The Hu Lab

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The Hu lab is interested in studying signaling pathways and mechanisms involved in neuro-degeneration.

We are interested in dissecting the disease mechanism of Frontal temporal lobe degeneration (FTLD) due to mutations in the progranulin gene. Progranulin encodes a secreted growth factor that has been implicated in wound healing and cell proliferation. But its function in the nervous system is still unclear. In FTLD patients with progranulin mutation, a DNA and RNA binding protein called TDP-43 was found to accumulate in the cytoplasm in ubiquitinated, phosphorylated and cleaved forms. We are interested in studying pathways that control progranulin trafficking and progranulin signaling. We have shown progranulin is delivered into lysosomes by sortilin. We are interested in further exploring potential functions of progranulin in lysosomes and how that’s related to neurodegeneration.

Recent studies also identified TMEM106B as a new risk factor for FTLD with progranulin mutations. Our preliminary studies have shown TMEM106B might affect lysosomal function. We are in the process of dissecting TMEM106B functions in the lysosomes and in the disease progression of FTLD with progranulin mutations.

Finally we are also investigating mechanisms involved in regulating TDP-43 aggregation and clearance using mammalian cell culture and zebrafish models.

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.


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, where she was awarded a Postdoctoral Fellowship from Paralyzed Veteran of American foundation.

Selected Publications

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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