed. A significant reduction of the contractile activity was also elicited after stimulation with caffeine, an activator of Ca2+-release through RyRs. In the adults, no differences were detected between wild-type and mutant mice. These results are the first demonstrations of a physiological role of RyR3 in excitation-contraction coupling mechanisms of skeletal muscle, and support the model of a two-channel system regulating skeletal muscle contraction. In order to further characterize the RyR3-1- mouse, [3H]ryanodine binding experiments were performed on diaphragm and total hindlimb skeletal muscles from RyR3+/+ and RyR3-1- mice. Preliminary results will be presented and discussed.
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Steer, Emma Jane. "The action of flecainide on the wild-type cardiac ryanodine receptor." Thesis, University of Leeds, 2017. http://etheses.whiterose.ac.uk/18395/.

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The genetic disorder catecholaminergic polymorphic ventricular tachycardia (CPVT) causes the function of the sarcoplasmic reticulum (SR) Ca2+ release channel (RyR2) to be altered and induces fatal arrhythmias during stress or exercise. Flecainide, a class 1C sodium channel (Nav1.5) inhibitor and anti-arrhythmic agent, was recently observed to be effective against CPVT arrhythmias. Controversially, it was suggested that flecainide acted directly on RyR2, alongside its action on Nav1.5. The present study sought to establish whether flecainide affected RyR2 activity to prevent pro-arrhythmic Ca2+ waves in wild type (WT) cardiomyocytes and if so, to elucidate the mechanisms responsible. Flecainide or flecainide-FITC was applied to intact or saponin permeabilised cardiomyocytes isolated from WT rat ventricle. Confocal microscopy was used to image SR Ca2+ release after application of flecainide or trans-sarcolemmal movement of fluorescent flecainide-FITC. In intact myocytes, flecainide decreased pro-arrhythmic Ca2+ wave frequency although Ca2+ spark properties were unchanged, indicating no effect on RyR2 despite prolonged flecainide exposure (45 min). Flecainide-FITC traversed the sarcolemma over a period of hours and primarily accumulated in the mitochondria. In permeabilised myocytes, where flecainide had immediate access to RyR2 and Nav1.5 was non-functional, a 10-20% decrease in wave frequency was apparent, accompanied by sustained changes in Ca2+ spark properties. The effect on waves was potentiated when the SR counter-current was inhibited by substitution of K+ with Cs+. These results suggest that flecainide has an anti-arrhythmic effect on RyR2 in permeabilised WT cardiomyocytes. However, slow cytosolic accumulation and the requirement for an increased drug concentration may explain the absence of an effect on RyR2 in intact cells. Nevertheless, these findings support the concept that RyR2 channel activity can be pharmacologically manipulated and that RyR2 represents a potential pharmacological target in patients with arrhythmia.
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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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Vincent, Karla Kristine. "Transactivation of Beta 2 Adrenergic Receptor by Bradykinin type 2 Receptor via heterodimerization." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/37117.

