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Jeffrey Robbins, PhD Executive Co-Director, Heart Institute
Executive Co-Director, Heart Institute
Director, Molecular Cardiovascular Biology
Professor, UC Department of Pediatrics
Structure function relationships for the contractile proteins; cardiac-specific gene manipulation in transgenic rabbits; the contractile protein myosin and human heart failure; molecular studies of human valve disease
Visit the Robbins Lab.
Gupta MK, Robbins J. Post-translational control of cardiac hemodynamics through myosin binding protein C. Pflugers Arch: European journal of physiology. 2014 Feb;466(2):231-6.
Mun JY, Previs MJ, Yu HY, Gulick J, Tobacman LS, Beck Previs S, Robbins J, Warshaw DM, Craig R. Myosin-binding protein C displaces tropomyosin to activate cardiac thin filaments and governs their speed by an independent mechanism. Proc Natl Acad Sci U S A. 2014 Feb 11;111(6):2170-5.
Sandri M, Robbins J. Proteotoxicity: An underappreciated pathology in cardiac disease. J Mol Cell Cardiol. 2014 Jun;71c:3-10.
Wang X, Robbins J. Proteasomal and lysosomal protein degradation and heart disease. J Mol Cell Cardiol. 2014 Jun;71c:16-24.
James J, Robbins J. Ablating a cardiac protein: Causality at last. Circ Res. 2013;112:1415-1419.
Razzaque MA, Gupta M, Osinska H, Gulick J, Blaxall BC, Robbins J. An endogenously produced fragment of cardiac myosin-binding protein C is pathogenic and can lead to heart failure. Circ Res. 2013 Aug 16;113(5):553-61.
Gupta MK, Gulick J, James J, Osinska H, Lorenz JN, Robbins J. Functional dissection of myosin binding protein C phosphorylation. J Mol Cell Cardiol. 2013;64C:39-50.
Bhuiyan MS, Pattison JS, Osinska H, James J, Gulick J, McLendon PM, Hill JA, Sadoshima J, Robbins J. Enhanced autophagy ameliorates cardiac proteinopathy. J Clin Invest. 2013;123(12):5284-97.
Pattison JS, Robbins J. Desmin and heart disease. In: Kavallaris M, ed. Cytoskeleton and human disease. New York, NY: Humana Press; 2012:411-424.
Bhuiyan MS, Gulick J, Osinska H, Gupta M, Robbins J. Determination of the critical residues responsible for cardiac myosin binding protein C's interactions. J Mol Cell Cardiol. 2012;53:838-847.
Cardiac Signaling in the Normal and Abnormal Heart. Principal Investigator. National Heart, Lung, and Blood Institute. Sep 2013-May 2018. #P01 HL69779.
Proteotoxicity: an underappreciated factor in cardiac disease. North American Coordinator. Leducq Transatlantic Alliance For Cardiovascular Disease. 2011-2016.
Burns C. Blaxall, PhD, FAHA, FACC, FAPS Director of Translational Science, Heart Institute
is interested in understanding the molecular mechanisms associated with the development and progression of heart failure. We are particularly interested in developing novel heart failure therapeutics targeting myocardial function and fibrosis. To this end, we also seek to understand the pathologic role of cardiac myocyte and non-myocyte (i.e.. fibroblast) intercellular communication.
Director of Translational Science, Heart Institute
Co-Director, Heart Institute Research Core & Biorepository
Molecular and signaling mechanisms of heart failure; cardiac fibrosis; drug and therapeutic discovery
Visit the Blaxall Lab.
Dr. Burns C. Blaxall has focused his entire career on understanding the molecular mechanisms of heart failure. He received his PhD in pharmacology from the University of Colorado Health Sciences Center, and postdoctoral training at Duke University Medical Center. He then rose through the faculty ranks at the University of Rochester Medical Center and the Aab Cardiovascular Research Institute, where he also directed the Howard Hughes Medical Institute Med-into-Grad Fellowship in Cardiovascular Science.
