Fenghua Hu is an Assistant Professor in the Department of Molecular Biology and Genetics and is a member of the Weill Institute for Cell and Molecular Biology (Weill Institute). She received her B.S. in Biochemistry from Peking University in China in 1997 and her Ph.D. from Baylor College of Medicine in 2002. She did her postdoctoral training at Yale University. She is presently a member of the graduate Fields of Biochemistry, Molecular, and Cell Biology (BMCB), Genetics, Genomics and Development (GGD), and Biological and Biomedical Sciences (BBS).
The Hu lab is interested in studying molecular and cellular mechanisms involved in neurodegeneration, particularly frontotemporal Lobar Degeneration (FTLD) and Amyotrophic Lateral Sclerosis (ALS). We are trying to understand the cellular and physiological functions of several genes associated with ALS/FTLD, such as PGRN, TMEM106B and C9orf72. We hope our studies will not only shed light on the molecular and cellular mechanisms of FTLD but also on the regulation of normal cellular functions and physiology by these FTLD proteins, such as regulation of autophagy-lysosome functions by PGRN, TMEM106B and C9orf72.
Fenghua currently teaches BIOMG 6360, "Functional organization of eukaryotic cells", and participates in BMCB graduate courses.
Awards and Honors
- New Investigator Award (2013) Alzheimer's Association
- Pilot grant (2012) AFTD
- Zhou, X., Sullivan, P. M., Sun, L., & Hu, F. (2017). The interaction between progranulin and prosaposin is mediated by granulins and the linker region between saposin B and C. JNC: Journal of Neurochemistry. 143:236-243.
- Zhou, X., Paushter, D. H., Feng, T., Sun, L., Reinheckel, T., & Hu, F. (2017). Lysosomal processing of progranulin. Molecular Neurodegeneration. 12:6.
- Zhou, X., Paushter, D. H., Feng, T., Pardon, C. M., Mendoza, C. S., & Hu, F. (2017). Regulation of cathepsin D activity by the FTLD protein progranulin. Acta Neuropathologica. 134:151-153.
- Zhou, X., Sun, L., Bracko, O., Choi, J. W., Jia, Y., Nana, A. L., Brady, O. A., Hernandez, Jean C. Cruz,, Nishimura, N., Seeley, W. W., & Hu, F. (2017). Impaired prosaposin lysosomal trafficking in frontotemporal lobar degeneration due to progranulin mutations. Nature Communications. 8:14.
- Zhou, X., Sun, L., Brady, O. A., Murphy, K. A., & Hu, F. (2017). Elevated TMEM106B levels exaggerate lipofuscin accumulation and lysosomal dysfunction in aged mice with progranulin deficiency. Acta Neuropathologica Communications. 5:9.
- Sullivan, P. M., Zhou, X., Robins, A., Paushter, D., Kim, D., Smolka, M., & Hu, F. (2016). The ALS/FTLD associated protein C9orf72 associates with SMCR8 and WDR41 to regulate the autophagy-lysosome pathway. Acta Neuropathologica Communications. 4.
- Zhou, X., Sun, L., Oliveria, F., Qi, X., Brown, W. J., Smolka, M., Sun, Y., & Hu, F. (2015). Prosaposin facilitates sortilin independent lysosomal targeting of progranulin. JCB: The Journal of Cell Biology. 210:991.
- Brady, O. A., Zheng, Y., Murphy, K., Huang, M., & Hu, F. (2013). The frontotemporal lobar degeneration risk factor, TMEM106B, regulates lysosomal morphology and function. Human Molecular Genetics. 22:685-695.
- Zheng, Y., Brady, O., Meng, P., Mao, Y., & Hu, F. (2011). C-terminus of Progranulin interacts with the beta-propeller region of Sortilin to regulate Progranulin trafficking. PLOS One. 6:e21023.
- Hu, F., Padukkavidana , T., Brady, O. A., Zheng, Y., & Strittmatter, S. (2010). Sortilin1-Mediated Endocytosis Determines Levels of the Fronto-Temporal Dementia Protein, Progranulin. Neuron. 68:654-67 .