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Although a long standing convention maintained that G Protein Coupled Receptors (GPCRs) exist in the plasma membrane solely as monomers, substantial work over the last two decades has demonstrated that these ubiquitous receptors can and in many cases, preferentially, exist as homodimers, heterodimers, or higher order oligomers. Often, two GPCRs of the same class heterodimerize; it is less common for two GPCRs of different signaling pathways to interact. The work presented here studied the physical and functional interaction of two GPCRs from discrete classes, the Beta 2 Adrenergic Receptor (β2AR), a Gαs-coupled receptor, and Bradykinin type 2 Receptor (Bk2R), a Gαq coupled receptor. These data show that Bk2R and β2AR are physically coupled when heterologously expressed in Xenopus oocytes, and in pheochromocytoma (PC12) cells and in freshly isolated murine ventricular myocytes, two systems that endogenously express these receptors. This physical coupling led to functional consequences in heterologous and endogenous expression systems, as Bk2R was able to transactivate β2AR signaling via its direct interaction with the receptor. Furthermore, coexpression of Bk2R shifted the dose response curve of β2AR for its selective agonist rightward in Xenopus oocyte electrophysiology experiments, suggesting the presence of Bk2R negatively affected β2AR native pharmacology. Up to thirty minutes of either bradykinin (BK) or isoproterenol exposure did not change the relative amount of Bk2R/β2AR heterodimer in PC12 cells, a rat adrenal medulla tumor cell line that endogenously expresses these receptors. Despite the obvious signaling consequences, the Bk2R/β2AR heterodimer accounted for only 10% of the total β2AR protein detected and 20% of the total Bk2R protein detected. When other Bk2R-specific ligands were also tested to examine the extent of β2AR transactivation, our data showed that both Lys-des-Arg-Bradykinin, a Bk2R partial agonist and NPC 567, a Bk2R antagonist, transactivated β2AR to the same extent as BK. Taken together, our data provide a novel mode of receptor regulation and signaling via Bk2R/β2AR heterodimerization. Because a large percentage of therapeutics target GPCRs, a greater understanding of how a GPCR heterodimer functions could be beneficial for targeting new drugs and refining existing drugs. Understanding the Bk2R/β2AR heterodimer provides a new perspective on the myriad of fucntional consequences that occur when a GPCR is activated.
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Hower, Amy Elizabeth. "Receptor Functions of the Receptor-Type Protein Tyrosine Phosphatase PTPRO." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/303.

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Protein tyrosine phosphorylation regulates many aspects of cell growth and differentiation. Since cellular tyrosine phosphorylation levels are controlled by the antagonizing actions of the protein tyrosine kinases (PTKs) and the protein tyrosine phosphatases (PTPs), these enzymes play a direct role in regulating processes as diverse as oncogenesis and neuronal development. In particular, the transmembrane group of PTPs, known as the receptor-type protein tyrosine phosphatases (RPTPs), has been linked to regulation of axon growth and guidance during development and regeneration. The regulation of activity of these RPTPs is of clear importance, yet the fundamental mechanisms underlying this regulation are poorly understood. While extracellular ligands are well known to dimerize and activate the receptor protein tyrosine kinases, the extent to which RPTP regulation parallels this scenario is largely unknown. We have examined the dimerization state and the relationship this state has with the phosphatase activity of the neuronal RPTP, PTPRO. We have found that PTPRO, a Type III RPTP, can exist in a dimerized state, likely regulated by disulfide linkages in the intracellular domain. Ligand addition to a chimeric PTPRO increases dimerization of the transmembrane and intracellular domains. Ligand addition to the chimeric PTPRO also decreases its phosphatase activity towards artificial peptides and a putative substrate, TrkC, a protein also known to be important in neuronal development. PTPRO's regulation of TrkC may be physiologically relevant as the proteins can be co-precipitated from transfected cells and PTPRO's dephosphorylation of TrkC is efficient compared to that of other RPTPs. The decrease in PTPRO's activity upon ligand-induced dimerization was unexpected as dimerization of a structurally-similar RPTP family member suggested the opposite functional outcome. This work suggests a complex relationship between dimerization and activity for the Type III RPTPs, which include PTPRO. The results presented in this dissertation will extend the current knowledge on RPTP functions and the cellular processes they regulate.
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Hatcher-Solis, Candice N. "PHARMACOLOGICAL IMPLICATIONS OF ADENOSINE 2A RECEPTOR- DOPAMINE TYPE 2 RECEPTOR HETEROMERIZATION." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4458.