In 2012, he was recruited to the Heart Institute of Cincinnati Children’s Hospital Medical Center, where he is director of translational science. Dr. Blaxall has received many academic honors, including the Early Career Investigator Award from the American Heart Association (AHA), the Outstanding Achievement Award from the Founder’s AHA Affiliate, the Merit Award for Research Achievement from Mended Hearts, and election as fellow of the AHA.
PhD: University of Colorado HSC, Denver, CO, 1999.
Fellowship: Duke University Medical Center, Durham, NC.
Kamal FA, Mickelsen DM, Wegman KM, Travers JG, Moalem J, Hammes SR, Smrcka AV, Blaxall BC. Simultaneous adrenal and cardiac g-protein-coupled receptor-gβγ inhibition halts heart failure progression. J Am Coll Cardiol. 2014;63(23):2549-57.
Ram R, Wescott AP, Varandas K, Dirksen RT, Blaxall BC. Mena associates with Rac1 and modulates connexin 43 remodeling in cardiomyocytes. Am J Physiol Heart Circ Physiol. 2014;306(1):H154-9.
Belmonte SL, Ram R, Mickelsen DM, Gertler FB, Blaxall BC. Cardiac overexpression of Mammalian enabled (Mena) exacerbates heart failure in mice. Am J Physiol Heart Circ Physiol. 2013;305(6):H875-84.
Martin ML, Blaxall BC. Cardiac intercellular communication: are myocytes and fibroblasts fair-weather friends? J Cardiovasc Transl Res. 2012;5(6):768-82.
Aguilar F, Belmonte SL, Ram R, Noujaim SF, Dunaevsky O, Protack TL, Jalife J, Todd Massey H, Gertler FB, Blaxall BC. Mammalian enabled (Mena) is a critical regulator of cardiac function. Am J Physiol Heart Circ Physiol. 2011;300(5):H1841-52.
Belmonte S, Blaxall BC. G-protein coupled receptor kinases as therapeutic targets in cardiovascular disease. Circ Res. 2011;109(3):309-19.
Jaffré F, Friedman AE, Hu Z-Y, Mackman N and Blaxall BC. Beta-adrenergic receptor stimulation transactivates Protease-Activated Receptor 1 via MMP-13 in heart. Circulation. 2012;125(24):2993-3003.
Ram R, Mickelsen DM, Theodoropoulos C, Blaxall BC. New approaches in small animal echocardiography: imaging the sounds of silence. Amer J Pathol Heart Circ Physiol. 2011;301(5):H1765-80.
Casey LM, Pistner AR, Belmonte S, Jaffre F, Migdalovic D, Stolpnik O, Nwakanma F, Vorobiof G, Dunaevsky O, Smrcka AV, Blaxall BC. Small molecule targeting of G beta gamma prevents heart failure progression. Circ Res. 2010;107(4):532-9.
Bullard TA, Protack TL, Aguilar F, Bagwe S, Massey HT, Blaxall BC. Identification of Nogo as a novel indicator of heart failure. Physiolog Genom. 2008;32(2):182-9.
James D. Gulick, MS
Instructor, UC Department of Pediatrics
Understanding how certain mutations in contractile protein genes are able to alter the function of the heart
Michalek AJ, Howarth JW, Gulick J, Previs MJ, Robbins J, Rosevear PR, Warshaw DM. Phosphorylation modulates the mechanical stability of the cardiac Myosin-binding protein C motif. Biophys J. 2013 Jan 22;104(2):442-52.
Bhuiyan MS, Gulick J, Osinska H, Gupta M, Robbins J. Determination of the critical residues responsible for cardiac myosin binding protein C's interactions. J Mol Cell Cardiol. 2012 Dec;53(6):838-47.
Weith AE, Previs MJ, Hoeprich GJ, Previs SB, Gulick J, Robbins J, Warshaw DM. The extent of cardiac myosin binding protein-C phosphorylation modulates actomyosin function in a graded manner. J Muscle Res Cell Motil. 2012 Dec;33(6):449-59.
