Relevant bibliographies by topics / Endothelin receptor – type B

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  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Endothelin receptor – type B'

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Published: 31 January 2023

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Journal articles on the topic "Endothelin receptor – type B"

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Pollock, David M., and Markus P. Schneider. "Clarifying Endothelin Type B Receptor Function." Hypertension 48, no. 2 (August 2006): 211–12. http://dx.doi.org/10.1161/01.hyp.0000229908.62191.6e.

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Zhang, Junlan, Yiqun Ling, Liping Tang, Bao Luo, David M. Pollock, and Michael B. Fallon. "Attenuation of experimental hepatopulmonary syndrome in endothelin B receptor-deficient rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 4 (April 2009): G704—G708. http://dx.doi.org/10.1152/ajpgi.90627.2008.

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Experimental hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL) in rat is accompanied by increased lung vascular endothelial endothelin B (ETB) receptor expression and increased circulating levels of endothelin-1 (ET-1). The onset of HPS is hypothesized to be triggered by ET-1/ETB receptor activation of endothelial nitric oxide synthase (eNOS)-derived NO production in the pulmonary endothelium. However, whether functional pulmonary vascular ETB receptors are required for the development of experimental HPS is not defined. We evaluated the effects of vascular ETB receptor deficiency on the development of experimental HPS. The molecular and physiological alterations of HPS were compared in 2-wk CBDL wild-type and ETB receptor-deficient (transgenic sl/sl) rats. Relative to wild-type rats, basal hepatic and plasma ET-1 levels were elevated in sl/sl controls although, unlike wild-type animals circulating ET-1 levels, did not increase further after CBDL in sl/sl animals. In contrast to wild-type animals, ETB receptor-deficient rats did not develop increased Akt and eNOS expression and activation and did not develop gas exchange abnormalities of HPS after CBDL. There was a similar degree of pulmonary intravascular monocyte accumulation in both 2-wk CBDL sl/sl and wild-type animals. In conclusion, ETB receptor deficiency inhibits lung Akt/eNOS activation and prevents the onset of experimental HPS after CBDL. This effect is independent of inhibition of pulmonary intravascular monocyte accumulation. These results demonstrate that ET-1/ETB receptor signaling plays a key role in the initiation of experimental HPS.
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Seccia, Teresa M., and Lorenzo A. Calò. "Endothelin-1-induced endothelial mesenchimal transition via endothelin type B receptor stimulation." Journal of Hypertension 35, no. 6 (June 2017): 1329–30. http://dx.doi.org/10.1097/hjh.0000000000001344.

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Lau, Denise, Katalin Szöcs, Anna Klinke, Tanja Rudolph, Volker Rudolph, Thomas Streichert, Stefan Blankenberg, and Stephan Baldus. "Myeloperoxidase upregulates endothelin receptor type B expression." Journal of Molecular and Cellular Cardiology 69 (April 2014): 76–82. http://dx.doi.org/10.1016/j.yjmcc.2013.12.007.

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Okamoto, Yasuo, Haruaki Ninomiya, and Tomoh Masaki. "Posttranslational Modifications of Endothelin Receptor Type B." Trends in Cardiovascular Medicine 8, no. 8 (November 1998): 327–29. http://dx.doi.org/10.1016/s1050-1738(98)00027-9.

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Lau, Denise, Katalin Szöcs, Anna Klinke, and Stephan Baldus. "Myeloperoxidase Modulates Endothelin Receptor Type B Expression." Free Radical Biology and Medicine 49 (January 2010): S145. http://dx.doi.org/10.1016/j.freeradbiomed.2010.10.404.

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Terada, Koji, Takahiro Horinouchi, Tsunehito Higashi, Prabha Nepal, and Soichi Miwa. "Ubiquitination-regulated receptor trafficking of endothelin type A and type B receptors." Folia Pharmacologica Japonica 145, no. 1 (2015): 4–9. http://dx.doi.org/10.1254/fpj.145.4.

