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Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease.

JACC. Basic to translational science

Grisanti LA, Schumacher SM, Tilley DG, Koch WJ.
PMID: 30175279
JACC Basic Transl Sci. 2018 Aug 28;3(4):550-562. doi: 10.1016/j.jacbts.2017.12.002. eCollection 2018 Aug.

The new horizon for cardiac therapy may lie beneath the surface, with the downstream mediators of G protein-coupled receptor (GPCR) activity. Targeted approaches have shown that receptor activation may be biased toward signaling through G proteins or through GPCR...

Cite
Grisanti LA, Schumacher SM, Tilley DG, et al. Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease. JACC Basic Transl Sci. 2018;3(4):550-562doi: 10.1016/j.jacbts.2017.12.002.
Grisanti, L. A., Schumacher, S. M., Tilley, D. G., & Koch, W. J. (2018). Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease. JACC. Basic to translational science, 3(4), 550-562. https://doi.org/10.1016/j.jacbts.2017.12.002
Grisanti, Laurel A, et al. "Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease." JACC. Basic to translational science vol. 3,4 (2018): 550-562. doi: https://doi.org/10.1016/j.jacbts.2017.12.002
Grisanti LA, Schumacher SM, Tilley DG, Koch WJ. Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease. JACC Basic Transl Sci. 2018 Aug 28;3(4):550-562. doi: 10.1016/j.jacbts.2017.12.002. eCollection 2018 Aug. PMID: 30175279; PMCID: PMC6115700.
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A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure.

Science signaling

Coleman RC, Eguchi A, Lieu M, Roy R, Barr EW, Ibetti J, Lucchese AM, Peluzzo AM, Gresham K, Chuprun JK, Koch WJ.
PMID: 33785612
Sci Signal. 2021 Mar 30;14(676). doi: 10.1126/scisignal.abb5968.

Aberrant changes in gene expression underlie the pathogenesis and progression of pressure-overload heart failure, leading to maladaptive cardiac hypertrophy, ventricular remodeling, and contractile dysfunction. Signaling through the G protein G

Cite
Coleman RC, Eguchi A, Lieu M, et al. A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure. Sci Signal. 2021;14(676)doi: 10.1126/scisignal.abb5968.
Coleman, R. C., Eguchi, A., Lieu, M., Roy, R., Barr, E. W., Ibetti, J., Lucchese, A. M., Peluzzo, A. M., Gresham, K., Chuprun, J. K., & Koch, W. J. (2021). A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure. Science signaling, 14(676), . https://doi.org/10.1126/scisignal.abb5968
Coleman, Ryan C, et al. "A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure." Science signaling vol. 14,676 (2021). doi: https://doi.org/10.1126/scisignal.abb5968
Coleman RC, Eguchi A, Lieu M, Roy R, Barr EW, Ibetti J, Lucchese AM, Peluzzo AM, Gresham K, Chuprun JK, Koch WJ. A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure. Sci Signal. 2021 Mar 30;14(676). doi: 10.1126/scisignal.abb5968. PMID: 33785612; PMCID: PMC8092419.
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G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure.

Drug discovery today. Therapeutic strategies

Schumacher-Bass SM, Traynham CJ, Koch WJ.
PMID: 24839449
Drug Discov Today Ther Strateg. 2012;9(4):e155-e162. doi: 10.1016/j.ddstr.2014.01.002.

An ever-increasing number of people world-wide are developing and suffering from heart failure, and existing therapies, although improved are not ideal. Therefore, innovative treatment strategies are urgently needed. As our understanding of the underlying dysfunction of the myocardium increases,...

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Schumacher-Bass SM, Traynham CJ, Koch WJ. G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure. Drug Discov Today Ther Strateg. 2012;9(4):e155-e162doi: 10.1016/j.ddstr.2014.01.002.
Schumacher-Bass, S. M., Traynham, C. J., & Koch, W. J. (2012). G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure. Drug discovery today. Therapeutic strategies, 9(4), e155-e162. https://doi.org/10.1016/j.ddstr.2014.01.002
Schumacher-Bass, Sarah M, et al. "G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure." Drug discovery today. Therapeutic strategies vol. 9,4 (2012): e155-e162. doi: https://doi.org/10.1016/j.ddstr.2014.01.002
Schumacher-Bass SM, Traynham CJ, Koch WJ. G protein-coupled Receptor Kinase 2 as a Therapeutic Target for Heart Failure. Drug Discov Today Ther Strateg. 2012;9(4):e155-e162. doi: 10.1016/j.ddstr.2014.01.002. PMID: 24839449; PMCID: PMC4019414.
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[No title available]

Molecular pharmacology

Wang J, Pani B, Gokhan I, Xiong X, Kahsai AW, Jiang H, Ahn S, Lefkowitz RJ, Rockman HA.
PMID: 34561298
Mol Pharmacol. 2021 Dec;100(6):568-579. doi: 10.1124/molpharm.121.000359. Epub 2021 Sep 24.