Previs MJ, Previs SB, Gulick J, Robbins J, Warshaw DM. Molecular mechanics of cardiac myosin binding protein C in native thick filaments. Science. 2012 Sept 7; 337 (6099): 1215-8.
Weith A, Sadayappan S, Gulick J, Previs MJ, Vanburen P, Robbins J, Warshaw DM. Unique single molecule binding of cardiac myosin binding protein-C to actin and phosphorylation-dependent inhibition of actomyosin motility requires 17 amino acids of the motif domain. J Mol Cell Cardiol. 2012 Jan;52(1):219-27.
Tranter M, Liu Y, He S, Gulick J, Ren X, Robbins J, Jones WK, Reineke TM. In vivo delivery of nucleic acids via glycopolymer vehicles affords therapeutic infarct size reduction in vivo. Mol Ther. 2012 Mar;20(3):601-8.
Jeyaraj D, Haldar SM, Wan X, McCauley MD, Ripperger JA, Hu K, Lu Y, Eapen BL, Sharma N, Ficker E, Cutler MJ, Gulick J, Sanbe A, Robbins J, Demolombe S, Kondratov RV, Shea SA, Albrecht U, Wehrens XH, Rosenbaum DS, Jain MK. Circadian rhythms govern cardiac repolarization and arrhythmogenesis. Nature. 2012 Mar 1;483(7387):96-9.
Jeanne M. James, MD
Cardiovascular genetics; echocardiography; congenital heart disease; medical education; molecular cardiology; ventricular remodeling; cardiac hypertrophy.
Visit the James Lab website.
Jeanne James, MD, is an associate professor of pediatrics at University of Cincinnati College of Medicine and is currently the director of the Cardiology Fellowship Training Program at Cincinnati Children's Hospital Medical Center.
A native of West Virginia, Dr. James earned her bachelor and medical degrees from West Virginia University in Morgantown, WV. She completed her pediatric residency and pediatric cardiology fellowship at Vanderbilt University Medical Center in Nashville, TN. Dr. James has been an attending staff member of the Division of Cardiology at Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine since 1995.
Dr. James' academic interests are in translational research on heart muscle disease, cardiovascular genetics and echocardiography. She has made numerous scholarly contributions to the field with publications describing both laboratory-based and clinical research. She serves as a grant reviewer for the American Heart Association and is a peer-reviewer for a number of scientific and medical journals.
Dr. James has established collaborative relationships with laboratory researchers at Cincinnati Children’s Hospital Medical Center, the University of Cincinnati College of Medicine and investigators across the United States. As the director of the Mouse Echocardiography Core, she uses non-invasive imaging to evaluate phenotypes of transgenic mice, including embryonic mice.
Dr. James serves as an attending physician in clinical echocardiography laboratory as well as the inpatient cardiology ward and consult team. Dr. James is a member of the Cardiovascular Genetics (CVG) service and has significant responsibilities in the CVG outpatient clinic. Dr. James is a member of the American Society of Echocardiography, the American Heart Association and the Society for Pediatric Research.
MD: West Virginia University, Morgantown, WV, 1987.
Residency: Vanderbilt University Medical Center, Nashville, TN, 1987-90.
Fellowship: Vanderbilt University Medical Center, Nashville, TN, 1991-94.
Certification: Pediatrics, 1990 - present.
Certified: Pediatric Cardiology, 1996 - present.
Cheek J, Wirrig E, Alfieri C, James J, Yutzey K. Differential activation of valvulogenic, chondrogenic and osteogenic pathways in mouse models of myxomatous and calcific aortic valve disease. J Mol Cell Cardio. 2012 Mar;52(3):689-700.
Sadayappan S, Gulick J, Martin L, Osinska H, Barefield D, Cuello F, Avkiran M, Lasko V, Lorenz J, Maillet M, Martin J, Heller-Brown J, Bers D, Molkentin J, James J, Robbins J. A critical function for Ser-282 in cardiac myosin binding protein-C phosphorylation and cardiac function. Circ Res. 2011; 109(2):141-50.