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Okuta, Akiko, Kazutoshi Tani, Shoko Nishimura, Yoshinori Fujiyoshi, and Tomoko Doi. "Thermostabilization of the Human Endothelin Type B Receptor." Journal of Molecular Biology 428, no. 11 (June 2016): 2265–74. http://dx.doi.org/10.1016/j.jmb.2016.03.024.

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Chiou, W. J., S. R. Magnuson, D. Dixon, S. Sundy, T. J. Opgenorth, and J. R. Wu-wong. "Dissociation Characteristics of Endothelin Receptor Agonists and Antagonists in Cloned Human Type-B Endothelin Receptor." Endothelium 5, no. 3 (January 1997): 179–89. http://dx.doi.org/10.3109/10623329709053397.

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Mazaki, Yuichi, Tsunehito Higashi, Yasuhito Onodera, Jin-Min Nam, Ari Hashimoto, Shigeru Hashimoto, Takahiro Horinouchi, and Soichi Miwa. "GRP78 promotes ERK activation through endothelin type B receptor." Proceedings for Annual Meeting of The Japanese Pharmacological Society 92 (2019): 1—P—110. http://dx.doi.org/10.1254/jpssuppl.92.0_1-p-110.

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Dissertations / Theses on the topic "Endothelin receptor – type B"

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Guyonnet, Léa. "Rôle du récepteur myéloïde à l’endothéline (ETB) au cours de l’hypertension artérielle." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB018.

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L’hypertension artérielle (HTA) est un problème de santé publique. Largement répandue dans le monde, elle touchait 40% des adultes âgés de plus de 25 ans et causait 9.4 millions de décès en 2008. Cette pathologie est la cause la plus commune de décès dans les pays développés et constitue un facteur de risque majeur d’atteintes cardiaques, rénales et cérébrales. Bien qu'étudiés depuis maintenant plus d'un demi-siècle, les mécanismes des atteintes systémiques liées à l'hypertension restent encore peu connus. L'augmentation de la pression artérielle est multifactorielle et découle aussi du dérèglement de certains systèmes tels le système rénine-angiotensine et le système endothéline. De récentes études ont suggéré un rôle de l’immunité innée dans le développement de l’HTA et des lésions qui y sont associées. L’endothéline-1 est un puissant vasoconstricteur. Sa production est déclenchée par différents stimuli dont l’AngII et des cytokines pro-inflammatoires. L’ET-1 agit via deux récepteurs : ETAR et ETBR. Pour ce projet, nous avons généré des souris ne possédant pas le récepteur ETB myéloïde (LysM-Cre Ednrb lox/lox). Ces souris ont été soumises à une perfusion chronique d’AngII associée à un régime hyper-sodé. Nous avons observé que les deux groupes de souris développent la même hypertension et les mêmes atteintes cardiaques. En revanche les atteintes des organes cibles sont moins importantes chez les souris LysM-Cre Ednrb lox/lox. La fonction rénale de ces dernières est préservée et, histologiquement, moins de lésions sont observées. Cette protection semble être due à l’incapacité des cellules myéloïdes à infiltrer les reins. En effet, la chimioattraction des cellules myéloïdes vers ET-1 est dépendante du récepteur ETB myéloïde. De plus, les cellules inflammatoires qui sont observées dans les reins des souris LysM-Cre Ednrb lox/lox présentent un phénotype anti-inflammatoire contrairement à leur contrôles
Arterial hypertension is a major risk factor for atherosclerosis, coronary artery disease, stroke, and chronic kidney disease (CKD) and is one of the most prominent contributors to death worldwide. However, despite the frequency of hypertension, its cause in the majority of adults is unknown. Hypertension is complex, with no single mechanism entirely explaining the blood pressure (BP) rise in any given model. The past 50 years have seen growing evidence implicating the immune system. Recent data suggest that macrophages (M)/monocytes contribute to, and protect from, hypertension and its associated end organ injury. Endothelin-1 (ET-1) is the most potent endogenous vasoconstrictor. Its production is triggered by multiple stimuli including Ang II and pro-inflammatory cytokines. ET-1 acts by binding to two distinct receptors, the endothelin-A (ETA) and the endothelin-B (ETB) receptors. Interestingly, ET antagonism can blunt BP elevation in an Ang II model suggesting that ET-1 largely mediates the effects of Ang II. Here, we have generated mice specifically lacking ETB receptors on myeloid cells. We have shown that the development of hypertension associated with Ang II infusion is not dependent on these cells. Similarly, the cardiac dysfunction seen after 6 weeks of Ang II was similar between knockout and control mice. Interestingly, mice deficient of ETB receptors on myeloid cells alone were protected from Ang II induced vascular dysfunction and kidney injury. This protection appeared to relate to an inability for ETB receptor deficient Mto infiltrate the kidneys due to impaired chemokinesis towards ET-1. Furthermore, the Minfiltrating he kidney in response to Ang II in myeloid ETB receptor deficient mice overwhelmingly possessed an anti-inflammatory phenotype
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Sedkaoui, Melissa. "Single-chain variable fragments and molecularly imprinted polymers directed against endothelin receptors – type B for cancer cells targeting." Thesis, Compiègne, 2021. http://www.theses.fr/2021COMP2636.