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G protein-coupled receptors (GPCRs) are heptahelical, transmembrane proteins that mediate a plethora of physiological functions by binding ligands and releasing G proteins that interact with downstream effectors. GPCRs signal as monomers, complexes of the same receptor subtype (homomers), or complexes of different receptor subtypes (heteromers). Recently, heteromeric GPCR complexes have become attractive targets for drug development since they exhibit distinct signaling and cell-specific localization from their homomeric counterparts. Yet, the effect of heteromerization on the pharmacology of many GPCR homomers remains unknown. Therefore, we have undertaken the task to examine the effect of heteromerization on Gs signaling through the adenosine 2A receptor (A2AR) and Gi signaling through the dopamine type 2 receptor (D2R) since the A2AR-D2R heteromer is an emerging therapeutic target for Parkinson’s disease (PD). We examined the effect of heteromerization on A2AR and D2R homomeric signaling using electrophysiology and the Xenopus laevis oocyte heterologous expression system. G protein-coupled inwardly rectifying potassium channels (GIRKs) were used as reporters for Gi signaling because activation leads to direct Gbeta-gamma (Gβγ)-mediated stimulation of the GIRK current. We also coupled GIRK channels to Gs signaling by overexpressing Gαs and signaling throughGαsβγ. Our electrophysiological assay is innovative because it allows us to optimize the conditions of heteromerization and directly observe GPCR signaling at the G protein level. Our data demonstrate that heteromer formation alone decreases dopamine-elicited Gi signaling through the D2R and CGS-21680-elicited Gs signaling through the A2AR. Furthermore, this reciprocal antagonism was predominately due to changes in efficacy versus potency. We also examined crosstalk observing that applying agonists or antagonists to the adjacent receptor further modulate this inhibition with the combination of agonists and antagonists relieving inhibition. Mutating the A2AR-D2R heteromer interface abrogated all of the aforementioned ligand-induced effects on G protein signaling through the A2AR-D2R heteromer. We are currently aiming to validate our results from the oocyte experiments with an in vivo model. Our data further elucidate the effect of various ligands on G protein signaling through the A2AR- D2R heteromer, which may facilitate future studies that examine A2AR-D2R heteromer signaling.
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Phillips, Timothy Trevor. "A study of metabotropic glutamate receptor type 2." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624330.

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Puente, de Las Cuevas Elena. "Molecular genetic studies on the ryanodine receptor (sarcoplasmic reticulum Ca'2'+ channel) from Heliothis virescens (Lepidoptera: Noctuidae)." Thesis, University of Reading, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394523.

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Viana, Dias Jose Miguel. "Insights into the regulation of the ryanodine receptor Differential effects of calcium(2+), magnesium(2+) and pharmacological agents on ATP binding /." Ann Arbor, Mich. : ProQuest, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3244456.

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Thesis (Ph.D. in Molecular and Cell Biology)--S.M.U., 2007.
Title from PDF title page (viewed Mar. 18, 2008). Source: Dissertation Abstracts International, Volume: 67-12, Section: B, page: 6904. Adviser: Pia D. Vogel. Includes bibliographical references.
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Books on the topic "Ryanodine receptor type 2"

1

Flavin, Nora. Cloning and characterisation of the bovine activin receptor type II gene (ActRII): Its localisation to chromosome 2 (BTA2) by somatic cell genetic analysis and the genotyping of an associated microsatelltie UCD2. Dublin: University College Dublin, 1996.

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Rainey, Susan. Cloning and characterization of the insulin receptor-related receptor (IRR) reveals that it is closely associated with trkA in the genome and maps to human chromosome 1q22, A type 2 diabetes susceptibility locus. 2002.

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Lorent, Kristin. Expression of the Alpha-2-Macroglobulin Receptor System and the Amyloid Precursor Protein Family in Embryos and in Adult Brain of Wild Type and transg: Enic Mice (Acta Biomedica Lovaniensia , No 148). Coronet Books Inc, 1997.

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Nielsen, David A., Dmitri Proudnikov, and Mary Jeanne Kreek. The Genetics of Impulsivity. Edited by Jon E. Grant and Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.
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Hohmann, Andrea G. Control of pain initiation by endogenous cannabinoids. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0033.

