Main.Research History

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#Woo L, Tkachenko S, Ding M, Plowright AT, Engkvist O, Andersson H, Drowley L, Barrett I, Firth M, Wolf MJ, Bekiranov S, Brautigan DL, Wang QD, *Saucerman JJ. High-content phenotypic screen for compounds that induce proliferation of human iPSC-derived cardiomyocytes. Circulation 2016;134:A18674. AHA Scientific Sessions Abstract [[http://circ.ahajournals.org/content/134/Suppl_1/A18674 | link]].
to:
#Woo L, Tkachenko S, Ding M, Plowright AT, Engkvist O, Andersson H, Drowley L, Barrett I, Firth M, Wolf MJ, Bekiranov S, Brautigan DL, Wang QD, *Saucerman JJ. High-content phenotypic screen for compounds that induce proliferation of human iPSC-derived cardiomyocytes. Circulation 2016;134:A18674. AHA Scientific Sessions Abstract [[http://circ.ahajournals.org/content/134/Suppl_1/A18674 | (link)]].
Changed line 3 from:
#Woo L, Tkachenko S, Ding M, Plowright AT, Engkvist O, Andersson H, Drowley L, Barrett I, Firth M, Wolf MJ, Bekiranov S, Brautigan DL, Wang QD, *Saucerman JJ. High-content phenotypic screen for compounds that induce proliferation of human iPSC-derived cardiomyocytes. Circulation 2016;134:A18674. AHA Scientific Sessions Abstract.
to:
#Woo L, Tkachenko S, Ding M, Plowright AT, Engkvist O, Andersson H, Drowley L, Barrett I, Firth M, Wolf MJ, Bekiranov S, Brautigan DL, Wang QD, *Saucerman JJ. High-content phenotypic screen for compounds that induce proliferation of human iPSC-derived cardiomyocytes. Circulation 2016;134:A18674. AHA Scientific Sessions Abstract [[http://circ.ahajournals.org/content/134/Suppl_1/A18674 | link]].
Changed lines 39-42 from:
#''Yang JH'', Saucerman JJ. Phospholemman is a negative feed-forward regulator of Ca2+ in β-adrenergic signaling, accelerating β-adrenergic inotropy. J Mol Cell Cardiol. 2012; 52(5):1048-55. PMCID: 3327824. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22289214 | Pubmed]]]

#Amanfu, RK, Muller, J, Saucerman JJ. Automated image analysis of cardiac myocyte Ca2+ dynamics. Conf Proc IEEE Eng Med Biol Soc 2011. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22255377 | Pubmed]]]
to:
#Amanfu RK, Saucerman JJ. Modeling the effects of beta1-adrenergic receptor blockers and polymorphisms on cardiac myocyte Ca2+ handling. Mol Pharmacol 2014 May 27. pii: mol.113.090951.
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#'^1^'Sample V, '^1^'DiPilato LM, '^1^'Yang JH, Ni Q, Saucerman JJ, Zhang J. Regulation of nuclear PKA revealed by spatiotemporal manipulation of cAMP. Nature Chemical Biology. ''in press''. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22366721 | Pubmed]]]

#Greenwald EC, Saucerman JJ. Bigger, Better, Faster: Principles and Models of AKAP Anchoring Protein Signaling. J Cardiovasc Pharmacol. 2011 Nov
;58(5):462-9. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/21562426 | Pubmed]]]\\\
to:
#Saucerman JJ, Greenwald EC, Polanowska-Grabowska R. Mechanisms of cyclic AMP compartmentation revealed by computational models. J Gen Physiol. 2014 Jan;143(1):39-48. PMCID: 3874575.

#Yang JH, Polanowska-Grabowska RK, Smith JS, Shields CW, Saucerman JJ
. PKA catalytic subunit compartmentation regulates contractile and hypertrophic responses to β-adrenergic stimulation. J Mol Cell Cardiol, 2013 Nov 10;66C:83-93.[Epub ahead of print]. PMCID: 3927644.
Deleted lines 54-62:
'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca'^2+^' signals also activate their own pathways such as Ca'^2+^'-calmodulin-dependent protein kinase (CaMKII), which can synergize with the β-adrenergic pathway to modulate short and long-term heart function.
\\\

#Soltis AR, Saucerman JJ. "Synergy between CaMKII substrates and β-adrenergic signaling in regulation of cardiac myocyte Ca(2+) handling." Biophys J. 2010;99(7):2038-47. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/20923637 | Pubmed]]]. '''Selected as a “Must Read” 8/10 by [=[=][[http://f1000.com/5952956 | Faculty of 1000]]].'''

