Research Topics
Genomes and Genes | R P XiaoSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
|
Detail Information
Publications
The enigma of beta2-adrenergic receptor Gi signaling in the heart: the good, the bad, and the uglyWeizhong Zhu
Circ Res 97:507-9. 2005- Subtype-specific alpha1- and beta-adrenoceptor signaling in the heartRui Ping Xiao
Institute of Molecular Medicine, Peking University, Beijing 100871, China
Trends Pharmacol Sci 27:330-7. 2006.... 
Age-associated reductions in cardiac beta1- and beta2-adrenergic responses without changes in inhibitory G proteins or receptor kinasesR P Xiao
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224, USA
J Clin Invest 101:1273-82. 1998..Neither GRKs nor Gi proteins appear to contribute to the age-associated reduction in cardiac beta-AR responsiveness...- Enhanced G(i) signaling selectively negates beta2-adrenergic receptor (AR)--but not beta1-AR-mediated positive inotropic effect in myocytes from failing rat heartsRui Ping Xiao
The Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
Circulation 108:1633-9. 2003.... - Subtype-specific beta-adrenoceptor signaling pathways in the heart and their potential clinical implicationsRui-Ping Xiao
Laboratory of Cardiovascular Science, National Institute on Aging/NIH, Baltimore, MD 21224, USA
Trends Pharmacol Sci 25:358-65. 2004 - Beta-adrenergic signaling in the heart: dual coupling of the beta2-adrenergic receptor to G(s) and G(i) proteinsR P Xiao
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, MD 21224, USA
Sci STKE 2001:re15. 2001..Because of these differences, selective activation of cardiac beta2AR may provide catecholamine-dependent inotropic support without cardiotoxic consequences, which might have beneficial effects in the failing heart... - Coupling of beta2-adrenoceptor to Gi proteins and its physiological relevance in murine cardiac myocytesR P Xiao
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, MD, USA
Circ Res 84:43-52. 1999.... - Recent advances in cardiac beta(2)-adrenergic signal transductionR P Xiao
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, MD 21224, USA
Circ Res 85:1092-100. 1999.... - beta2-adrenergic cAMP signaling is uncoupled from phosphorylation of cytoplasmic proteins in canine heartM Kuschel
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, MD, USA
Circulation 99:2458-65. 1999.... - Dual modulation of cell survival and cell death by beta(2)-adrenergic signaling in adult mouse cardiac myocytesW Z Zhu
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
Proc Natl Acad Sci U S A 98:1607-12. 2001..The survival effect appears to predominate and is mediated by the G(i)-G(beta gamma)-PI3K-Akt signaling pathway... - G(i)-dependent localization of beta(2)-adrenergic receptor signaling to L-type Ca(2+) channelsY Chen-Izu
Laboratory of Cardiovascular Sciences, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224 6823, USA
Biophys J 79:2547-56. 2000..Our results suggest that the dual coupling of beta(2)-AR to both G(s)- and G(i)-proteins leads to a highly localized beta(2)-AR signaling pathway to modulate sarcolemmal L-type Ca(2+) channels in rat ventricular myocytes... - beta-Adrenergic stimulation synchronizes intracellular Ca(2+) release during excitation-contraction coupling in cardiac myocytesL S Song
Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA
Circ Res 88:794-801. 2001.... - {Beta}2-adrenergic receptor agonists inhibit the proliferation of 1321N1 astrocytoma cellsL Toll
SRI International, Menlo Park, California, USA
J Pharmacol Exp Ther 336:524-32. 2011..Because a significant portion of brain tumors contain β(2)-ARs to a greater extent than whole brain, (R,R')-fenoterol, or some analog, may be useful in the treatment of brain tumors after biopsy to determine β(2)-AR expression... - Phosphatidylinositol 3-kinase offsets cAMP-mediated positive inotropic effect via inhibiting Ca2+ influx in cardiomyocytesVeronique Leblais
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, MD 21224, USA
Circ Res 95:1183-90. 2004.... - Heterodimerization of beta1- and beta2-adrenergic receptor subtypes optimizes beta-adrenergic modulation of cardiac contractilityWei Zhong Zhu
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA
Circ Res 97:244-51. 2005.... - The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathyP Liao
Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
Proc Natl Acad Sci U S A 98:12283-8. 2001.... - Linkage of beta1-adrenergic stimulation to apoptotic heart cell death through protein kinase A-independent activation of Ca2+/calmodulin kinase IIWei Zhong Zhu
Laboratory of Cardiovascular Science, National Institute on Aging, NIH, Baltimore, Maryland 21224, USA
J Clin Invest 111:617-25. 2003..These findings indicate that CaMKII constitutes a novel PKA-independent linkage of beta(1)AR stimulation to cardiomyocyte apoptosis that has been implicated in the overall process of chronic heart failure... - The third intracellular loop and the carboxyl terminus of beta2-adrenergic receptor confer spontaneous activity of the receptorKhalid Chakir