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The landmark paper discussed in this chapter, published by Calignano et al. in 1998, focuses on the control of pain initiation by endogenous cannabinoids. In the paper, analgesic lipid mediators are shown to be present in peripheral paw tissue where they control the ability of pain signals to ascend to the central nervous system (CNS). Anandamide acts through a peripheral mechanism to suppress inflammatory pain via cannabinoid type 1 receptors. Palmitoylethanolamine, subsequently identified as an endogenous ligand for peroxisome proliferator-activated receptor-α‎, produces peripheral antinociceptive effects via a mechanism similar to that for the cannabinoid type 2 receptor. These lipids do not serve redundant functions and, in combination, produce synergistic antinociceptive effects. These observations suggested that drug-development efforts targeting peripheral control of pain may elucidate improved pharmacotherapies that lack the unwanted CNS side effects of current treatments.
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Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.

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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.
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Gnudi, Luigi, Giorgio Gentile, and Piero Ruggenenti. The patient with diabetes mellitus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0149_update_001.

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About one third of patients with type 1 diabetes develop diabetic nephropathy long-term (usually not before at least 10 years of diabetes), though this proportion is falling as standards of care have risen. Nephropathy is strongly associated with other microvascular complications of diabetes, so that some degree of retinopathy is to be expected, and evidence of neuropathy is common. Patients with type 2 diabetes are equally susceptible, but this is an older group in which vascular disease and other pathologies are also more likely. The rise in type 2 diabetes accounts for diabetes being the most common recorded cause of end stage renal disease (ESRD) in the developed world.Diabetic nephropathy is characterized by a progression through hyperfiltration, microalbuminuria, hypertension, overt proteinuria, nephrotic syndrome, loss of GFR, to ESRD. Risk factors for developing it include genetic factors (though no major single gene effects have been identified), and quality of glycaemic control.The risk of progression can at early stages be reduced by improved glycaemic control, and control of hypertension also slows progression. However angiotensin converting enzyme inhibitors or receptor blockers (ACEi, ARB) are the standard of care for patients with microalbuminuria or overt proteinuria, as they have been shown to reduce the risk of renal endpoints. Combination therapy with both ACEi and ARB together has been associated with a high risk of AKI, hyperkalaemia and other adverse effects so is not generally recommended. Other promising agents in combination are under investigation but none adequately proven at this stage.Patients who reach ESRD have reduced survival on all modalities compared to age-matched patients with other diagnoses. Best rehabilitation and survival for those who are suitable is through renal transplantation, though combined pancreas-renal transplantation may offer still better outcomes for selected patients.
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Book chapters on the topic "Ryanodine receptor type 2"

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Sheikh, Søren Paludan. "Angiotensin Type 2 Receptor." In Encyclopedia of Signaling Molecules, 320–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_451.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "Angiotensin Type 2 Receptor." In Encyclopedia of Signaling Molecules, 106–13. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_451.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "Angiotensin II Receptor Type 2." In Encyclopedia of Signaling Molecules, 106. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100061.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "C-Type Mannose Receptor 2." In Encyclopedia of Signaling Molecules, 481. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100327.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda, et al. "Mannose Receptor, C-type 2." In Encyclopedia of Signaling Molecules, 1042. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100743.

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Nissley, S. Peter. "Type 2 IGF Receptor-Mediated Events." In The IGF System, 165–97. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-712-3_8.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "C-type Lectin-Like Receptor 2." In Encyclopedia of Signaling Molecules, 481. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100324.

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Suzuki-Inoue, Katsue. "C-Type Lectin-Like Receptor 2 (CLEC-2)." In C-Type Lectin Receptors in Immunity, 83–98. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56015-9_6.

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Fluharty, Steven J., Lawrence P. Reagan, and Daniel K. Yee. "The Angiotensin Type 1 and Type 2 Receptor Families." In Advances in Experimental Medicine and Biology, 193–215. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-0952-7_11.

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Fearon, D. T., and J. M. Ahearn. "Complement Receptor Type 1 (C3b/C4b Receptor; CD35) and Complement Receptor Type 2 (C3d/Epstein-Barr Virus Receptor; CD21)." In Current Topics in Microbiology and Immunology, 83–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74977-3_5.

