Core Faculty

Huabo Su, PhD

Huabo su, PhD

Associate Professor, Vascular Biology Center
Pharmacology & Toxicology

More about Dr Su

Contact Info

Phone: (706) 721-9152
Fax: (706) 721-9799
Office: CB-3704
Lab: CB-3705, 3908

Education and Training

Research Assistant Professor
University of South Dakota, Molecular cardiovascular biology.

Post-Doctoral Training
Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD.

Biochemistry and Molecular Biology
Fudan University, Shanghai, China

Molecular Biology
Guangxi University, Nanning, China

Guangxi Normal University, Guilin, China

Society Memberships

American Heart Association

American Physiology Society

International Society of Heart Research


Post-translational modifications (PTMs) by a family of small protein modifiers, including ubiquitin (Ub) and Ub-like proteins, represent a vital mechanism regulating protein function and are integral to cellular homeostasis. Recent studies have consistently proven the fundamental importance of these PTMs in normal cell function and their implications in a wide array of diseases ranging from cancers, viral diseases, to neurodegenerative disorders and cardiovascular diseases. However, the biological functions of novel ubiquitin-like proteins in the heart remain poorly understood.

We are particularly interested in the roles of NEDD8 (Neural precursor cell expressed, developmentally downregulated 8) and Ufm1 (Ubiquitin-like protein modifier 1), two novel Ub-like proteins, in the heart. NEDD8 and Ufm1 modify protein targets via their specific conjugation enzymes, termed neddylation and ufmylation, respectively. Our research aims to address three major questions: 1) does neddylation or ufmylation have any roles in the developing and stressed hearts? 2) how does neddylation or ufmylation control cardiomyocyte function and survial? and 3) what cellular proteins are modified by NEDD8 or Ufm1 and how such modifications alter their molecular, cellular, organismal functions? We use a combination of novel genetically engineered mouse models with advanced molecular, cellular, physiological and pathological, and proteomic descriptors to tackle these questions.

Current Projects

  • Atypical neddylation and cardiac protein quality control
  • Role of neddylation in cardiac development
  • Unrecognized role of neddylation in post-mitotic cardiomyocytes
  • Pathophysiological significance of non-Cullin neddylation in the heart
  • Ufmylation, ER stress signaling and cardiac remodeling.


Su Lab

Jie Li, M.D., Ph.D. - Assistant Research Scientist

Jianqiu Zou, Ph.D. - Assistant Research Scientist

Rodney Littlejohn,  - M.D./Ph.D. candidate

Yali Yao, M.S. - Research Assistant

Yuan Wen, Ph.D. - Visiting Scholar

Recent Publications

More Publications from PubMed

Zou J, Ma W, Littlejohn R, Li J, Stansfield BK, Kim IM, Liu J, Zhou J, Weintraub NL, Su H*. Transient inhibition of neddylation at neonatal stage evokes reversible cardiomyopathy and predisposes the heart to isoproterenol-induced heart failure. Am J Physiol Heart Circ Physiol. 2019 Mar 29. doi: 10.1152/ajpheart.00806.2018. [Epub ahead of print]. PMID: 30925068

Li J, Yue G, Ma W, Zhang A, Zou J, Cai Y, Tang X, Wang J, Liu J, Li H, Su H*. The ufm1 specific ligase 1 regulates endoplasmic reticulum homeostasis and protects against heart failure. Circ Heart Fail. 2018 Oct;11(10):e004917. doi: 10.1161/CIRCHEARTFAILURE.118.004917. PMID: 30354401
(Editorial comment: Putting the Stress on UFM1 (Ubiquitin-Fold Modifier 1). Sutherland JD, Barrio R. Circ Heart Fail. 2018 Oct;11(10):e005455. doi: 10.1161/CIRCHEARTFAILURE.118.005455.)

Zou J, Ma W, Li J, Littlejohn R, Zhou H, Kim IM, Fulton DJR, Chen W, Weintraub NL, Zhou J, Su H*. Neddylation is required for ventricular chamber maturation through repression of Hippo signaling. Proc Natl Acad Sci U S A. 2018 Apr 24;115(17):E4101-E4110. PMID: 29632206.

Li J, Ma W, Yue G, Tang Y, Kim IL, Weintraub NL, Wang X, Su H*. Cardiac proteasome functional insufficiency plays a pathogenic role in diabetic cardiomyopathy. J Mol Cell Cardiol. 2017 Jan;102:53-60. PMID: 27913284.
(Comment in: Targeting the ubiquitin proteasome system in diabetic cardiomyopathy. Bozi LHM, Campos JC. J Mol Cell Cardiol. 2017 Aug;109:61-63.)

Li J, Johnson JA, Su H*. Ubiquitin and ubiquitin-like proteins in cardiac disease and protection. Curr Drug Targets. 2018; 19(9):989-1002. doi: 10.2174/1389450117666151209114608. PMID: 26648080.

Su H, Li J, Zhang H, Ma W, Wei N, Liu J, Wang X. COP9 Signalosome Controls the Degradation of Cytosolic Misfolded Proteins and Protects Against Cardiac Proteotoxicity. Circ Res. 2015 Nov 6;117(11):956-66. PubMed PMID: 26383969.
(Comment in: Breaking down the COP9 Signalsome in the heart: how inactivating a protein ubiquitin ligase increases protein ubiquitylation and protects the heart. Glembotski CC. Circ Res. 2015 Nov 6;117(11):914-6. PMID: 26541679)

Li J, Ma W, Li H, Hou N, Wang X, Kim IM, Li F, Su H*. NEDD8 Ultimate Buster-1 Long (NUB1L) Protein Suppresses Atypical Neddylation and Promotes Proteasomal Degradation of Misfolded Proteins. J Biol Chem. 2015 Sep 25;290(39):23850-62. PubMed PMID: 26260793.

Kandala S, Kim IM, Su H*. Neddylation and deneddylation in cardiac biology. Am J Cardiovasc Dis. 2014 Dec 29;4(4):140-58. PMID: 25628956.