James J, Kinnett K, Ittenbach R, Wang Y, Benson D, Cripe L. Electrocardiographic abnormalities in very young Duchenne muscular dystrophy patients precede the onset of cardiac dysfunction. Neuromuscul Disord. 2011; 21(7):462-7.
Combs M, Braitsch C, Lange A, James J, Yutzey K. NFATc1 promotes epicardium-derived cell (EPDC) invasion into myocardium. Development. 2011; 138(9):1747-57.
James J, Robbins J. Signaling and myosin binding protein C. J Biol Chem. 2011;286(12):9913-9.
Stanley BA, Graham DR, James J, Mitsak M, Tarwater PM, Robbins J, Van Eyk JE. Altered myofilament stoichiometry in response to heart failure in a cardioprotective a-myosin heavy chain transgenic rabbit model. Proteomics Clin Appl. 2011; 5(3-4):147-58.
Acehan D, Vaz F, Houtkooper R, James J, Moore V, Tokunaga C, Kulik W, Wansapura J, Toth M, Strauss A, Khuchua Z. Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome. J Biol Chem. 2010; 286(2):899-908.
Hinton R, Adelman-Brown J, Witt S, Krishnamurthy V, Gruber M, Osinska H, Sakthivel B, James J, Narmoneva D, Mecham R, Benson D. Elastin haploinsufficiency results in latent progressive aortic valve disease in a mouse model. Circ Res. 2010; 107(4):549-57.
James J, Hor K, Moga M, Martin L, Robbins J. Effects of myosin heavy chain manipulation in experimental heart failure. J Mol Cell Cardiol. 2010; 48(5):999-1006.
Suzuki T, Palmer B, James J, Wang Y, Chen V, VanBuren P, Maughan D, Robbins J, LeWinter M. Effects of cardiac myosin isoform variation on myofilament function and cross-bridge kinetics in transgenic rabbits. Circ Heart Fail. 2009; 2(4):334-41.
Pattison J, Waggoner J, James J, Martin L, Gulick J, Osinska H, Klevitsky R, Kranias E, Robbins J. Phospholamban overexpression in transgenic rabbits. Transgenic Research. 2008; 17(2):157-70.
Zaza Khuchua, PhD
research interests are mitochondrial structure, function, biogenesis and recycling in normal and pathological heart muscle. More specifically we are interested in defects in cardiac lipid and phospholipid metabolism. We employ genetically engineered mice to model human genetic disorders.
Associate Professor, UC Department of Pediatrics
Mitochondrial function; structure and dynamics in cardiac cells in normal and pathological conditions; role of mitochondrial phospholipids in aerobic metabolism in heart; role of lipid molecules in cell signaling systems
MS: Moscow State University, Moscow, Russia, 1981.
PhD: All Union Cardiology Research Center, Moscow, Russia, 1987.
Acehan D, Vaz F, Houtkooper RH, James J, Moore V, Tokunaga C, Kulik W, Wansapura J, Toth MJ, Strauss A, Khuchua Z. Cardiac and skeletal muscle defects in a mouse model of human Barth syndrome. J Biol Chem. 2011 Jan 14;286(2):899-908.
Acehan D, Khuchua Z, Houtkooper RH, Malhotra A, Kaufman J, Vaz FM, Ren M, Rockman HA, Stokes DL, Schlame M. Distinct effects of Tafazzin deletion in differentiated and undifferentiated mitochondria. Mitochondrion.
Tchekneva EE, Khuchua Z, Davis LS, Kadkina V, Dunn SR, Bachman S, Ishibashi K, Rinchik EM, Harris RC, Dikov MM, Breyer MD. Single amino acid substitution in aquaporin 11 causes renal failure. J Am Soc Nephrol. 2008 10:1955-64.
Marjorie Maillet, PhD
Signaling pathways; cellular biology; cardiac hypertrophy and heart failure
PhD: Paris XI University, Orsay, France, 2003.
