Small ubiquitin-like modifier 2 (SUMO2) is critical for memory processes in mice.


Small ubiquitin-like modifier (SUMO1-3) conjugation (SUMOylation), a posttranslational modification, modulates almost all major cellular processes. Mounting evidence indicates that SUMOylation plays a crucial role in maintaining and regulating neural function, and importantly its dysfunction is implicated in cognitive impairment in humans. We have previously shown that simultaneously silencing SUMO1-3 expression in neurons negatively affects cognitive function. However, the roles of the individual SUMOs in modulating cognition and the mechanisms that link SUMOylation to cognitive processes remain unknown. To address these questions, in this study, we have focused on SUMO2 and generated a new conditional Sumo2 knockout mouse line. We found that conditional deletion of Sumo2 predominantly in forebrain neurons resulted in marked impairments in various cognitive tests, including episodic and fear memory. Our data further suggest that these abnormalities are attributable neither to constitutive changes in gene expression nor to alterations in neuronal morphology, but they involve impairment in dynamic SUMOylation processes associated with synaptic plasticity. Finally, we provide evidence that dysfunction on hippocampal-based cognitive tasks was associated with a significant deficit in the maintenance of hippocampal long-term potentiation in Sumo2 knockout mice. Collectively, these data demonstrate that protein conjugation by SUMO2 is critically involved in cognitive processes.





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Publication Info

Yu, Shu, Francesca Galeffi, Ramona M Rodriguiz, Zhuoran Wang, Yuntian Shen, Jingjun Lyu, Ran Li, Joshua D Bernstock, et al. (2020). Small ubiquitin-like modifier 2 (SUMO2) is critical for memory processes in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(11). pp. 14750–14767. 10.1096/fj.202000850rr Retrieved from

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Huaxin Sheng

Associate Professor in Anesthesiology

We have successfully developed various rodent models of brain and spinal cord injuries in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma, subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression injury. We also established cardiac arrest and hemorrhagic shock models for studying multiple organ dysfunction.  Our current studies focus on two projects. One is to examine the efficacy of catalytic antioxidant in treating cerebral ischemia and the other is to examine the efficacy of post-conditioning on outcome of subarachnoid hemorrhage induced cognitive dysfunction.


Dennis Alan Turner

Professor of Neurosurgery

Current clinical research interests include clinical trials regarding adaptive or closed-loop deep brain stimulation with novel devices, cellular, and gene therapy in Parkinson disease. Additional trials have included gene therapy for Alzheimer's disease and sensory restoration for development of brain machine interfaces. Clinical treatments include deep brain stimulation, which is now a common procedure for treating Parkinson disease and tremor. Translational approaches include testing new devices and stimulation patterns in the operating room. Pre-clinical research interests focus on evaluation of cerebral perfusion and metabolism changes with stroke, aging and Alzheimer's disease, using both in vivo and in vitro approaches. These basic science interests include new approaches to cerebral blood flow enhancement with brain stimulation, optical imaging of the brain, cellular understanding of metabolism using direct substrate recordings (ie, oxygen, glucose, lactate, respirometry) and developing new methods to understand neurovascular coupling, analyzing complex interactions between neurons, astrocytes and blood vessels.  Further interests include changes in cerebral blood flow with stroke and enhanced recovery after stroke.


William Christopher Wetsel

Associate Professor in Psychiatry and Behavioral Sciences

Last Updated: 27 October 2020

My laboratory uses genetically-modified mice to study the roles that certain genes and gene products play in the presentation of abnormal neuroendocrine, neurological, and psychiatric responses. Traditionally, the identification of neuroendocrine dysfunction has involved biochemical analyses of hormonal responses, those for neurological disorders have relied upon behavioral and postmortem analyses, and those for psychiatric conditions have depended upon phenomenology.  The use of genetic technologies has allowed specific genes in selected cells and in neural pathways to be related to certain molecular, biochemical, cellular, physiological, and behavioral dysfunctions. As the Director of the Mouse Behavioral and Neuroendocrine Analysis Core Facility at Duke University (, we have phenotyped many different lines of inbred and mutant mice for my own work as well as for investigators at Duke and at other research institutions. As a consequence, we have helped to develop many different mouse genetic models of neuroendocrine and neuropsychiatric illness. We are working also with academic medicinal chemists and/or certain pharmacological/biotechnological companies to identify novel compounds that will ameliorate abnormal responses in various mutant mouse models. Some of these preclinical studies have formed a basis for clinical trials in humans.


Wei Yang

Professor in Anesthesiology

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