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Les récepteurs aux endothélines sont des récepteurs couples aux protéines G desquels deux variants existent, type A (ETAR) et type B (ETBR). Ils sont principalement décrits pour leur rôle physiologique de régulation du flux sanguin dans tous les types de vaisseaux via les mécanismes de vasoconstriction et de dilatation, respectivement. Cependant, les récepteurs aux endothélines sont impliqués dans plusieurs désordres physiologiques dont le cancer ou l’expression de l’un ou des deux récepteurs aux endothélines est dérégulée. Nous avons développé deux stratégies complémentaires pour le ciblage des récepteurs ETB, visant à inhiber son action quand il est surexprimé : la sélection de single-chain variable fragment (scFv) à partir d’une banque large et naïve par la technologie du phage-display, et la synthèse sur mesure, assistée par une matrice de polymères à empreintes moléculaires (MIP) comme « anticorps en plastique ». La sélection de scFv a été réalisée par biopanning sur cellules transfectées entières afin de maintenir la conformation native de ETBR. Phage-scFv qui se lient uniquement à la cible et ceux qui sont internalisés suite à l’interaction scFv- récepteur ont été isolés séparément. Après confirmation de la reconnaissance des cellules CHO-ETBR par rapport aux cellules CHO-WT par les phages-scFv polyclonaux en utilisant un test ELISA et la microscopie électronique à balayage (MEB), nous avons sélectionné au total 17 clones qui ont montré une capacité de liaison augmentée par phage-ELISA monoclonal sur cellules transfectées entières, mais également sur UACC-257, une lignée cellulaire de mélanome avec une surexpression de ETBR. Des résultats préliminaires obtenus par cryométrie en flux ont montré une reconnaissance augmentée de CHO-ETBR par l’un des clones sélectionnés. La viabilité cellulaire a été affectée par certains de ces clones. Des MIP nanoparticules ont été synthétisées en utilisant un peptide synthétique comme molécule matrice qui mime un « épitope » de ETBR. Nous avons réalisé la synthèse sur une phase solide afin d’obtenir une exposition orientée de la matrice, résultant en la production de MIP avec des cavités homogènes. Les particules MIP d’une taille de l’ordre du nanomètre ont été obtenus et ont par la suite été testés pour leur capacité à reconnaitre le récepteur entier exprimé sur la surface cellulaire par imagerie cellulaire. Des nano-MIP fluorescents ont montré une reconnaissance sélective des cellules transfectées par rapport à leurs homologues non transfectées
Endothelin receptors are G-protein coupled receptors of which two variants exist, type A (ETAR) and type B (ETBR). They are mainly described for their physiological role of regulating the blood flow in all vessel types via vasoconstriction and vasodilatation mechanisms, respectively. However, endothelin receptors are involved in several physiological disorders including cancer in which the expression of one or both endothelin receptors are deregulated.We have developed two complementary strategies for targeting ETB receptors, aiming to inhibit its action when it is overexpressed: selection of single-chain variable fragments (scFv) from a large naive library by phage-display technology as « biologic antibodies », and tailor-made template-assisted synthesis of Molecularly Imprinted Polymers (MIP) as « plastic antibodies ». The selection of scFv was performed by biopanning on whole transfected cells in order to maintain the native conformation of ETBR. Phage-scFv that only bind to the target and the ones that are internalized subsequently to scFv-receptor interaction were isolatedseparately. After confirming the recognition of CHO-ETBR cells over CHO-WT cells by polyclonal phage-scFv using an ELISA assay and Scanning Electron Microscopy (S.E.M), we have selected in total 17 clones that showed increased binding ability by monoclonal phage-ELISA on whole transfected cells but also to UACC-257, a melanoma cell line with an overexpression of ETBR. Preliminary results obtained by flow cytometry showed an enhanced recognition of CHO-ETBR by one of the selected clones. Cell viability was shown to be affected by some of these clones. MIP nanoparticles were synthesized using a synthetic peptide as template molecule that mimics an « epitope » of ETBR. We performed the synthesis on a solid phase in order to obtain an oriented exposition of the template resulting in the production of MIPs with homogenous cavities. MIP particles of a size in the nanometer range were obtained and were subsequently tested for their ability to recognize the whole receptor expressed oncell surface by cell imaging. Fluorescent nano-MIPs were shown to recognize selectively transfected cells with regard to their non-transfected counterparts
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Swire, Matthew. "Investigating endothelin receptor B signalling during myelination." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28912.