Fellowship: Cincinnati Children’s Hospital, Cincinnati, Ohio.
van Berlo JH, Maillet M, Molkentin JD. Signaling effectors underlying pathologic growth and remodeling of the heart. J Clin Invest. 123, 37-45. 2013.
Maillet M, van Berlo JH, Molkentin JD. Molecular basis of physiological heart growth: fundamental concepts and new players. Nat Rev Mol Cell Biol. 14, 38-48. 2012.
Lynch JM, Maillet M, Vanhoutte D, Schloemer A, Sargent MA, Blair NS, Lynch KA, Okada T, Aronow BJ, Osinska H, Prywes R, Lorenz JN, Mori K, Lawler J, Robbins J, Molkentin JD. A thrombospondin-dependent pathway for a protective ER stress response. Cell. 149, 1257-68. 2012.
Le Grand F, Grifone R, Mourikis P, Houbron C, Gigaud C, Pujol J, Maillet M, Pages G, Rudnicki M, Tajbakhsh S, Maire P. Six1 regulates stem cell repair potential and self-renewal during skeletal muscle regeneration. J Cell Biol. 198, 815-32. 2012.
Drawnel FM, Wachten D, Molkentin JD, Maillet M, Aronsen JM, Swift F, Sjaastad I, Liu N, Catalucci D, Mikoshiba K, Hisatsune C, Okkenhaug H, Andrews SR, Bootman MD, Roderick HL. Mutual antagonism between IP(3)RII and miRNA-133a regulates calcium signals and cardiac hypertrophy. J Cell Biol. 199, 783-98. 2012.
Davis J, Maillet M, Miano JM, Molkentin JD. Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research. Circ Res. 111, 761-77. 2012.
Sadayappan S, Gulick J, Osinska H, Barefield D, Cuello F, Avkiran M, Lasko VM, Lorenz JN, Maillet M, Martin JL, Brown JH, Bers DM, Molkentin JD, James J, Robbins J. A critical function for ser-282 in cardiac Myosin binding protein-C phosphorylation and cardiac function. Circ Res. 109, 141-50. 2011.
Qian L, Wythe JD, Liu J, Cartry J, Vogler G, Mohapatra B, Otway RT, Huang Y, King IN, Maillet M, Zheng Y, Crawley T, Taghli-Lamallem O, Semsarian C, Dunwoodie S, Winlaw D, Harvey RP, Fatkin D, Towbin JA, Molkentin JD, Srivastava D, Ocorr K, Bruneau BG, Bodmer R. Tinman/Nkx2-5 acts via miR-1 and upstream of Cdc42 to regulate heart function across species. J Cell Biol. 193, 1181-96. 2011.
Kehat I, Davis J, Tiburcy M, Accornero F, Saba-El-Leil MK, Maillet M, York AJ, Lorenz JN, Zimmermann WH, Meloche S, Molkentin JD. Extracellular signal-regulated kinases 1 and 2 regulate the balance between eccentric and concentric cardiac growth. Circ Res. 2011 Jan 21;108(2):176-83.
Nakayama H, Bodi I, Maillet M, DeSantiago J, Domeier TL, Mikoshiba K, Lorenz JN, Blatter LA, Bers DM, Molkentin JD. The IP3 receptor regulates cardiac hypertrophy in response to select stimuli. Circ Res. 2010 Sep 3;107(5):659-66
Douglas Millay, PhD
Assistant Professor, UC Department of Pediatrics
BS: Northern Kentucky University, Highland Heights, KY, 2002.
PhD: University of Cincinnati, Cincinnati, OH, 2008.
Fellowship: University of Texas Southwestern, Dallas, TX, 2014.
Millay DP, O’Rourke JR, Sutherland LB, Bezprozvannaya S, Shelton JM, Bassel-Duby R, Olson EN. Myomaker is a membrane activator of myoblast fusion and muscle formation. Nature. 2013 Jul 18;499 (7458).
Millay DP, Olson EN. Making muscle or mitochondria by selective splicing of PGC1α. Cell Metab. 2013 Jan 8;17(1):3-4.