#Saucerman JJ, Bers DM. "Calmodulin mediates differential sensitivity of CaMKII and calcineurin to local Ca2+ in cardiac myocytes." Biophys J. 2008 Nov 15;95(10):4597-612. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/18689454 | Pubmed]]]\\\

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National Institutes of Health, National Science Foundation, American Heart Association, Coulter Foundation, University of Virginia
to:
National Institutes of Health, National Science Foundation, American Heart Association, AstraZeneca, Coulter Foundation, University of Virginia
Changed lines 23-26 from:
#Ryall KA, *Saucerman JJ. Automated imaging reveals a concentration-dependent delay in reversibility of cardiac myocyte hypertrophy. J Mol Cell Cardiol, 2012 53(2):282-90. PMCID: 3389167. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22575844 | Pubmed]]]

#Bass GT
, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. 2012; 52(5):923-30. PMCID: 3299901. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]
\\\
to:
#Ryall KA, *Saucerman JJ. Automated Microscopy of Cardiac Myocyte Hypertrophy: A Case Study on the Role of Intracellular α-Adrenergic Receptors. Methods Mol Biol. 2015; 1234:123-34.

#Ryall, K
. A., V. J. Bezzerides, A. Rosenzwieg, Saucerman JJ. Phenotypic screen quantifying differential regulation of cardiac myocyte hypertrophy identifies CITED4 regulation of myocyte elongation. J Mol Cell Cardiol 2014 [Epub ahead of print], 10.1016/j.yjmcc.2014.02.013.
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'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
\\\

#Ryall KA, *Saucerman JJ. Automated imaging reveals a concentration-dependent delay in reversibility of cardiac myocyte hypertrophy. J Mol Cell Cardiol, 2012 53(2):282-90. PMCID: 3389167. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22575844 | Pubmed]]]

#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. 2012; 52(5):923-30. PMCID: 3299901. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]
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#Woo L, Tkachenko S, Ding M, Plowright AT, Engkvist O, Andersson H, Drowley L, Barrett I, Firth M, Wolf MJ, Bekiranov S, Brautigan DL, Wang QD, *Saucerman JJ. High-content phenotypic screen for compounds that induce proliferation of human iPSC-derived cardiomyocytes. Circulation 2016;134:A18674. AHA Scientific Sessions Abstract.
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#*Lindsey ML, Saucerman JJ, DeLeon-Pennell K. Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction. Biochim Biophys Acta. 2016 May 27. pii: S0925-4439(16)30129-6. doi: 10.1016/j.bbadis.2016.05.013. [Epub ahead of print]

#Zeigler AC, Richardson WJ, Holmes JW, *Saucerman JJ. A computational model of cardiac fibroblast signaling predicts context-dependent drivers of myofibroblast differentiation. J Mol Cell Cardiol. 2016 May;94:72-81.

#Zeigler, AC, Richardson WJ, Holmes JW, *Saucerman JJ. Computational modeling of cardiac fibroblasts and fibrosis. J Mol Cell Cardiol. 2016 Apr;93:73-83.\\\
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'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
\\\

#Ryall KA, *Saucerman JJ. Automated imaging reveals a concentration-dependent delay in reversibility of cardiac myocyte hypertrophy. J Mol Cell Cardiol, 2012 53(2):282-90. PMCID: 3389167. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22575844 | Pubmed]]]

#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. 2012; 52(5):923-30. PMCID: 3299901. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]
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June 09, 2016, at 09:55 AM EST by 184.5.136.108 -
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%center%

http://bme.virginia.edu/saucerman/images/bARsignaling300.jpg
June 09, 2016, at 09:52 AM EST by 184.5.136.108 -
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'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca'^2+^' dynamics.
to:
'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
Changed lines 6-9 from:
#''Yang JH'', Saucerman JJ. Phospholemman is a negative feed-forward regulator of Ca2+ in β-adrenergic signaling, accelerating β-adrenergic inotropy. J Mol Cell Cardiol. 2012; 52(5):1048-55. PMCID: 3327824. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22289214 | Pubmed]]]