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Conference papers on the topic "Ryanodine receptor type 2"

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Goldblatt, D. L., A. Fouts, G. Valverde-Ha, M. Martinez-Moczygemba, D. Huston, M. J. Tuvim, B. F. Dickey, and S. E. Evans. "Aerosolized Toll-Like Receptor Agonists Modulate Type 2 Allergic Inflammation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1347.

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Kertels, O., M. Breun, H. Hänscheid, M. Kircher, P. Hartrampf, A. Schirbel, CM Monoranu, et al. "Peptide Receptor Radionuclide Therapy in Patients with Neurofibromatosis Type 2 – Initial Experience." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708361.

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Boss, M., L. Deden, M. Brom, S. van Lith, and M. Gotthardt. "Pituitary GLP-1 receptor expression in the pathophysiology of type 2 diabetes." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683647.

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Daigle, Noelle, Thomas G. Knapp, Suzann Duan, David W. Jones, Ali Azhdarinia, Sukhen C. Ghosh, Solmaz AghaAmiri, et al. "Combined multiphoton microscopy and somatostatin receptor type 2 imaging of pancreatic neuroendocrine tumors." In Multimodal Biomedical Imaging XVIII, edited by Fred S. Azar, Xavier Intes, and Qianqian Fang. SPIE, 2023. http://dx.doi.org/10.1117/12.2648113.

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Mar, Ai-Chung. "Abstract 1361: The decoy receptor interleukin-1 receptor type 2 acts as an angiogenic factor in human colorectal cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1361.

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Agudelo, C., S. Mendizuri, E. Area-Gomez, Y. Xu, P. Geraghty, I. J. Goldberg, R. F. Foronjy, and I. Garcia-Arcos. "Type 2 Cell Low Density Lipoprotein Receptor Related Protein 1 (LRP1) Regulates Surfactant Homeostasis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4448.

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Cooper, Simon J., Christina Von Roemeling, Laura Marlow, Han W. Tun, and John A. Copland. "Abstract 2173: Negative transcriptional regulation of the human type III TGFβ receptor in ccRCC." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2173.

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Chen, Kristen, Majid Zeidi, Nithin Reddy, Barbara White, and Victoria Werth. "FRI0307 LENABASUM, A CANNABINOID TYPE 2 RECEPTOR AGONIST, REDUCES CD4 CELL POPULATIONS AND DOWNREGULATES TYPE 1 AND 2 INTERFERON ACTIVITIES IN LESIONAL DERMATOMYOSITIS SKIN." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7759.

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Uemura, Hiroji, Yusuke Ito, Aya Naiki-Ito, Hiroyuki Kato, Shugo Suzuki, Toshiya Kuno, and Satoru Takahashi. "Abstract 254: Chemopreventive effects of angiotensin II receptor type 2 agonist on prostate carcinogenesis by the downregulation of the androgen receptor." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-254.

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Talbot, H., A. Abbaci, S. Saada, N. Gachard, J. Abraham, A. Jaccard, D. Bordessoule, AL Fauchais, T. Naves, and MO Jauberteau. "SPOT-008 Neurotensin receptor type 2 protects B-cell chronic lymphocytic leukaemia cells from apoptosis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.41.

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Reports on the topic "Ryanodine receptor type 2"

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Zhuo, Chuanjun, Hongjun Tian, Lina Wang, Xiangyang Gao, Li Ding, and Ming Liu. Comparative safety of glucagon like peptide‑1 receptor agonists in patients with type 2 diabetes: a network meta-analysis of cardiovascular outcome trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0122.

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Deo, Salil, David McAllister, Naveed Sattar, and Jill Pell. The time-varying cardiovascular benefits of glucagon like peptide-1 agonist (GLP-RA)therapy in patients with type 2 diabetes mellitus: A meta-analysis of multinational randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0097.