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A key process enabling the correct functioning of neural circuits involves the formation of multi‐layered membranous myelin sheaths around axons. Myelin sheaths, made by specialised glial cells called oligodendrocytes in the central nervous system (CNS), metabolically support underlying axons and speed up electrical impulse conduction, aiding efficient communication between neurons. As only a subset of axons in the CNS are myelinated, with unique patterns developed therein, it raises the questions: how does an oligodendrocyte choose which axon to myelinate and what regulates the amount of myelin made? The production of myelin sheaths by the oligodendrocyte, is under strong influence from of a range of signals including those mediated by G protein‐coupled receptor (GPR) superfamily members. One GPR, Endothelin receptor B (EDNRB), best known for regulating blood flow, had previously been demonstrated to both positively and negatively influence myelination. I have investigated how EDNRB regulates myelination using an in vitro myelination assay, alongside in vivo analysis in zebrafish and mice. These systems identified a direct signalling role for EDNRB in the promotion of myelin sheath number. Furthermore, profiling the protein signalling cascade downstream of this receptor identified a range of known and novel factors involved in the regulation of myelin sheath number including the MAPK pathway, Src family kinases, ErbB receptors, protein kinase C ε, NMDAR and AMPAR. Functional analyses of a subset of these factors elucidate how EDNRB signalling, potentially connecting signals from a range of cell types, ensures correct adequate myelination in the CNS.
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Bagnall, Alan. "Role of the endothelin B receptor in cardiovascular homeostasis." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24786.