No abstract available.

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Wang J, Pani B, Gokhan I, et al. . Mol Pharmacol. 2021;100(6):568-579doi: 10.1124/molpharm.121.000359.
Wang, J., Pani, B., Gokhan, I., Xiong, X., Kahsai, A. W., Jiang, H., Ahn, S., Lefkowitz, R. J., & Rockman, H. A. (2021). . Molecular pharmacology, 100(6), 568-579. https://doi.org/10.1124/molpharm.121.000359
Wang, Jialu, et al. "." Molecular pharmacology vol. 100,6 (2021): 568-579. doi: https://doi.org/10.1124/molpharm.121.000359
Wang J, Pani B, Gokhan I, Xiong X, Kahsai AW, Jiang H, Ahn S, Lefkowitz RJ, Rockman HA. . Mol Pharmacol. 2021 Dec;100(6):568-579. doi: 10.1124/molpharm.121.000359. Epub 2021 Sep 24. PMID: 34561298; PMCID: PMC8626783.
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[No title available]

Molecular pharmacology

Wang J, Pani B, Gokhan I, Xiong X, Kahsai AW, Jiang H, Ahn S, Lefkowitz RJ, Rockman HA.
PMID: 34561298
Mol Pharmacol. 2021 Dec;100(6):568-579. doi: 10.1124/molpharm.121.000359. Epub 2021 Sep 24.

No abstract available.

Cite
Wang J, Pani B, Gokhan I, et al. . Mol Pharmacol. 2021;100(6):568-579doi: 10.1124/molpharm.121.000359.
Wang, J., Pani, B., Gokhan, I., Xiong, X., Kahsai, A. W., Jiang, H., Ahn, S., Lefkowitz, R. J., & Rockman, H. A. (2021). . Molecular pharmacology, 100(6), 568-579. https://doi.org/10.1124/molpharm.121.000359
Wang, Jialu, et al. "." Molecular pharmacology vol. 100,6 (2021): 568-579. doi: https://doi.org/10.1124/molpharm.121.000359
Wang J, Pani B, Gokhan I, Xiong X, Kahsai AW, Jiang H, Ahn S, Lefkowitz RJ, Rockman HA. . Mol Pharmacol. 2021 Dec;100(6):568-579. doi: 10.1124/molpharm.121.000359. Epub 2021 Sep 24. PMID: 34561298; PMCID: PMC8626783.
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Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure.

Drug discovery today. Disease mechanisms

Brinks H, Koch WJ.
PMID: 21218155
Drug Discov Today Dis Mech. 2010;7(2):e129-e134. doi: 10.1016/j.ddmec.2010.07.007.

In the human body, over 1000 different G protein-coupled receptors (GPCRs) mediate a broad spectrum of extracellular signals at the plasma membrane, transmitting vital physiological features such as pain, sight, smell, inflammation, heart rate and contractility of muscle cells....

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Brinks H, Koch WJ. Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure. Drug Discov Today Dis Mech. 2010;7(2):e129-e134doi: 10.1016/j.ddmec.2010.07.007.
Brinks, H., & Koch, W. J. (2010). Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure. Drug discovery today. Disease mechanisms, 7(2), e129-e134. https://doi.org/10.1016/j.ddmec.2010.07.007
Brinks, Henriette, and Koch, Walter J. "Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure." Drug discovery today. Disease mechanisms vol. 7,2 (2010): e129-e134. doi: https://doi.org/10.1016/j.ddmec.2010.07.007
Brinks H, Koch WJ. Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure. Drug Discov Today Dis Mech. 2010;7(2):e129-e134. doi: 10.1016/j.ddmec.2010.07.007. PMID: 21218155; PMCID: PMC3014615.
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Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure.

Drug discovery today. Disease mechanisms

Brinks H, Koch WJ.
PMID: 21218155
Drug Discov Today Dis Mech. 2010;7(2):e129-e134. doi: 10.1016/j.ddmec.2010.07.007.

In the human body, over 1000 different G protein-coupled receptors (GPCRs) mediate a broad spectrum of extracellular signals at the plasma membrane, transmitting vital physiological features such as pain, sight, smell, inflammation, heart rate and contractility of muscle cells....

Cite
Brinks H, Koch WJ. Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure. Drug Discov Today Dis Mech. 2010;7(2):e129-e134doi: 10.1016/j.ddmec.2010.07.007.
Brinks, H., & Koch, W. J. (2010). Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure. Drug discovery today. Disease mechanisms, 7(2), e129-e134. https://doi.org/10.1016/j.ddmec.2010.07.007
Brinks, Henriette, and Koch, Walter J. "Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure." Drug discovery today. Disease mechanisms vol. 7,2 (2010): e129-e134. doi: https://doi.org/10.1016/j.ddmec.2010.07.007
Brinks H, Koch WJ. Targeting G protein-coupled receptor kinases (GRKs) in Heart Failure. Drug Discov Today Dis Mech. 2010;7(2):e129-e134. doi: 10.1016/j.ddmec.2010.07.007. PMID: 21218155; PMCID: PMC3014615.
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GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation.

