The Hu Lab

The Hu lab is interested in studying molecular and cellular mechanisms involved in neuro-degeneration.

Frontotemporal Lobar Degeneration with ubiquitin and TDP-43 positive inclusions (FTLD-U) is a very common early onset dementia disease often associated with Amyotrophic Lateral Sclerosis (ALS). Mutations in Progranulin (PGRN), resulting in PGRN haplo-insufficiency, are one of the main causes of FTLD-TDP. A transmembrane protein of unknown function, TMEM106B, is a risk factor for FTLD-TDP with PGRN mutations. More recently, mutations in C9orf72, a gene of unknown function, were found to the main cause of mixed ALS/FTLD phenotypes. We are trying to understand the cellular functions of PGRN, TMEM106B and C9orf72 as well as other genes implicated in FTLD/ALS. 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 by these FTLD proteins, such as regulation of autophagy-lysosome functions by PGRN, TMEM106B and C9orf72.

Postdoctoral positions are currently available. We are seeking candidates who have a strong background in biochemistry, molecular biology, cell biology, or mouse genetics with interests in neurodegeneration.
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Fenghua Hu, PhD

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 received her postdoctoral training at Yale University.

Selected Publications

Zhou X, Sun L, Brady OA, Murphy KA, Hu F. Elevated TMEM106B levels exaggerate lipofuscin accumulation and lysosomal dysfunction in aged mice with progranulin deficiency Acta Neuropathologica Communications. 2017 Jan 26;5(9).

Sullivan PM, Zhou X, Robins AM, Paushter DH, Kim D, Smolka MB, Hu F. The ALS/FTLD associated protein C9orf72 associates with SMCR8 and WDR41 to regulate the autophagy-lysosome pathway. Acta Neuropathologica Communications. 2016 May 18:4(51).

Zhou X, Sun L, Oliveira F, Qi X, Brown WJ, Smolka M, Sun Y, Hu F. Prosaposin facilitates sortilin independent lysosomal targeting of progranulin. J Cell Biol. 2015 Sep 14;210(6):991-1002.

Hsu F, Hu F, Mao Y. Spatiotemporal control of phosphatidylinositol 4-phosphate by Sac2 regulates endocytic recycling. J Cell Biol. 2015 Apr 13;209(1):97-110.

Brady OA, Zhou X, Hu F. Regulated intramembrane proteolysis of the frontotemporal lobar degeneration (FTLD) risk factor,TMEM106B, by Signal Peptide Peptidase-like 2a (SPPL2a). J Biol Chem. 2014 Jul 11;289(28):19670-19680.

Brady OA, Zheng Y , Hu F.  The Frontotemporal Lobe degeneration risk factor, TMEM106B, regulates lysosomal morphology and function. Hum Mol Genet. 2012 Nov 6.

Zheng Y, Brady OA, Meng PS, Mao Y, Hu F. C-terminus of Progranulin interacts with the beta-propeller region of Sortilin to regulate Progranulin trafficking. PLoS One 2011 Jun 15; 6(6): e21023.

Brady OA, Meng PS, Zheng Y, Mao Y, Hu F.Regulation of TDP-43 aggregation by phosphorylation and p62/SQSTM1. Journal of Neurochemistry  2011 Jan; 116(2): 248-59.

Hu F, Padukkavidana T, Vægter CB, Brady OA, Zheng Y, Mackenzie IR, Feldman HH, Nykjaer A, Strittmatter SM.
Sortilin-Mediated Endocytosis Determines Levels of the Frontotemporal Dementia Protein, Progranulin. Neuron 2010 Nov 18;68(4): 654-67.

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