Zhong Lab

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Molecular Regeneration and Neuroimaging Laboratory

The primary interest of Zhong lab is to elucidate the molecular mechanisms that drive and direct axon growth and regeneration during early development and especially after injury or degenerative disease. We make extensive use of genetically modified mice to model disease conditions and to manipulate axon growth-related signaling cascades in vivo

Signaling pathways controlling axon growth and regeneration 

The goal of our research is to enable axon regeneration in the injured central nervous system, using experimental models of spinal cord injury and glaucoma. Several lines of genetically modified mice allow us to selectively activate or inactivate specific signaling molecules in neurons of interest in vivo. We assess regeneration phenotypes using high-resolution imaging, and we test for possible recovery of motor or visual behaviors. 

Develop new treatment options for the RASopathies in mouse models 

The RASopathies (also referred to as neuro-cardio-facio-cutaneous syndromes) are a related group of complex neurodevelopmental disorders affecting up to 1 in1000 live births. Mutations affecting the RAS–RAF–MAP kinase signaling pathway have been causally linked to the RASopathies. We have developed several mouse models which mimic the neurological aspects of human RASopathies’ syndromes. We investigate the underlying pathological causes of devise symptoms and test possible therapeutic strategies. 

Zhong lab conducting research.

Zhong lab conducting research.

Featured Research Projects

RESEARCH PROJECT: 
In Progress
We have recently identified the B-RAF kinase signaling as a key player in embryonic axon growth signaling, and are testing B-RAF as a possible driver of regenerative growth.
RESEARCH PROJECT: 
In Progress
The reliable tracing of axonal connections is essential for any deeper understanding of nervous system function.
RESEARCH PROJECT: 
In Progress
The NCFCS, which include Leopard Syndrome, Noonan Syndrome and Neurofibromatosis type I, are linked to loss- and gain-of function mutations in the RAF signaling pathway.