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Review question / Objective: P - patients with type 2 diabetes melllitus already receiving routine medical therapy; I - patients receiving glucagon like peptide 1 receptor agonist (GLP1 receptor agonist) therapy (semaglutide, dulaglutide, liraglutide, exenatide, lixisenatide, efpeglenatide, abiglutide); C - patients receiving standard therapy for diabetes mellitus but not receiving GLP1 agonist therapy; O - composite end point as per invididual trial, cardiovascular mortality, all-cause mortality, myocardial infarction, stoke. Condition being studied: Type 2 diabetes mellitus. Study designs to be included: Randomised controlled trials which enroll a large number of patients (defined as > 500) and are multinational in origin. Studies included will need to have published Kaplan and Meier curves for the end-points presented in the manuscript.
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Zhang, Mingzhu, Wujisiguleng Bao, Luying Sun, Zhi Yao, and Xiyao Li. Efficacy and safety of finerenone in chronic kidney disease associated with type 2 diabetes: meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0020.

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Review question / Objective: To assess the beneficial effect and safety of finerenone for patients with chronic kidney disease associated with type 2 diabetes. Condition being studied: Chronic kidney disease (CKD) is a major contributor to morbidity and mortality from non-communicable diseases, affecting almost 700 million people worldwide. Approximately 40% of patients with diabetes have CKD, which exposes them to a 3-fold higher risk of cardiovascular death versus those with T2D alone. Strategies to protect the kidneys of patients with CKD and T2D may reduce their risk of cardiovascular events. Finerenone, a nonsteroidal, selective mineralocorticoid receptor antagonist, reduced composite kidney and cardiovascular outcome in trials involving patients with chronic kidney disease. Recently, quite a few clinical studies have been conducted to compare finerenone and placebo. Our meta-analysis aimed to investigate the efficacy and safety of finerenone in chronic kidney disease associated with T2D. 1st author* - Mingzhu Zhang and Wujisiguleng Bao contributed equally to this study.
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yu, luyou, jinping yang, xi meng, and yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.

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Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.
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Sisler, Edward C., Raphael Goren, and Akiva Apelbaum. Controlling Ethylene Responses in Horticultural Crops at the Receptor Level. United States Department of Agriculture, October 2001. http://dx.doi.org/10.32747/2001.7580668.bard.

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Ethylene is a plant hormone that controls many plant responses, such as growth, senescence, ripening, abscission and seed germination. Recently, 1-methy- cyclopropene (1-MCP), was shown to bind to ethylene receptor for a certain period of time and prevent ethylene action. The objectives of this research were to synthesize analogues of 1-MCP and test their potency to block the ethylene receptor and inhibit ethylene action. During the course of this project, procedures for synthesis and shipment of the cyclopropene compounds were developed as well assay procedures for each compound were worked out. Thirteen new compounds were synthesized. All of them are structural analogues of 1-MCP, with substitution in the 1-position and a side chain containing 2 to 10 carbons. After preliminary studies, nine promising compounds were selected for in-depth study. The potency of the compounds to inhibit ethylene action was tested on a wide scope of systems like: climacteric fruits (banana, avocado and tomato), the triple response (etiolated peas), and leaf abscission (citrus). As the putative inhibitors are suspected to compete for the site of binding and a competitive type of inhibition could be considered, a high concentration of ethylene (300 m1.L-1) was used to induce ripening and other physiological processes. The tests were conducted under extreme conditions which hasten ripening like treatment and storage at 22 to 25oC. There were fluctuations in the responses as related to the concentrations of the inhibitors. Some required much higher concentration to exert the same effect, while some, when applied at the same concentration, blocked the receptor for a longer period of time than the others. Some fruits and other plant organs responded differently to the same inhibitor, indicating differences in characteristics and availability of the ethylene receptors in the various tissues. The potency of the putative inhibitors was found to be greatly affected by their molecular structural and size. In addition, it was found that treatment with the inhibitor should be given before the onset of ethylene action In the case of fruit, treatment should be carried out before the pre-climacteric stage. Simultaneous treatment with ethylene and the inhibitors reduced the inhibitors' effect. The relationship between ethylene and the inhibitors is of a non-competitive nature. All the fruits treated with the putative inhibitors resumed normal ripening after recovery from the inhibition. This fact is of great importance when considering the inhibitors for practical use. The advantage of using inhibitors of ethylene action over inhibitors of ethylene production lies in the ability of the inhibitors of ethylene action to protect the tissue against both endogenous and exogenous ethylene, thus providing better overall protection. Our findings indicate that 1-MCP and its structural analogues are potent inhibitors of ethylene action capable of providing good protection against endogenous and exogenous ethylene. The fact that the compounds are in a gas phase and are non-phytotoxic, odorless and effective at minute concentrations, renders them promising candidates for commercial use. However, the development of water-soluble inhibitors will expand the potential use of the inhibitors in agriculture.
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Avni, Adi, and Gitta L. Coaker. Proteomic investigation of a tomato receptor like protein recognizing fungal pathogens. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600030.bard.

