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Yunbo Ke, PhD

Academic Title:

Assistant Professor

Primary Appointment:



20 Penn Street, Baltimore, MD 21201

Phone (Primary):

(410) 706-2572

Phone (Secondary):

(312) 217-3879

Education and Training


1978 - 1982: BS, Biology, Huazhong Normal University

1990 - 2005: PhD , Biochemistry, The Ohio State University

Thesis Topic: Regulation by introns: Splicing signals are required for growth-stimulated expression of thymidylate synthase gene in mouse fibroblasts

Thesis Advisor: Lee F Johnson, professor and chairman of Department of Molecular Genetics


Post-Graduate Education and Training

1995 - 1998: Postdoctoral Fellowship - Cardiology Section, University of Chicago, Chicago, IL

1998 - 2003: Other - Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL


Dr. Yunbo Ke has been studying signal tranduction in cardiovascular systems. He and his colleagues have discovered a novel kinase/phosphatase signaling module mediated by p21 activated kinase-1 and PP2A that bring about important functional effects in cardiac and endothelial cells. In cardiomyocytes and in the heart, the siganling pathways antagonize the effects of beta-adrenergic activities and regulate heart rate, myofilament contractility and hypertrophy. In endothelial cells, the signaling pathways modulate myosin II activities and regulate enothelial barrier function. Dr. Ke now studies multiple signaling molecles from G-protein coupled receptors, small G proteins and their downstream effectors in regulation of endothelial barrier function and vascular permeability in the lungs.

Research/Clinical Keywords

acute lung injury, endothelial barrier function, signal transduction, G proteins, protein kinases, cytoskeleton, actomyosin, focal adhesion, microtubule, genetically modified mice, LPS, trauma, inflammation, cytokines

Highlighted Publications

Yunbo Ke, Katherine Sheehan, E. Eroume A Egom, Ming Lei and R. John Solaro. Novel bradykinin signaling in adult rat cardiac myocytes through activation of p21 activated kinase. Am J Physiol Heart Circ Physiol. 2010 Apr;298(4):H1283-9. Epub 2010 Feb 12.PMID: 20154261 PMC2853422

Ke Y, Lei M, Wang X, Solaro RJ.  Unique catalytic activities and scaffolding f p21 activated kinase-1 in cardiovascular signaling. Front Pharmacol. 2013 Sep 27;4:116. Review. PMID:24098283

Davis RT 3rd, Simon JN, Utter M, Mungai P, Alvarez MG, Chowdhury SA, Heydemann A, Ke Y, Wolska BM, Solaro RJ. Knockout of p21-activated kinase-1 attenuates exercise-induced cardiac remodeling through altered calcineurin siganling. Cardiovasc Res. 2015 Dec 1;108(3):335-47. doi: 10.1093/cvr/cvv234. Epub 2015 Oct 12. PMID: 26464331

Monasky MM, Taglieri DM, Patel BG, Chernoff J, Wolska BM, Ke Y, and Solaro RJ. p21-activated kinase improves cardiac contractility during ischemia-reperfusion concomitant with changes in troponin-T and myosin light chain 2 phosphorylation. PMID: 22037191. Am J Physiol Heart Circ Physiol 2012 Jan, 302: H224-230.

Egom EE, Bae JS, Capel R, Richards M, Ke Y, Pharithi RB, Maher V, Kruzliak P, Lei M. Effect of sphingosine-1-phosphate on L-type calcium and Ca(2+) transient in rat ventricular myocytes. Mol Cell Biochem. 2016 Aug;419(1-2):83-92. doi: 10.1007/s11010-016-2752-8. Epub 2016 Jul 2. PMID: 27372350


Research Interests

Endothelial barrier dysfunction is an underlying cause of acute lung injury which occurs during inflammation, sepsis and trauma. Normal endothelial function is maintained by dynamic balance among internal tension, focal adhesion, adhesive junction and microtubule network. A variety of signaling molecules from G-protein coupled receptors to protein kinase/phosphatases for examples, regulate assemble/disassemble and activities of these cytoskeletal components, and modulate vascular permeability in the lungs. Cell signaling mediated by Rac1-Pak1 is among those that antagonize LPS-induced loss of endothelial barrier integrity and promote certain phospholipid-stimulated barrier restoration through reduction of internal contractility, dissolution of focal adhesion and enhancement of adhesive junction with amelioration of lung vascular leak. Multiple signaling pathways are also coordinated by scaffolding proteins that respond to different extracellular cues and switch binding partners that finally affect endothelial sensitivity or resistance in pathological conditions. My research is to demonstrate the intracellular processes for regulation of endothelial barrier function, and develop novel therapeutics for acute lung injury.

Professional Activity


Aug. 2003 - July, 2015




Aug. 2015 - Dc. 2016





Jan. 2017-Present


Research Assistant Professor, Department of Physiology and Biophysics

University of Illinois at Chicago

Chicago, IL


Research professional

Department of Medicine, Section of Pulmonary and Critical Care

University of Chicago

Chicago, IL


Assistant professor

Department of Anesthesiology,

University of Maryland Medical School

Baltimore, MD

Lab Techniques and Equipment

Genetically modified mouse models related to regulation of acute lung injury, trachea infusion of LPS, high tidal ventilation in mouse lungs, Nostril infusion of MRSA, Evans blue staining of mouse lungs for vascular permeability, optical imaging of lungs in live animals, survival surgery, in vitro and in vivo delivery with adenoviral vectors, cell culture,  ELISA, ECIS and recombinant DNA technology