Laboratory of Cardiovascular Science, Gerontology Research Center, NIA, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA
Mol Pharmacol 64:1048-58. 2003.... - Sustained beta1-adrenergic stimulation modulates cardiac contractility by Ca2+/calmodulin kinase signaling pathwayWang Wang
Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
Circ Res 95:798-806. 2004..This finding may bear important etiological and therapeutical ramifications in understanding beta1AR signaling in chronic heart failure... - Acidosis-induced p38 MAPK activation and its implication in regulation of cardiac contractilityMing Zheng
The Institute of Cardiovascular Sciences, Peking University, Beijing 100083, China
Acta Pharmacol Sin 25:1299-305. 2004..To determine the possible role of pH in mediating activation of p38 mitogen-activated protein kinase (MAPK) and the consequent function of activated p38 MAPK in regulating cardiac contractility... - Ca2+/calmodulin kinase II-dependent phosphorylation of ryanodine receptors suppresses Ca2+ sparks and Ca2+ waves in cardiac myocytesDongmei Yang
Laboratory of Cardiovascular Science, National Institute on Aging, NIH, Baltimore, MD 21224, USA
Circ Res 100:399-407. 2007.... - High basal protein kinase A-dependent phosphorylation drives rhythmic internal Ca2+ store oscillations and spontaneous beating of cardiac pacemaker cellsTatiana M Vinogradova
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, MD 21224-6825, USA
Circ Res 98:505-14. 2006.... - Enantioselective separation and online affinity chromatographic characterization of R,R- and S,S-fenoterolFarideh Beigi
Laboratory of Clinical Investigation, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA
Chirality 18:822-7. 2006..Further evaluation of R-F will determine if it has enhanced selectivity and specificity for beta2-AR/G(s) activation and if it can be used in the treatment of congestive heart failure... - Calmodulin regulation of excitation-contraction coupling in cardiac myocytesDongmei Yang
National Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing, China
Circ Res 92:659-67. 2003..A novel finding of this study is that expression of a Ca2+-insensitive CaM mutant can lead to activation of CaMKII in cardiac myocytes... - p38 Mitogen-activated protein kinase mediates a negative inotropic effect in cardiac myocytesPu Liao
Department of Physiology, School of Medicine, University of Maryland, Baltimore, MD 21224, USA
Circ Res 90:190-6. 2002..These findings reveal a novel function of p38 MAPK and shed a new light on our understanding of the coincidence of p38 MAPK activation and the onset of heart failure... - Dual site phospholamban phosphorylation and its physiological relevance in the heartDirk Hagemann
National Institute on Aging, NIH, Gerontology Research Center, Laboratory of Cardiovascular Science, Baltimore, MD 21224, USA
Trends Cardiovasc Med 12:51-6. 2002..Further studies are required to determine the exact process of dual site PLB phosphorylation and its functional roles in healthy and diseased hearts... - Phosphatidylinositol 3-kinase functionally compartmentalizes the concurrent G(s) signaling during beta2-adrenergic stimulationSu-Hyun Jo
Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, National Institute of Health, Baltimore, MD 21224, USA
Circ Res 91:46-53. 2002..Thus, PI3K constitutes a key downstream event of beta2-AR-G(i) signaling, which confines and negates the concurrent beta2-AR/G(s)-mediated PKA signaling... - Mitofusin-2 is a major determinant of oxidative stress-mediated heart muscle cell apoptosisTao Shen
Institute of Cardiovascular Sciences, Peking University, Beijing 100083, China
J Biol Chem 282:23354-61. 2007.... - Activation of CaMKIIdeltaC is a common intermediate of diverse death stimuli-induced heart muscle cell apoptosisWeizhong Zhu
Laboratory of Cardiovascular Science, Gerontology Research Center, NIA, National Institutes of Health, Baltimore, Maryland 21224
J Biol Chem 282:10833-9. 2007..Thus, activation of CaMKII(deltaC) constitutes a common intermediate by which various death-inducing stimuli trigger cardiomyocyte apoptosis via the primary mitochondrial death pathway... - Ca(2+) signaling in cardiac myocytes overexpressing the alpha(1) subunit of L-type Ca(2+) channelLong Sheng Song
Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
Circ Res 90:174-81. 2002..These results also suggest that a modest but sustained increase in Ca(2+) influx triggers a coordinated remodeling of Ca(2+) handling to maintain Ca(2+) homeostasis... - MCC-134, a single pharmacophore, opens surface ATP-sensitive potassium channels, blocks mitochondrial ATP-sensitive potassium channels, and suppresses preconditioningNorihito Sasaki
Laboratory of the Institute of Molecular Cardiobiology, Johns Hopkins University, Baltimore, MD 21205, USA