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The aim of this project was to precisely determine the role of the endothelial cell (EC) ETB receptor in the regulation of vascular tone, blood pressure and clearance of ET-1. Cre-loxP recombination was utilised to conditionally regulate ETB receptor expression in vivo. Mice featuring loxP sites flanking exons 2 and 3 of the ETB receptor gene (floxed ETB receptor mice) were generated by standard gene targeting techniques in embryonic stem cells. Floxed ETB mice were crossed with Tie2-Cre transgenic mice to produce mice in which recombination-mediated removal of ETB receptor coding regions was limited to EC (Flox/Flox Tie2). EC ETB receptor binding of 125I ET-1 and in vitro aortic and tracheal ring myography were performed to assess endothelial function and the response to selective ETB receptor agonists. Pulmonary EC ET-1 binding was decreased by ~80% in EC-specific ETB receptor knockout mice (cpm/50μg membrane protein ± SEM; Flox/Flox Tie2 581 ± 67; W/W -/- 3175 ± 268; n=3; p<0.001). Cell-specificity of ETB receptor down-regulation was demonstrated by maintenance of normal ETB receptor-mediated tracheal constriction. Blood pressure was increased in Flox/Flox Tie2 mice (MAP 137.2 ± 6.4mmHg (n=5); W/W -/-, 113.7 ± 4.7mmHg (n=6; p<0.05) but was not affected by dietary salt. Plasma ET-1 was increased ~4 fold following EC ETB receptor down-regulation (mean plasma [ET-1] pg/ml ± SEM; Flox/Flox Tie2 12.40 ± 2.95; W/W -/- 2.94 ± 0.83; n=6; p<0.001). Aortic rings from Flox/Flox Tie2 mice demonstrated impaired endothelium-dependant vasodilatation to ETB receptor selective agonists and acetylcholine but normal endothelium-independent vasodilatation. Recombination-mediated removal of exons 2 and 3 of the ETB receptor is sufficient to prevent expression of functional ETB receptors. The ‘floxed’ ETB receptor mouse thereby facilitates the cell type-specific down-regulation of ETB receptor expression in vivo. The EC ETB receptor plays an important role in the determination of blood pressure under normal physiological conditions. The mechanism underlying this effect may involve loss of EC ETB receptor-mediated vasodilatation or impaired clearance of ET-1 with a consequent increase in ETA receptor activity.
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Leslie, Stephen James. "The effect of endothelin A and endothelin B receptor ligands on the cardiovascular system of man." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29221.

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ET-1 vasoconstricts in the skin microcirculation and it appears that endothelin converting enzyme (ECE) activity is present as big ET-1 also vasoconstricts. ECE and neutral endopeptidase (NEP) blockade both cause vasodilatation suggesting skin basal resting ET tone. ET-1 (1-31) is also a vasoconstrictor in the skin microcirculation. Plasma concentrations of ET-1(1-31) are not elevated in patients with CHF. ETARA improves systemic haemodynamics in patients with CHF while concomitant ETBRA attenuates this effect. In the isolated human myocardium ET is positively inotropic but there is no resting ET inotropy with no effect on basal twitch force with ETRA. In addition, ET attenuates beta-adrenergic activation in isolated human myocardium. In hypercholesterolaemia, forearm vascular effects are similar to those previously reported in healthy volunteers. Treatment with statin therapy for 8 weeks caused a trend towards an increase in ETA mediated vasodilatation. Conclusions: The novel finding that ET(1-31) is a vasoconstrictor in the skin microcirculation may represent a novel pathway of ET production. The haemodynamic benefits of selective ETARA over dual ETA/BRA is a unique finding with considerable importance and supports the development of selective ETARAs as clinical therapies in CHF. The finding of antagonism between the ET system and the beta-adrenergic stimulation may represent a protective adaptation in conditions where there beta-adrenergic stimulation is detrimental and there is activation of the ET system, such as CHF.
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Elez, Danka. "Production of recombinant human endothelin B receptor in different hosts and its subsequent solubilization and purification." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970794746.

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Kelland, Nicholas. "The role of the endothelial cell endothelin B receptor in cardiovascular function." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1899.