The journal of cardiovascular aging

Grimmett ZW, Venetos NM, Premont RT, Stamler JS.
PMID: 34790976
J Cardiovasc Aging. 2021;1. doi: 10.20517/jca.2021.25. Epub 2021 Oct 13.

S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme responsible for reverting protein S-nitrosylation (SNO). In this issue, Salerno

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Grimmett ZW, Venetos NM, Premont RT, et al. GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation. J Cardiovasc Aging. 2021;1doi: 10.20517/jca.2021.25.
Grimmett, Z. W., Venetos, N. M., Premont, R. T., & Stamler, J. S. (2021). GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation. The journal of cardiovascular aging, 1. https://doi.org/10.20517/jca.2021.25
Grimmett, Zachary W, et al. "GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation." The journal of cardiovascular aging vol. 1 (2021). doi: https://doi.org/10.20517/jca.2021.25
Grimmett ZW, Venetos NM, Premont RT, Stamler JS. GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation. J Cardiovasc Aging. 2021;1. doi: 10.20517/jca.2021.25. Epub 2021 Oct 13. PMID: 34790976; PMCID: PMC8594876.
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Propranolol inhibits cavernous vascular malformations by β1 adrenergic receptor antagonism in animal models.

The Journal of clinical investigation

Li W, Shenkar R, Detter MR, Moore T, Benavides C, Lightle R, Girard R, Hobson N, Cao Y, Li Y, Griffin E, Gallione C, Zabramski JM, Ginsberg MH, Marchuk DA, Awad IA.
PMID: 34596055
J Clin Invest. 2021 Oct 01;131(19). doi: 10.1172/JCI154909.

No abstract available.

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Li W, Shenkar R, Detter MR, et al. Propranolol inhibits cavernous vascular malformations by β1 adrenergic receptor antagonism in animal models. J Clin Invest. 2021;131(19)doi: 10.1172/JCI154909.
Li, W., Shenkar, R., Detter, M. R., Moore, T., Benavides, C., Lightle, R., Girard, R., Hobson, N., Cao, Y., Li, Y., Griffin, E., Gallione, C., Zabramski, J. M., Ginsberg, M. H., Marchuk, D. A., & Awad, I. A. (2021). Propranolol inhibits cavernous vascular malformations by β1 adrenergic receptor antagonism in animal models. The Journal of clinical investigation, 131(19), . https://doi.org/10.1172/JCI154909
Li, Wenqing, et al. "Propranolol inhibits cavernous vascular malformations by β1 adrenergic receptor antagonism in animal models." The Journal of clinical investigation vol. 131,19 (2021). doi: https://doi.org/10.1172/JCI154909
Li W, Shenkar R, Detter MR, Moore T, Benavides C, Lightle R, Girard R, Hobson N, Cao Y, Li Y, Griffin E, Gallione C, Zabramski JM, Ginsberg MH, Marchuk DA, Awad IA. Propranolol inhibits cavernous vascular malformations by β1 adrenergic receptor antagonism in animal models. J Clin Invest. 2021 Oct 01;131(19). doi: 10.1172/JCI154909. PMID: 34596055; PMCID: PMC8483741.
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A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure.

Science signaling

Coleman RC, Eguchi A, Lieu M, Roy R, Barr EW, Ibetti J, Lucchese AM, Peluzzo AM, Gresham K, Chuprun JK, Koch WJ.
PMID: 33785612
Sci Signal. 2021 Mar 30;14(676). doi: 10.1126/scisignal.abb5968.

Aberrant changes in gene expression underlie the pathogenesis and progression of pressure-overload heart failure, leading to maladaptive cardiac hypertrophy, ventricular remodeling, and contractile dysfunction. Signaling through the G protein G

Cite
Coleman RC, Eguchi A, Lieu M, et al. A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure. Sci Signal. 2021;14(676)doi: 10.1126/scisignal.abb5968.
Coleman, R. C., Eguchi, A., Lieu, M., Roy, R., Barr, E. W., Ibetti, J., Lucchese, A. M., Peluzzo, A. M., Gresham, K., Chuprun, J. K., & Koch, W. J. (2021). A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure. Science signaling, 14(676), . https://doi.org/10.1126/scisignal.abb5968
Coleman, Ryan C, et al. "A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure." Science signaling vol. 14,676 (2021). doi: https://doi.org/10.1126/scisignal.abb5968
Coleman RC, Eguchi A, Lieu M, Roy R, Barr EW, Ibetti J, Lucchese AM, Peluzzo AM, Gresham K, Chuprun JK, Koch WJ. A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure. Sci Signal. 2021 Mar 30;14(676). doi: 10.1126/scisignal.abb5968. PMID: 33785612; PMCID: PMC8092419.
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Showing 1 to 10 of 10 entries