#Amanfu, RK, Muller, J, Saucerman JJ. Automated image analysis of cardiac myocyte Ca2+ dynamics. Conf Proc IEEE Eng Med Biol Soc 2011. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22255377 | Pubmed]]]
to:
#Ryall KA, *Saucerman JJ. Automated imaging reveals a concentration-dependent delay in reversibility of cardiac myocyte hypertrophy. J Mol Cell Cardiol, 2012 53(2):282-90. PMCID: 3389167. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22575844 | Pubmed]]]

#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. 2012; 52(5):923-30. PMCID: 3299901. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]
Changed lines 13-19 from:
'''cAMP/PKA compartmentation.''' cAMP and PKA are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure.
\\\

#'^1^'Sample V, '^1^'DiPilato LM, '^1^'Yang JH, Ni Q, Saucerman JJ, Zhang J. Regulation of nuclear PKA revealed by spatiotemporal manipulation of cAMP. Nature Chemical Biology. ''in press''. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22366721 | Pubmed]]]

#Greenwald EC, Saucerman JJ. Bigger, Better, Faster: Principles and Models of AKAP Anchoring Protein Signaling. J Cardiovasc Pharmacol. 2011 Nov;58(5):462-9. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/21562426 | Pubmed]]]
\\\
to:
'''Cardiac Regeneration.''' While cardiac regeneration was once thought to be limited to organisms such newts and zebrafish, recent studies have demonstrated that mammals also have some regenerative capacity. We are combining genomic and high-throughput microscopy experiments with computational models to map the molecular networks and identify compounds that stimulate cardiac myocyte proliferation.\\\
Changed lines 18-22 from:
'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
to:
'''Cardiac inflammation and extracellular matrix remodeling.''' Cardiac macrophages and fibroblasts play important roles in inflammation and wound healing following cardiac injury. Yet systems and therapeutic approaches targeting these cells have been limited. We are collaborating with investigators at UVA and externally to reconstruct the molecular networks in fibroblasts and macrophages in the context of myocardial infarction.\\\

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'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca'^2+^' dynamics
.
Changed lines 25-27 from:
#Ryall KA, *Saucerman JJ. Automated imaging reveals a concentration-dependent delay in reversibility of cardiac myocyte hypertrophy. J Mol Cell Cardiol, 2012 53(2):282-90. PMCID: 3389167. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22575844 | Pubmed]]]

#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. 2012; 52(5):923-30. PMCID: 3299901. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]
to:
#''Yang JH'', Saucerman JJ. Phospholemman is a negative feed-forward regulator of Ca2+ in β-adrenergic signaling, accelerating β-adrenergic inotropy. J Mol Cell Cardiol. 2012; 52(5):1048-55. PMCID: 3327824. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22289214 | Pubmed]]]

#Amanfu, RK, Muller, J, Saucerman JJ. Automated image analysis of cardiac myocyte Ca2+ dynamics. Conf Proc IEEE Eng Med Biol Soc 2011. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22255377 | Pubmed]]]
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'''cAMP/PKA compartmentation.''' cAMP and PKA are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure.
\\\

#'^1^'Sample V, '^1^'DiPilato LM, '^1^'Yang JH, Ni Q, Saucerman JJ, Zhang J. Regulation of nuclear PKA revealed by spatiotemporal manipulation of cAMP. Nature Chemical Biology. ''in press''. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22366721 | Pubmed]]]

#Greenwald EC, Saucerman JJ. Bigger, Better, Faster: Principles and Models of AKAP Anchoring Protein Signaling. J Cardiovasc Pharmacol. 2011 Nov;58(5):462-9. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/21562426 | Pubmed]]]\\\
October 02, 2012, at 09:17 AM EST by 128.143.234.226 -
Changed lines 6-8 from:
#Kraeutler MJ, Soltis AR, Saucerman JJ. "Modeling cardiac β-adrenergic signaling with normalized-Hill differential equations: comparison with a biochemical model." BMC Syst Biol. 2010;4:157. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/21087478 | Pubmed]]]