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Maximizing food production with minimal negative effects on the environment remains a long-term challenge for sustainable food production. Microbial pathogens cause devastating diseases, minimizing crop losses by controlling plant diseases can contribute significantly to this goal. All plants possess an innate immune system that is activated after recognition of microbial-derived molecules. The fungal protein Eix induces defense responses in tomato and tobacco. Plants recognize Eix through a leucine-rich-repeat receptor- like-protein (LRR-RLP) termed LeEix. Despite the knowledge obtained from studies on tomato, relatively little is known about signaling initiated by RLP-type immune receptors. The focus of this grant proposal is to generate a foundational understanding of how the tomato xylanase receptor LeEix2 signals to confer defense responses. LeEix2 recognition results in pattern triggered immunity (PTI). The grant has two main aims: (1) Isolate the LeEix2 protein complex in an active and resting state; (2) Examine the biological function of the identified proteins in relation to LeEix2 signaling upon perception of the xylanase elicitor Eix. We used two separate approaches to isolate receptor interacting proteins. Transgenic tomato plants expressing LeEix2 fused to the GFP tag were used to identify complex components at a resting and activated state. LeEix2 complexes were purified by mass spectrometry and associated proteins identified by mass spectrometry. We identified novel proteins that interact with LeEix receptor by proteomics analysis. We identified two dynamin related proteins (DRPs), a coiled coil – nucleotide binding site leucine rich repeat (SlNRC4a) protein. In the second approach we used the split ubiquitin yeast two hybrid (Y2H) screen system to identified receptor-like protein kinase At5g24010-like (SlRLK-like) (Solyc01g094920.2.1) as an interactor of LeEIX2. We examined the role of SlNRC4a in plant immunity. Co-immunoprecipitation demonstrates that SlNRC4a is able to associate with different PRRs. Physiological assays with specific elicitors revealed that SlNRC4a generally alters PRR-mediated responses. SlNRC4a overexpression enhances defense responses while silencing SlNRC4 reduces plant immunity. We propose that SlNRC4a acts as a non-canonical positive regulator of immunity mediated by diverse PRRs. Thus, SlNRC4a could link both intracellular and extracellular immune perception. SlDRP2A localizes at the plasma membrane. Overexpression of SlDRP2A increases the sub-population of LeEIX2 inVHAa1 endosomes, and enhances LeEIX2- and FLS2-mediated defense. The effect of SlDRP2A on induction of plant immunity highlights the importance of endomembrane components and endocytosis in signal propagation during plant immune . The interaction of LeEIX2 with SlRLK-like was verified using co- immunoprecipitation and a bimolecular fluorescence complementation assay. The defence responses induced by EIX were markedly reduced when SlRLK-like was over-expressed, and mutation of slrlk-likeusing CRISPR/Cas9 increased EIX- induced ethylene production and SlACSgene expression in tomato. Co-expression of SlRLK-like with different RLPs and RLKs led to their degradation, apparently through an endoplasmic reticulum-associated degradation process. We provided new knowledge and expertise relevant to expression of specific be exploited to enhance immunity in crops enabling the development of novel environmentally friendly disease control strategies.
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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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Sessa, Guido, and Gregory B. Martin. molecular link from PAMP perception to a MAPK cascade associated with tomato disease resistance. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597918.bard.