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Endothelin-1 (ET-1) binds to endothelin A (ETA) and B (ETB) receptors on vascular smooth muscle cells, resulting in profound vasoconstriction and cellular proliferation. In contrast, activation of endothelial cell (EC) ETB receptors releases nitric oxide (NO) and prostacyclin (PGI2), which are anti-mitotic and mediate vasodilatation. ETB receptors are also responsible for the clearance of ET-1 from the circulation and renal ETB receptors contribute to sodium and water balance. Pharmacological blockade and genetic models featuring total ETB ablation, demonstrate salt sensitive hypertension. However, these do not allow the role of the EC ETB in cardiovascular homeostasis to be determined. Mice featuring loxP sites flanking exons 3 and 4 of the ETB gene (floxed ETB mice: FF/--) were crossed with Tie2-Cre mice (WW/Tie2-Cre), in which the expression of a Cre recombinase cDNA transgene is limited to EC, to generate EC-specific ETB down-regulated mice (FF/Tie2-Cre). Having demonstrated EC-specific down-regulation of ETB receptors using autoradiography, the role and relative contribution of the EC ETB to the regulation of systemic BP, to the clearance of ET-1 from the plasma, as well as to the development of pulmonary arterial hypertension were investigated. Autoradiography revealed significant down-regulation of ETB in EC-rich tissues such as lung of FF/Tie2-Cre animals (8 ± 3 amol.mm-2) compared to controls (80 ± 21 amol.mm-2) (n=4; p<0.05). Levels of ETA expression were preserved despite higher concentrations of plasma ET-1 in the FF/Tie2-Cre samples (12.4 ± 3.0 pg.ml-1) compared to controls (3.0 ± 0.8 pg.ml-1) (n=6; p<0.001). Using radiotelemetry, mean arterial blood pressure of FF/Tie2 mice was not significantly different to that of FF/- controls on low salt (FF/Tie2-Cre: 122.7 ± 1.52 mmHg, n=10; FF/--: 125.7 ± 0.58 mmHg, n=12), normal salt (FF/Tie2-Cre: 133.8 ± 4.0 mmHg, n=10; FF/--: 131.5 ± 3.33 mmHg, n=12) or high salt diet (FF/Tie2-Cre: 149.2 ± 2.71 mmHg, n=10; FF/--: 143.9 ± 2.97 mmHg, n=12). Similarly no differences in SBP, DBP or HR were seen between genotypes. The clearance of an intravenous bolus of radiolabelled ET-1 was significantly impaired in FF/Tie2-Cre mice (0.054 ± 0.006 ml.sec-1) compared to control mice (0.175 ± 0.032 ml.sec-1) (n=5; p<0.01). ETB blockade of control mice reduced ET-1 clearance to that of untreated FF/Tie2-Cre animals (n=4). Two weeks of hypobaric hypoxia induced an exaggerated increase in systolic right ventricular pressure in FF/Tie2-Cre mice (34.4 ± 1.2 mmHg, n=10) compared with FF/-- mice (24.6 ± 1.4mmHg, n=10; p<0.05), associated with an increased right ventricular/ left ventricular + septum ratio in FF/Tie2-Cre mice (normoxia: 0.224 ± 0.009; hypoxia: 0.285 ± 0.017; p<0.01), but not in FF/-- mice. Hypoxia increased the percentage of remodeled vessels in FF/-- mice (normoxia: 5.6 ± 0.6%; hypoxia: 11.4 ± 0.6%; n=6; p<0.001), and this was augmented in FF/Tie2-Cre mice (normoxia: 7.1 ± 0.5%; hypoxia: 18.5 ± 1.2%; n=6; p<0.001). The EC ETB receptor does not play a significant role in the BP response to salt, suggesting that ETB signalling on other cell types is responsible for ETB mediated natriuresis. However, the EC ETB receptor is crucial to the elimination of ET-1 from the circulation and is protective against the development of pulmonary arterial hypertension, most likely by preventing remodeling of small pulmonary arteries.
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Wu, Sumin [Verfasser]. "Structural and functional basis of Endothelin-1 type A receptor (ETAR) activation / Sumin Wu." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1179779118/34.

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Lowenstein, Marcia. "Interactions between Endothelin Receptor B and Transcription Factors Sox10 and Pax3 in the Melanocyte Lineage." FIU Digital Commons, 2009. http://digitalcommons.fiu.edu/etd/117.