#Amanfu, RK, Muller, J, Saucerman JJ
. Automated image analysis of cardiac myocyte Ca2+ dynamics. Conf Proc IEEE Eng Med Biol Soc 2011: in press.
to:
#''Yang JH'', Saucerman JJ. Phospholemman is a negative feed-forward regulator of Ca2+ in β-adrenergic signaling, accelerating β-adrenergic inotropy. J Mol Cell Cardiol. 2012; 52(5):1048-55. PMCID: 3327824. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22289214 | Pubmed]]]

#Amanfu, RK, Muller, J, Saucerman JJ
. Automated image analysis of cardiac myocyte Ca2+ dynamics. Conf Proc IEEE Eng Med Biol Soc 2011. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22255377 | Pubmed]]]
Changed lines 26-29 from:
#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. Accepted. 2011. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]\\\
to:
#Ryall KA, *Saucerman JJ. Automated imaging reveals a concentration-dependent delay in reversibility of cardiac myocyte hypertrophy. J Mol Cell Cardiol, 2012 53(2):282-90. PMCID: 3389167. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22575844 | Pubmed]]]

#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. 2012; 52(5):923-30. PMCID: 3299901. [=[=
][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]
\\\
Changed lines 16-17 from:
#'^1^'Sample V, '^1^'DiPilato LM, '^1^'Yang JH, Ni Q, Saucerman JJ, Zhang J. Regulation of nuclear PKA revealed by spatiotemporal manipulation of cAMP. Nature Chemical Biology. Accepted 2011.
to:
#'^1^'Sample V, '^1^'DiPilato LM, '^1^'Yang JH, Ni Q, Saucerman JJ, Zhang J. Regulation of nuclear PKA revealed by spatiotemporal manipulation of cAMP. Nature Chemical Biology. ''in press''. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/22366721 | Pubmed]]]
Deleted line 39:
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'''cAMP/PKA compartmentation.''' cAMP and PKA are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure.
to:
#Kraeutler MJ, Soltis AR, Saucerman JJ. "Modeling cardiac β-adrenergic signaling with normalized-Hill differential equations: comparison with a biochemical model." BMC Syst Biol. 2010;4:157. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/21087478 | Pubmed]]]

#Amanfu, RK, Muller, J, Saucerman JJ. Automated image analysis
of cardiac myocyte Ca2+ dynamics. Conf Proc IEEE Eng Med Biol Soc 2011: in press.
Changed lines 10-13 from:
'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
to:
----\\\

'''cAMP/PKA compartmentation.''' cAMP and PKA are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure.
Changed lines 15-22 from:
'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca'^2+^' signals also activate their own pathways such as Ca'^2+^'-calmodulin-dependent protein kinase (CaMKII), which can synergize with the β-adrenergic pathway to modulate short and long-term heart function.
to:
#'^1^'Sample V, '^1^'DiPilato LM, '^1^'Yang JH, Ni Q, Saucerman JJ, Zhang J. Regulation of nuclear PKA revealed by spatiotemporal manipulation of cAMP. Nature Chemical Biology. Accepted 2011.

#Greenwald EC, Saucerman JJ. Bigger
, Better, Faster: Principles and Models of AKAP Anchoring Protein Signaling. J Cardiovasc Pharmacol. 2011 Nov;58(5):462-9. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/21562426 | Pubmed]]]\\\

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'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges
.
Added lines 24-37:

#Bass GT, Ryall KA, Katikapalli A, Taylor BE, Dang ST, Acton ST, Saucerman JJ. Automated image analysis identifies signaling pathways regulating distinct signatures of cardiac myocyte hypertrophy. J Mol Cell Cardiol. Accepted. 2011. [=[=][[http://dx.doi.org/10.1016/j.yjmcc.2011.11.009 | Link]]]\\\

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'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca'^2+^' signals also activate their own pathways such as Ca'^2+^'-calmodulin-dependent protein kinase (CaMKII), which can synergize with the β-adrenergic pathway to modulate short and long-term heart function.
\\\

#Soltis AR, Saucerman JJ. "Synergy between CaMKII substrates and β-adrenergic signaling in regulation of cardiac myocyte Ca(2+) handling." Biophys J. 2010;99(7):2038-47. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/20923637 | Pubmed]]]. '''Selected as a “Must Read” 8/10 by [=[=][[http://f1000.com/5952956 | Faculty of 1000]]].'''

