Yarui Diao

Assistant Professor of Cell Biology

Amgen Faculty Mentor

CMB - Cell Biology

DSCB - Developmental Genetics

Campus mail: 349 Nanaline Duke Building, Durham, NC 27705

Phone: (919) 684-8553

I lead a functional genomics lab at Duke Cell Biology. We are particularly interested in developing and applying cutting-edge functional genomics tools to understand the transcriptional regulatory mechanisms controlling tissue regeneration in healthy and disease conditions.

Education and Training

University of Hong Kong (China), Ph.D. 2011

Selected Grants and Awards

Publications

A compendium of promoter-centered long-range chromatin interactions in the human genome.

A large number of putative cis-regulatory sequences have been annotated in the human genome, but the genes they control remain poorly defined.

A Molecular Switch Regulating Cell Fate Choice between Muscle Progenitor Cells and Brown Adipocytes.

During mouse embryo development, both muscle progenitor cells (MPCs) and brown adipocytes (BAs) are known to derive from the same Pax7+/Myf5+ progenitor cells. However, the underlying mechanisms for the cell fate control remain unclear.

A new class of temporarily phenotypic enhancers identified by CRISPR/Cas9-mediated genetic screening.

With <2% of the human genome coding for proteins, a major challenge is to interpret the function of the noncoding DNA.

A tiling-deletion-based genetic screen for cis-regulatory element identification in mammalian cells.

Millions of cis-regulatory elements are predicted to be present in the human genome, but direct evidence for their biological function is scarce.

Chromatin architecture reorganization during stem cell differentiation.

Higher-order chromatin structure is emerging as an important regulator of gene expression.

Circular ecDNA promotes accessible chromatin and high oncogene expression.

Oncogenes are commonly amplified on particles of extrachromosomal DNA (ecDNA) in cancer1,2, but our understanding of the structure of ecDNA and its effect on gene regulation is limited.

Genome-wide analysis of miRNA signature in the APPswe/PS1ΔE9 mouse model of alzheimer's disease.

Alzheimer's disease (AD) is the most common cause of dementia. One of the pathological hallmarks of AD is amyloid β (Aβ) deposition.

MicroRNAs 99b-5p/100-5p Regulated by Endoplasmic Reticulum Stress are Involved in Abeta-Induced Pathologies.

Alzheimer's disease (AD) is the most common cause of dementia. Amyloid β (Abeta, Aβ) deposition and intracellular tangles are the pathological hallmarks of AD.

miR-203, a tumor suppressor frequently down-regulated by promoter hypermethylation in rhabdomyosarcoma.

Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma found in children and young adults. It is characterized by the expression of a number of skeletal muscle-specific proteins, including MyoD and muscle α-actin.

NAD metabolic dependency in cancer is shaped by gene amplification and enhancer remodelling.

Precision oncology hinges on linking tumour genotype with molecularly targeted drugs1; however, targeting the frequently dysregulated metabolic landscape of cancer has proven to be a major challenge2.

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Yarui Diao

Education and Training

Selected Grants and Awards

Publications

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