Yue Feng, MD, PhD

(she/her)

Professor, Department of Pharmacology and Chemical Biology, School of Medicine

MyNCBI Bibliography Department Website Lab Website

Graduate Programs

Full Member - Biochemistry, Cell and Developmental Biology
Full Member - Genetics and Molecular Biology

Education

PhD, Vanderbilt University, 1990
MD, Bejing Medical University, 1986

Contact Information

Email: yfeng@emory.edu

Phone: 404-727-0351

Address:
O. Wayne Rollins Research Center, Room 5025 1510 Clifton Road NE Atlanta, GA 30322 1940-001-1AF

Using a multidisciplinary strategy based on molecular, cellular, genetics and pharmacological approaches, we are investigating how RNA homeostasis and cellular behavior govern normal brain development and function and how RNA malfunction in distinct brain cell types leads to human brain disorders.

1) Non-coding RNA in human brain diseases
We investigate novel mechanisms that regulate the biogenesis and function of regulatory non-coding RNAs (ncRNAs), including long noncodoing RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), in human neuronal and glial development and how their dysregualtion leads to neuropsychiatric and neurodegenerative disorders, represented by schizophrenia and Alzheimer's disease. Using human neuronal and glial cells as well as mopuse models, we employ genetic and biochemical approaches to elucidate the functional interplay of cnRNAs with various RNA binding proteins that control broad gene networks involved in brain disorders.

2) Alternative splicing, homeostasis and translation of mRNAs in brain diseases
We currently focus on the selective RNA-binding protein QKI, a key factor controlling proliferation and differentiation of myelin producing glia and myelin formation via regulating pre-mRNA splicing, biogenesis of non-coding RNAs, as well as mRNA stability and translation. Emerging evidence indicated the involvement of QKI function in several human diseases, including myelin repair in multiple sclerosis, white matter defects in schizophrenia, and glioma tumorigenesis. We have established molecular, cellular and animal models to investigate mRNA targets and cellular mechanisms that underlie QKI-dependent myelinogenesis and axonal protection. Genetic and pharmacological approaches are employed to manipulate QKI function to promote myelination.