Fang He, Ph.D.
Affiliations: | 1999-2001 | Biology | Jiangxi Institute of Education |
2001-2004 | Biochemistry and Molecular Biology | Nanjing University, Nanjing Shi, Jiangsu Sheng, China | |
2004-2011 | Biological Sciences | Louisiana State University, Baton Rouge, LA, United States | |
2011- | Neurology | University of Michigan, Ann Arbor, Ann Arbor, MI |
Area:
Fly Genetics, NeurodegenerationWebsite:
https://www.linkedin.com/pub/fang-he/95/812/8b0Google:
"Fang He"Bio:
Dr. He’s research mainly focuses on genetic factors in repeat associated neurodegenerative diseases and the molecular basis for their pathogenesis. Dr. He has a strong background in cell and molecular biology, with specific training and expertise in Drosophila genetics. As a PhD student, he developed and studied Drosophila model of human type II hyperprolinemia caused by null mutation of gene P5CDH, which carries symptoms of childhood mental retardation. He also conducted research on rRNA post-transcriptional modification by generation of Nopp140 knock-out Drosophila lines. As a post-doctoral fellow in University of Michigan, He applied Drosophila techniques to study fragile X-associated Tremor/Ataxia (FXTAS) and Amyotrophic Lateral Sclerosis C9 type (C9ALS). He developed several fly lines with different versions of CGG repeats to study FXTAS and fly lines with 5’ and intronic GGGGCC repeat in different sizes to study C9ALS. Using these flies he has made series important findings, including that the Repeat-associated Non-ATG (RAN) translation is an important component for both CGG and GGGGCC repeat toxicity.
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Publications
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He F, Flores BN, Krans A, et al. (2020) The carboxyl termini of RAN translated GGGGCC nucleotide repeat expansions modulate toxicity in models of ALS/FTD. Acta Neuropathologica Communications. 8: 122 |
Linsalata AE, He F, Malik AM, et al. (2019) DDX3X and specific initiation factors modulate FMR1 repeat-associated non-AUG-initiated translation. Embo Reports. e47498 |
Sellier C, Buijsen RA, He F, et al. (2017) Translation of Expanded CGG Repeats into FMRpolyG Is Pathogenic and May Contribute to Fragile X Tremor Ataxia Syndrome. Neuron |
Yang WY, He F, Strack RL, et al. (2016) Small Molecule Recognition and Tools to Study Modulation of r(CGG)exp in Fragile X-Associated Tremor Ataxia Syndrome. Acs Chemical Biology |
He F, Jones JM, Figueroa-Romero C, et al. (2016) Screening for novel hexanucleotide repeat expansions at ALS- and FTD-associated loci. Neurology. Genetics. 2: e71 |
Oh SY, He F, Krans A, et al. (2015) RAN translation at CGG repeats induces ubiquitin proteasome system impairment in models of fragile X-associated tremor ataxia syndrome. Human Molecular Genetics. 24: 4317-26 |
He F, James A, Raje H, et al. (2015) Deletion of Drosophila Nopp140 induces subcellular ribosomopathies. Chromosoma. 124: 191-208 |
He F, Krans A, Freibaum BD, et al. (2014) TDP-43 suppresses CGG repeat-induced neurotoxicity through interactions with HnRNP A2/B1. Human Molecular Genetics. 23: 5036-51 |
Todd PK, Oh SY, Krans A, et al. (2013) CGG repeat-associated translation mediates neurodegeneration in fragile X tremor ataxia syndrome. Neuron. 78: 440-55 |
Meisler MH, Grant AE, Jones JM, et al. (2013) C9ORF72 expansion in a family with bipolar disorder. Bipolar Disorders. 15: 326-32 |