#Saucerman JJ, Bers DM. "Calmodulin mediates differential sensitivity of CaMKII and calcineurin to local Ca2+ in cardiac myocytes." Biophys J. 2008 Nov 15;95(10):4597-612. [=[=][[http://www.ncbi.nlm.nih.gov/pubmed/18689454 | Pubmed]]]\\\

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Changed line 3 from:
'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca'^2+^' dynamics. ''Funding by American Heart Association.''
to:
'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca'^2+^' dynamics.
Changed line 5 from:
'''cAMP/PKA compartmentation.''' cAMP and PKA are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure. ''Funding by NIH.''
to:
'''cAMP/PKA compartmentation.''' cAMP and PKA are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure.
Changed line 7 from:
'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges. ''Funding by NSF and University of Virginia.''
to:
'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges.
Changed lines 9-12 from:
'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca'^2+^' signals also activate their own pathways such as Ca'^2+^'-calmodulin-dependent protein kinase (CaMKII), which can synergize with the β-adrenergic pathway to modulate short and long-term heart function. ''Funding by NIH and NSF.''
to:
'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca'^2+^' signals also activate their own pathways such as Ca'^2+^'-calmodulin-dependent protein kinase (CaMKII), which can synergize with the β-adrenergic pathway to modulate short and long-term heart function.
\\\
'''Funding:'''
National Institutes of Health, National Science Foundation, American Heart Association, Coulter Foundation, University of Virginia
Changed line 3 from:
'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca dynamics. ''Funding by American Heart Association.''
to:
'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca'^2+^' dynamics. ''Funding by American Heart Association.''
Changed line 9 from:
'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca signals also activate their own pathways such as CaMKII, which can synergize with the β-adrenergic pathway to modulate short and long-term heart function. ''Funding by NIH and NSF.''
to:
'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca'^2+^' signals also activate their own pathways such as Ca'^2+^'-calmodulin-dependent protein kinase (CaMKII), which can synergize with the β-adrenergic pathway to modulate short and long-term heart function. ''Funding by NIH and NSF.''
Changed lines 3-10 from:
Heart function and disease are controlled by complex molecular networks that are just beginning to be mapped out. Our lab develops mathematical models to understand how these molecular control systems work, and then we perform a variety of experiments to test this understanding. Experimental techniques include cell culture, live-cell imaging, and biochemical assays. These integrated approaches are helping us harness molecular networks to reverse the progression of heart disease.

Current projects include:
#Beta-adrenergic signaling and novel therapies in heart failure
#Live-cell imaging of cAMP compartmentation
#Multi-scale modeling
of signaling networks
#Calcium signaling pathways regulating heart contractility and growth
#Diagnosis of neonatal sepsis by its actions on the heart
to:
'''β-adrenergic signaling and beta blockers in heart failure.''' Do beta blockers work by suppressing or resensitizing the β-adrenergic pathway? Would patients with receptor polymorphisms benefit from personalized therapies? We are coupling integrated models of signaling and contractile function with video microscopy of Ca dynamics. ''Funding by American Heart Association.''
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'''cAMP/PKA compartmentation.''' cAMP and PKA
are central hubs transmitting signals from dozens of receptors to hundreds of effectors. We are studying how compartmentation (subcellular localization) of cAMP and PKA determines the input/output specificity of the network. Key methods are imaging genetically-encoded FRET biosensors and computational models with realistic cellular geometries. Dysregulated cAMP compartmentation is a key element of heart failure. ''Funding by NIH.''
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'''Cardiac hypertrophy.''' Dozens of pathways are implicated in cardiac myocyte growth, but little is known about the quantitative contribution of these pathways to myocyte shape, reversibility, sarcomeric organization, or many other factors affecting the progression of heart failure. We are combining high-throughput microscopy, automated image processing, and large-scale network modeling to address these challenges. ''Funding by NSF and University of Virginia.''
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'''Crosstalk between signaling networks and cardiac electrophysiology.''' Overstimulation of β-adrenergic signaling is a common trigger of cardiac arrhythmia. Electrical and Ca signals also activate their own pathways such as CaMKII, which can synergize with the β-adrenergic pathway to modulate short and long-term heart function. ''Funding by NIH and NSF.''
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#beta-adrenergic signaling and novel therapies in heart failure
to:
#Beta-adrenergic signaling and novel therapies in heart failure
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Our lab is particularly interested in the roles of complex signaling networks involved in the regulation of cardiovascular function and disease. We perform quantitative live-cell imaging of signaling dynamics and develop quantitative models to explain how signaling networks function. These systems approaches are currently helping us characterize mechanisms underlying regulation of cardiac contractility, ischemic heart disease, and pathways leading to cardiac growth. Such quantitative understanding will be critical for the future rational design of therapeutic agents for cardiovascular disease.\\\