Circulation 107:1183-8. 2003.... - Dysregulation of HSG triggers vascular proliferative disordersKuang Hueih Chen
The Institute of Cardiovascular Science and The Institute of Molecular Medicine, Peking University, Beijing 100083, China
Nat Cell Biol 6:872-83. 2004..Thus, rHSG functions as a cell proliferation suppressor, whereas dysregulation of rHSG results in proliferative disorders... - G-protein-coupled receptor chromatographic stationary phases. 2. Ligand-induced conformational mobility in an immobilized beta2-adrenergic receptorFarideh Beigi
Laboratory of Clinical Investigation and Laboratory of Cardiovascular Science, NIA, NIH, Baltimore, Maryland 21224 6825, USA
Anal Chem 76:7187-93. 2004..The data from this study suggest that the immobilized beta(2)-AR can be used to screen for ligand binding interactions in both the resting and active states of the receptor... - Comparative molecular field analysis of the binding of the stereoisomers of fenoterol and fenoterol derivatives to the beta2 adrenergic receptorKrzysztof Jozwiak
Department of Chemistry, Medical University of Lublin, Lublin, Poland
J Med Chem 50:2903-15. 2007.... - Dilated cardiomyopathy caused by tissue-specific ablation of SC35 in the heartJian Hua Ding
Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093 0651, USA
EMBO J 23:885-96. 2004..These studies raise a new paradigm for the etiology of certain human heart diseases of genetic or environmental origin that may be triggered by dysfunction in RNA processing... - Phosphoproteome analysis of cardiomyocytes subjected to beta-adrenergic stimulation: identification and characterization of a cardiac heat shock protein p20Guoxiang Chu
Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0575, USA
Circ Res 94:184-93. 2004..These findings suggest that cardiomyocytes undergo significant posttranslational modification via phosphorylation in a multitude of proteins to dynamically fine-tune cardiac responses to beta-adrenergic signaling... - Emerging concepts and therapeutic implications of beta-adrenergic receptor subtype signalingMing Zheng
Institute of Cardiovascular Sciences, Peking University, Beijing 100083, People's Republic of China
Pharmacol Ther 108:257-68. 2005.... - Nuclear Ca2+ sparks and waves mediated by inositol 1,4,5-trisphosphate receptors in neonatal rat cardiomyocytesDali Luo
Department of Pharmacology, School of Chemical Biology and Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China
Cell Calcium 43:165-74. 2008.... - Intracellular acidosis-activated p38 MAPK signaling and its essential role in cardiomyocyte hypoxic injuryMing Zheng
Institute of Cardiovascular Sciences, Peking University, Beijing, People's Republic of China
FASEB J 19:109-11. 2005..These results demonstrate, for the first time, that intracellular acidosis constitutes a necessary and sufficient link responsible for hypoxia-activated p38 MAPK signaling and the subsequent hypoxic cardiomyocyte injury and death... - Calmodulin kinase II inhibition protects against myocardial cell apoptosis in vivoYingbo Yang
Dept of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
Am J Physiol Heart Circ Physiol 291:H3065-75. 2006..These findings indicate CaMKII is proapoptotic in vivo and suggest that regulation of SR Ca(2+) content by PLN contributes to the antiapoptotic mechanism of CaMKII inhibition... - Role of inositol 1,4,5-trisphosphate receptors in alpha1-adrenergic receptor-induced cardiomyocyte hypertrophyDa li Luo
Department of Pharmacology, School of Chemical Biology and Pharmaceutical Sciences, Capital University of Medical Sciences, Beijing 100069, China
Acta Pharmacol Sin 27:895-900. 2006..Thus, we hypothesized that Ca2+ release through IP3Rs was necessary for alpha1AR-stimulated cardiac hypertrophy... - Cross-talk of opioid peptide receptor and beta-adrenergic receptor signalling in the heartSalvatore Pepe
Laboratory of Cardiac Surgical Research, Wynn Domain, Baker Heart Research Institute and The Alfred Hospital, Monash University Faculty of Medicine, Melbourne, Australia
Cardiovasc Res 63:414-22. 2004..This brief review will focus on the interaction between beta-AR and OPR and its potential physiological and pathophysiological relevance in the heart... - ASF/SF2-regulated CaMKIIdelta alternative splicing temporally reprograms excitation-contraction coupling in cardiac muscleXiangdong Xu
Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
Cell 120:59-72. 2005..Our results validate ASF/SF2 as a fundamental splicing regulator in the reprogramming pathway and reveal the central contribution of ASF/SF2-regulated CaMKIIdelta alternative splicing to functional remodeling in developing heart... - Distinct beta-adrenergic receptor subtype signaling in the heart and their pathophysiological relevanceMing Zheng
The Institute of Molecular Medicine, Peking University, Beijing 100083 China
Sheng Li Xue Bao 56:1-15. 2004....