Hatley ME, Tang W, Garcia MR, Finkelstein D, Millay DP, Liu N, Graff J, Galindo RL, Olson EN. A mouse model of rhabdomyosarcoma originating from the adipocyte lineage. Cancer Cell. 2012 Oct 16;22 (4): 536-46.
Zeve D, Seo J, Suh JM, Stenesen D, Tang W, Berglund ED, Wan Y, Williams LJ, Lim A, Martinez MJ, McKay RM, Millay DP, Olson EN, Graff JM. Wnt signaling activation in adipose progenitors promotes insulin-independent muscle glucose uptake. Cell Metab. 2012 Apr 4;15(4):492-504.
Pei J, Millay DP, Olson EN, Grishin NV. CREST--a large and diverse superfamily of putative transmembrane hydrolases. Biol Direct. 2011 Jul 6;6:37.
Goonasekera SA, Lam CK, Millay DP, Sargent MA, Hajjar RJ, Kranias EG, Molkentin JD. Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle. J Clin Invest. 2011 Mar;121(3):1044-52.
Wissing ER, Millay DP, Vuagniaux G, Molkentin JD. Debio-025 is more effective that prednisone in reducing muscular pathology in mdx mice. Neuromuscul Disord. 2010 Nov;20(11):753-60.
Millay DP, Goonasekera SA, Sargent MA, Molkentin JD. Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism. Proc Natl Acad Sci USA. 2009 Nov 10;106(45)19023-8.
Millay DP, Sargent MA, Roche JA, Maillet M, McNally EM, Bloch RJ, Molkentin JD. Genetic manipulation of dysferlin expression in skeletal muscle: Novel insights into muscular dystrophy. Am J Pathol. 2009 Nov;175(5):1817-23.
Millay DP, Sargent MA, Osinska H, Baines CP, Barton ER, Vuagniaux G, Sweeney HL, Robbins J, Molkentin JD. Genetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophy. Nat Med. 2008 Apr;14(4):442-7.
Jeffery D. Molkentin, PhD Professor | Howard Hughes Medical Institute Investigator
Professor | Howard Hughes Medical Institute Investigator
Dr. Molkentin's research aims to understand the intracellular signaling pathways and transcriptional regulatory circuits that control mammalian cell growth and differentiation. His work has advanced the understanding of molecular events behind heart disease and muscular dystrophy.
In 2008 he was named a Howard Hughes Medical Institute (HHMI) investigator.
For a full description of Dr. Molkentin's work, please see his Faculty Lab Site in the Division of Molecular and Cardiovascular Biology.
BS: Marquette University, Milwaukee, WI, 1989.
PhD: Medical College of Wisconsin, 1994.
Burr AR, Molkentin JD. Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy. Cell Death & Diff. 2015.
Kwong JQ, Lu X, Correll RN, Vagnozzi RJ, Sargent MA, York AJ, Zhang J, Bers DM, Molkentin JD. The mitochondrial calcium uniporter selectively matches metabolic output to acute contractile stress in the heart. Cell Reports. 2015;12:15-22.
Karch J, Molkentin JD. Regulated Necrotic Cell Death: The Passive Aggressive Side of Bax and Bak. Circ Res. 2015 May 22;116(11):1800-9.
Karch J, Kanisicak O, Brody MJ, Sargent MA, Michael DM. Molkentin JD. Necroptosis interfaces with MOMP and the MPTP in mediating cell death. PLOS one. 2015;10(6):e0130520.
Accornero F, van Berlo JH, Correll RN, Elrod JW, Sargent MA, York A, JE Rabinowitz, Leask A, Molkentin JD. Genetic analysis of CTGF as an effector of TGF signaling and cardiac remodeling. Mol Cell Biol. 2015;35:2154-2164.
Kwong JQ, Molkentin JD. In sickness and health: role of the mitochondrial permeability transition pore in the heart. Cell Metabolism. 2014;21:206-214.
