Russell W Mellen

Russell W Mellen,

Pre-doctoral Fellow

Business Phone: (352) 273-8600
Business Email:

About Russell W Mellen

Growing up in sunny southern California, Russell moved to Florida after receiving his Bachelors in Science in Biology from Azusa Pacific University in 2015. During his time as an undergraduate, Russell worked in the lab of Dr. Charles Chen, studying the effects of increased atmospheric carbon dioxide on the photosynthetic capacity of rice plants. This research project took Russell out of California and around the world, as much of the project was conducted in Tsukubamirai, Japan. It was during this time, while trudging through rice patties in the summer sun, that Russell realized that scientific research was where his passions lie. Growing up, Russell was always acutely aware of the life-altering effects of genetic disorders, as the autosomal recessive disorder phenylketonuria runs in his family and affects his close relatives. With his graduate studies looming, this led to Russell shifting his area of research focus to attempt to bring therapy to others who suffer from genetic disorders, ultimately culminating in Russell joining the Boye lab. When not in lab Russell can be found exercising at Southwest Recreation Center or exploring Florida’s beaches. Russell’s research focuses on CRISPR-Cas9 mediated knockout of dominant congenital diseases


Travel Grant Recipient
2019 · American Society for Gene and Cell Therapy

Research Profile

Mutations in GUCY2D, the gene encoding retinal guanylate cyclase-1 (retGC1), are the leading cause of autosomal dominant cone-rod dystrophy. GUCY2D-CORD6 patients present with loss of visual acuity, abnormal color vision, photophobia, visual field loss and macular atrophy within the first decade. Rod degeneration and peripheral visual field loss follow. We have made significant progress towards clinical application of a gene replacement therapy for LCA due to recessive mutations in GUCY2D (LCA1), but a different approach is needed for CORD6 where gain of function mutations are responsible for dysfunction and dystrophy. CRISPR/Cas9 has received considerable attention as a mechanism to permanently modify disease-causing genes. My dissertation research seeks to develop strategies for site-specific knock out of either the mutated allele or the entire GUCY2D gene in order to provide therapy.


Novel AAV44.9-Based Vectors Display Exceptional Characteristics for Retinal Gene Therapy.
Molecular therapy : the journal of the American Society of Gene Therapy. 28(6):1464-1478 [DOI] 10.1016/j.ymthe.2020.04.002. [PMID] 32304666.
Erratum for Shen et al., “Identification of a Novel Enhancer/Chromatin Opening Element Associated with High-Level γ-Globin Gene Expression”.
Molecular and cellular biology. 39(11) [DOI] 10.1128/MCB.00168-19. [PMID] 31088916.
Identification of a Novel Enhancer/Chromatin Opening Element Associated with High-Level γ-Globin Gene Expression.
Molecular and cellular biology. 38(19) [DOI] 10.1128/MCB.00197-18. [PMID] 30012865.


Bachelors of Science in Biology
2013-2015 · Azusa Pacific University
2011-2013 · Orange Coast College

Contact Details

(352) 273-8600