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Genetic interactions that underlie developmental processes such as cell differentiation and pattern formation are complex and difficult to elucidate. Neural Crest (NC) cells and their derivatives offer an optimal system in which to probe for these complex interactions as they acquire different cell fates and constitute a variety of structures. The transcription factors Sox10 and Pax3 as well as the transmembrane receptor Endothelin receptor b (Ednrb) are temporally and spatially co-expressed early in NC cells and mutations in these genes lead to similar hypopigmentation phenotypes due to a reduced number of NC-derived melanocyte precursors, the melanoblasts. The goal of this study was to establish whether Sox10 and Ednrb or Pax3 and Ednrb interact to promote normal murine melanocyte development. Crosses of Sox10 or Pax3 with Ednrb heterozygous mutants showed that the double heterozygous hypopigmentation phenotype was significantly more pronounced than phenotypes of single heterozygotes, implying that a synergistic interaction exists between Sox10 and Ednrb and Pax3 and Ednrb. This interaction was further explored by the attempt to rescue the Sox10 and Pax3 hypopigmentation phenotypes by the transgenic addition of Ednrb to melanoblasts. Pigmentation was completely restored in the Sox10 and partially restored in the Pax3 mutant mice. The comparison of the number of melanoblasts in transgenic and non-transgenic Sox10 mutant embryos showed that the transgenic rescue occurred as early as E11.5, a critical time for melanoblast population expansion. Cell survival assays indicated that the rescue was not due to an effect of the transgene on melanoblast survival. A novel phenotype arose when studying the interaction between Ednrb and Pax3. Newborns appeared normal but by 3.5 weeks of age, the affected pups were smaller than normal littermates and developed a dome-shaped head; some also developed thoracic kyphosis. Affected pups were dead by 4 weeks of age: 80% were Pax3Sp/+ and 75% were female. When compared to normal littermates, affected mice had brains with enlarged 4th ventricles and more glia while skeletal staining showed kyphosis, wider rib cages and pelvic differences. An epistatic interaction resulting from the mixing of genetic backgrounds that is exacerbated in the presence of Pax3 heterozygosity is suspected.
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Neder, Thomas Harry [Verfasser], and Charlotte [Akademischer Betreuer] Wagner. "The endothelin-A and endothelin-B receptor as potential factors to control synthesis and secretion of renin / Thomas Harry Neder ; Betreuer: Charlotte Wagner." Regensburg : Universitätsbibliothek Regensburg, 2018. http://d-nb.info/1155360753/34.

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Book chapters on the topic "Endothelin receptor – type B"

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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. "A-Type Endothelin Receptor." In Encyclopedia of Signaling Molecules, 176. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100096.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Endothelin Receptor Type A." In Encyclopedia of Signaling Molecules, 551. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100391.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Endothelin Type A Receptor." In Encyclopedia of Signaling Molecules, 551. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100392.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "ETA Type Endothelin Receptor." In Encyclopedia of Signaling Molecules, 602. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100408.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "Type A Endothelin Receptor." In Encyclopedia of Signaling Molecules, 1942. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101420.

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Heldin, Carl-Henrik, and Lars Rönnstrand. "Platelet-Derived Growth Factor B Type Receptor." In Receptor Purification, 303–14. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0461-9_15.

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Cantú, Silvana M., María I. Rosón, Adriana S. Donoso, Ana M. Puyó, and Marcelo R. Choi. "Natriuretic Peptide Receptor Type B (NPRB)." In Encyclopedia of Signaling Molecules, 3351–55. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101994.

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Cantú, Silvana M., María I. Rosón, Adriana S. Donoso, Ana M. Puyó, and Marcelo R. Choi. "Natriuretic Peptide Receptor Type B (NPRB)." In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101994-1.

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Yu, Hong. "HDL and Scavenger Receptor Class B Type I (SRBI)." In HDL Metabolism and Diseases, 79–93. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1592-5_6.

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Asai, Rieko, Yuichiro Arima, Daiki Seya, Ki-Sung Kim, Yumiko Kawamura, Yukiko Kurihara, Sachiko Miyagawa-Tomita, and Hiroki Kurihara. "Endothelin Receptor Type A-Expressing Cell Population in the Inflow Tract Contributes to Chamber Formation." In Etiology and Morphogenesis of Congenital Heart Disease, 289–90. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_40.

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Conference papers on the topic "Endothelin receptor – type B"

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Shirai, Tsuyoshi, Tomoyuki Mutoh, Tomonori Ishii, Hiroshi Fujii, and Hideo Harigae. "THU0317 IDENTIFICATION OF ENDOTHELIAL PROTEIN C RECEPTOR AND SCAVENGER RECEPTOR CLASS B TYPE 1 AS MAJOR AUTOANTIGENS IN TAKAYASU ARTERITIS." 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.602.