Davis J, Burr AR, Davis GF, Birnbaumer L, Molkentin JD. A TRPC6-dependent pathway for myofibroblast transdifferentiation and wound healing in vivo. Dev. Cell. 2012 23:705-715.
Auger-Messier M, Accornero F, Goonasekera SA, Bueno OF, Lorenz JN, van Berlo JH, Willette RN, Molkentin JD. Unrestrained p38 MAPK Activation in Dusp1/4 Double Null Mice Induces Cardiomyopathy. Circ Res. 2013 Jan 4:112(1):48-56.
Lorts A, Schwanekamp JA, Baudino TA, McNally EM, Molkentin JD. Deletion of periostin reduced muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-b pathway. Proc Natl Acad Sci USA. 2012 109:10978-10983.
Lynch JM, Maillet M, Vanhoutte D, Schloemer A, Sargent MA, Blair NS, Lynch KA, Okada T, Aronow BJ, Osinska H, Prywes R, Lorenz JN, Mori K, Lawler J, Robbins J, Molkentin JD. A thrombospondin-dependent pathway for a protective ER stress response. Cell. 2012 149,1257-1268.
Joshua S. Waxman, PhD
Understanding the molecular underlying nature of congenital heart defects; cardiomyocyte formation
Visit the Waxman Lab.
BA: New College, Sarasota, FL,1999.
PhD: University of Washington, Seattle, WA, 2004.
Postdoctoral Fellow: Skirball Institute/NYU School of Medicine, New York, NY, 2004-2009.
D’Aniello E, Rydeen A, Anderson J, Mandal A, Waxman JS.Depletion of retinoic acid receptors initiates a novel positive feedback mechanism that promotes teratogenic increases in retinoic acid. PLoS Genet. 2013 Aug; 9(8):e1003689.
Sorrell MR, Dohn TE, D’Aniello E, Waxman JS. Tcf7l1 proteins cell autonomously restrict cardiomyocyte and promote endothelial specification in zebrafish. Dev Biol. 2013;380(2); 199-210.
Mandal A, Rydeen A, Anderson J, Sorrell MR, Zygmunt T, Torres-Vázquez J, Waxman JS. Transgenic retinoic acid sensor lines in zebrafish indicate regions of available embryonic retinoic acid. Developmental Dynamics. 2013 Aug; 242(8); 989-1000.
Dohn TE, Waxman JS. Distinct phases of Wnt/β-catenin signaling direct cardiomyocyte formation in zebrafish. Dev Biol. 2012 Jan 15;361(2):364-76.
Sorrell MR, Waxman JS. Restraint of Fgf8 signaling by retinoic acid signaling is required for proper heart and forelimb formation. Dev. Biol. 2011 Oct 1; 358(1):44-55.
Waxman JS, Yelon D. Zebrafish retinoic acid receptors function as context-dependent transcriptional activators. Dev Biol. 2011; 352:128-40.
Feng L, Hernandez RE, Waxman JS, Yelon D, Moens CB. Dhrs3a regulates retinoic acid biosynthesis through a feedback inhibition mechanism. Dev Biol. 2010 Feb 1;338(1):1-14.
Waxman JS, Yelon D. Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling. Dev Dyn. 2009 May; 238(5):1207-13.
Linville A, Radtke K, Waxman JS, Yelon D, Schilling TF. Combinatorial roles for zebrafish retinoic acid receptors in the hindbrain, limbs and pharyngeal arches. Dev Biol. 2009 Jan 1; 325(1):60-70.
Waxman JS, Keegan BR, Roberts RW, Poss KD, Yelon D. Hoxb5b acts downstream of retinoic acid signaling in the forelimb field to restrict heart field potential in zebrafish. Dev Cell. 2008 Dec; 15(6):923-34.
Katherine Yutzey, PhD
is focused on the molecular mechanisms of heart development and disease. Particular emphasis is on signaling pathways and transcription factors that control heart valve development as well as contribute to pediatric and adult valve disease. Additional projects address the development of coronary vasculature, cardiac fibrosis and maturation of cardiac muscle after birth.