Our current projects are in
# Multi-scale integration from cell signaling networks to cardiac MRI
# Nonlinear systems analysis
of complex biochemical networks
# Calcium signaling pathways regulating cardiac contractility and growth
# Compartmentation of cAMP signaling in cardiac myocytes
to:
Heart function and disease are controlled by complex molecular networks that are just beginning to be mapped out. Our lab develops mathematical models to understand how these molecular control systems work, and then we perform a variety of experiments to test this understanding. Experimental techniques include cell culture, live-cell imaging, and biochemical assays. These integrated approaches are helping us harness molecular networks to reverse the progression of heart disease.

Current projects include:
#beta-adrenergic signaling and novel therapies in heart failure
#Live-cell imaging of cAMP compartmentation
#Multi-scale modeling of signaling networks
#Calcium signaling pathways regulating heart contractility and growth
#Diagnosis
of neonatal sepsis by its actions on the heart
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# [[Research/Multi-scale integration from cell signaling networks to cardiac MRI]]
# [[Research/Nonlinear systems analysis of complex biochemical networks]]
# [[Research/Calcium signaling pathways regulating cardiac contractility and growth]]
# [[Research/Compartmentation of cAMP signaling in cardiac myocytes]]
to:
# Multi-scale integration from cell signaling networks to cardiac MRI
# Nonlinear systems analysis of complex biochemical networks
# Calcium signaling pathways regulating cardiac contractility and growth
# Compartmentation of cAMP signaling in cardiac myocytes
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%center% http://bme.virginia.edu/saucerman/images/bARsignaling300.jpg \\\
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%center% http://bme.virginia.edu/saucerman/images/bARsignaling300.jpg
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Our lab is particularly interested in the roles of complex signaling networks involved in the regulation of cardiovascular function and disease. We perform quantitative live-cell imaging of signaling dynamics and develop quantitative models to explain how signaling networks function. These systems approaches are currently helping us characterize mechanisms underlying regulation of cardiac contractility, ischemic heart disease, and pathways leading to cardiac growth. Such quantitative understanding will be critical for the future rational design of therapeutic agents for cardiovascular disease.
to:
Our lab is particularly interested in the roles of complex signaling networks involved in the regulation of cardiovascular function and disease. We perform quantitative live-cell imaging of signaling dynamics and develop quantitative models to explain how signaling networks function. These systems approaches are currently helping us characterize mechanisms underlying regulation of cardiac contractility, ischemic heart disease, and pathways leading to cardiac growth. Such quantitative understanding will be critical for the future rational design of therapeutic agents for cardiovascular disease.\\\
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# [[Research/Multi-Scale Integration|Multi-scale integration from cell signaling networks to cardiac MRI]]
# [[Research/Nonlinear Systems Analysis|Nonlinear systems analysis of complex biochemical networks]]
# [[Research/Calcium Signaling Pathways|Calcium signaling pathways regulating cardiac contractility and growth]]
# [[Research/cAMP Signaling Compartmentation|Compartmentation of cAMP signaling in cardiac myocytes]]
to:
# [[Research/Multi-scale integration from cell signaling networks to cardiac MRI]]
# [[Research/Nonlinear systems analysis of complex biochemical networks]]
# [[Research/Calcium signaling pathways regulating cardiac contractility and growth]]
# [[Research/Compartmentation of cAMP signaling in cardiac myocytes]]