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Beeler, D., L. Fritze, G. Soff, R. Jackman, and R. Rosenberg. "HUMAN THROMBOMODULIN cDNA:SEQUENCE AND TRANSLATED STRUCTURE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643967.

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Abstract:
A 750 bp bovine Thrombomodulin (TM) cDNA fragment was used as an hybridization probe to screen an oligo-dT primed Lambda gtll. cDNA library prepared from human umbilical vein endothelial cell mRNA. A 2.4 kb positive human clone was isolated which showed an 80% nucleotide sequence homology with bovine TM cDNA. This clone and a 550 bp fragment from its 5' end were used to further screen the oligo-dT primed library as well as randomly primed library prepared from the same mRNA. The cDNA clones obtained allow us to describe the overall structure of human TM and reveal that it is extremely similar to the structure of bovine TM, especially as the bovine TM is organized like the receptor for low density lipoprotein (LDL R). Both TM and LDL R exhibit short cytoplasmic C-terminal tails which are either neutral or negatively charged. Other coated pit receptors such as the insulin receptor or the epidermal growth factor (EGF) receptor have very large cytoplasmic regions with a complex tyrosine kinase segment as well as multiple sites for phosphorylation. Both TM and LDL R possess a transmembrane region and an immediately adjacent extracellular serine/threonine rich region which in LDL R has been shown to bear 0-1inked sugars. Both TM and LDL R contain a more distal area of cysteine rich repeats, first noted in the EGF precursor and termed EGF type B. However, the TM EGF type B repeats appear to have been duplicated in TM resulting in their being 6 of them rather than the 3 found in LDL R. The N-terminal half of LDL R is thought to contain the ligand binding region of the receptor and is constructed from multiple cysteine rich repeats similar to those of Complement factor C9. The structure of this region of TM is quite different from that of LDL R, possessing few cysteines. We suspect that protein C and/or thrombin may bind to this unique domain of TM.
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Ye, Fei, Kazunari Yamada, Yue Liu, Jinny Choe, Anna Dembo, Jonathan L. Tso, Timothy F. Cloughesy, et al. "Abstract 3308: Endothelin 3/endothelin receptor B signaling pathway blockade depletes radio-chemoresistant glioblastoma stem cells." 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.am2011-3308.

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Folkert, Ian Wesley, Tsun Ki Jerrick To, Samir Devalaraja, Robert J. Norgard, and Malay Haldar. "Abstract 1776: Tumor-derived endothelins regulate antitumor immune responses through macrophage endothelin B receptor." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1776.

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Jungck, David, Jürgen Knobloch, Sandra Körber, Yingfeng Lin, Jürgen Konradi, Sarah Yanik, Erich Stoelben, and Andrea Koch. "Endothelin receptor B protects GM-CSF mRNA from degradation in human airway smooth muscle cells." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5112.

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Kappes, LM, S. Sommerlatte, C. Plattfaut, S. Pitann, G. Marschner, H. Heidecke, P. Lamprecht, et al. "AB0175 Inhibitory effect of endothelin-1 type a receptor antagonists on migration of neutrophils and tumour cells." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6173.

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Conficoni, Elisa, Massimiliano Palazzini, Enri Leci, Andrea Rinaldi, Cristina Bachetti, Francesca Terzi, Francesca Sciarra, et al. "Effects Of Long-Term Administration Of Epoprostenol Alone Or In Combination With Endothelin Receptor Antagonists And Phosphodiesterase Type-5 Inhibitors." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4799.

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Asundi, Jyoti, Paul Polakis, Jennifer A. Lacap, and Michelle Nannini. "Abstract 2924: MAPK pathway inhibition enhances the efficacy of an anti-endothelin B receptor drug conjugate by inducing target expression in melanoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2924.

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Warburton, Rod, Daniel S. Green, Chamila Rupasinghe, Jaime Wilson, Achani Yatawara, Christine Sallum, Linda Taylor, Dale Mierke, Nicholas S. Hill, and Peter Polgar. "A Cell Permeable Peptide Antagonist Of The Endothelin Receptor B Reduces Pulmonary Arterial Hypertension In The Rat In An ERK And AKT Dependent Manner." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4776.

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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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