Visit the Yutzey Lab.
Molecular regulation of heart development; valve development and disease mechanisms; cardiomyocyte proliferation; cardiac connective tissue lineages.
Visit Dr. Yutzey's lab website.
Katherine E. Yutzey, PhD, is a professor who joined the Division of Molecular Cardiovascular Biology at Cincinnati Children's Hospital Medical Center within the University of Cincinnati College of Medicine in 1995.
Dr. Yutzey is the first recipient of the Fifth Third Bank/Charlotte R. Schmidlapp Women Scholars Award and was also a recipient of a Children's Hospital Medical Center Trustee Award. Her work is also supported by grants from National Institutes of Health (NIH) and the American Heart Association.
The focus of Dr. Yutzey's research program is the regulation of normal and abnormal heart development. Congenital heart defects represent one of the most common classes of human birth defects. Increasing evidence exists for a genetic basis of certain instances of congenital heart disease.
Dr. Yutzey’s lab also studies molecular mechanisms of cardiac connective tissue cell lineage development and disease. This work focuses on heart valve development and disease as well as mechanisms of cardiac fibrosis.
BA: Oberlin College, Oberlin, OH, 1986.
PhD: Purdue University, West Lafayette, IN,1992
Fellowship: Cornell University Medical College, New York, NY,1992-1995.
Wirrig EE, Hinton RB, Gomez MV, Yutzey KE. Cox2 inhibition reduces aortic valve calcification in vivo. Arterioscler. Thromb Vasc Biol. 2015;35:938-947.
Yutzey KE. Neuregulin1 makes heart muscle. Nature. 2015;520:445-446.
Wirrig EE, Yutzey KE. Conserved transcriptional regulatory mechanisms in aortic valve development and disease. Arterioscler Thromb Vasc Biol. 2014;34:737-741.
Cole CR, Yutzey KE, Brar AK, Goessling LS, vanVickle-Chavez SJ, Cunningham MV, Eghtesady P. Congenital heart disease linked to maternal autoimmunity against cardiac myosin. J Immunol. 2014;192:4074-4082.
Yutzey KE. Cardiovascular Biology: Switched at birth. Nature. 2014;509:572-573.
Yutzey KE, Demer LL, Body SC, Huggins GS, Towler DA, Giachelli CM, Hofmann-Bowman MA, Mortlock DP, Rogers MB, Sadeghi MM, Aikawa E. Calcific aortic valve disease: A consensus summary from the Alliance of Investigators on Calcific Aortic Valve Disease. Arterioscler Thromb Vasc Biol. 2014;34:2387-2393.
Lee MP, Ratner N, Yutzey KE. Genome-wide Twist1 occupancy in endocardial cushion cells, embryonic limb buds and peripheral nerve sheath tumor cells. BMC Genomics. 2014;15:821.
Godby RC, Munjal C, Opoka AM, Smith JM, Yutzey KE, Narmoneva DA, Hinton RB. Cross talk between NOTCH signaling and biomechanics in human aortic valve disease pathogenesis. J Cardiovasc Dev Dis. 2014;1:237-256.
Fang M, Alfieri CM, Hulin A, Conway SJ, Yutzey KE. Loss of -catenin promotes chondrogenic differentiation of aortic valve interstitial cells. Arterioscler Thromb Vasc Biol. 2014;34:2601-2608.
Sengupta A, Kalinichenko VV, Yutzey KE. FoxO and FoxM1 transcription factors have antagonistic functions in neonatal cardiomyocyte cell cycle withdrawal and IGF1 gene regulation. Circ Res. 2013;112:267-277.
Wnt/-catenin signaling and cardiac fibrosis. National Institutes of Health Component Principal Investigator. 2002-2018. P01 HL069779.
Wnt signaling in heart valve development and disease. National Institutes of Health. Principal Investigator. 2012-2016. R01 HL094319.
Cell signaling mechanisms of calcific aortic valve disease. National Institutes of Health. Principal Investigator. 2012-2016. R01 HL114682.
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