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The research problem: The detection of pathogen-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs) is a key mechanism by which plants activate an effective immune response against pathogen attack. MAPK cascades are important signaling components downstream of PRRs that transduce the PAMP signal to activate various defense responses. Preliminary experiments suggested that the receptor-like cytoplasmickinase (RLCK) Mai5 plays a positive role in pattern-triggered immunity (PTI) and interacts with the MAPKKK M3Kε. We thus hypothesized that Mai5, as other RLCKs, functions as a component PRR complexes and acts as a molecular link between PAMP perception and activation of MAPK cascades. Original goals: The central goal of this research was to investigate the molecular mechanisms by which Mai5 and M3Kε regulate plant immunity. Specific objectives were to: 1. Determine the spectrum of PAMPs whose perception is transmitted by M3Kε; 2. Identify plant proteins that act downstream of M3Kε to mediate PTI; 3. Investigate how and where Mai5 interacts with M3Kε in the plant cell; 4. Examine the mechanism by which Mai5 contributes to PTI. Changes in research directions: We did not find convincing evidence for the involvement of M3Kε in PTI signaling and substituted objectives 1 and 3 with research activities aimed at the analysis of transcriptomic profiles of tomato plants during the onset of plant immunity, isolation of the novel tomato PRR FLS3, and investigation of the involvement of the RLCKBSKs in PTI. Main achievements during this research program are in the following major areas: 1. Functional characterization of Mai5. The function of Mai5 in PTI signaling was demonstrated by testing the effect of silencing the Mai5 gene by virus-induced gene silencing (VIGS) experiments and in cell death assays. Domains of Mai5 that interact with MAPKKKs and subcellular localization of Mai5 were analyzed in detail. 2. Analysis of transcriptional profiles during the tomato immune responses to Pseudomonas syringae (Pombo et al., 2014). We identified tomato genes whose expression is induced specifically in PTI or in effector-triggered immunity (ETI). Thirty ETI-specific genes were examined by VIGS for their involvement in immunity and the MAPKKK EPK1, was found to be required for ETI. 3. Dissection of MAP kinase cascades downstream of M3Kε (Oh et al., 2013; Teper et al., 2015). We identified genes that encode positive (SGT and EDS1) and negative (WRKY1 and WRKY2) regulators of the ETI-associated cell death mediated by M3Kε. In addition, the MKK2 MAPKK, which acts downstream of M3Kε, was found to interact with the MPK3 MAPK and specific MPK3 amino acids involved interaction were identified and found to be required for induction of cell death. We also identified 5 type III effectors of the bacterial pathogen Xanthomonaseuvesicatoria that inhibited cell death induced by components of ETI-associated MAP kinase cascades. 4. Isolation of the tomato PRR FLS3 (Hind et al., submitted). FLS3, a novel PRR of the LRR-RLK family that specifically recognizes the flagellinepitope flgII-28 was isolated. FLS3 was shown to bind flgII-28, to require kinase activity for function, to act in concert with BAK1, and to enhance disease resistance to Pseudomonas syringae. 5. Functional analysis of RLCKs of the brassinosteroid signaling kinase (BSK) family.Arabidopsis and tomato BSKs were found to interact with PRRs. In addition, certain ArabidospsisBSK mutants were found to be impaired in PAMP-induced resistance to Pseudomonas syringae. Scientific and agricultural significance: Our research activities discovered and characterized new molecular components of signaling pathways mediating recognition of invading pathogens and activation of immune responses against them. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease.
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