Dr. Haiyang Yu uses cutting-edge approaches in cell biology, molecular biology, and genetics to study neurodegenerative disorders such as frontotemporal dementia (FTD), Lou Gehrig’s disease (amyotrophic lateral sclerosis; ALS), and Alzheimer’s disease. He has also developed novel therapeutic strategies by specifically degrading cytoplasmic protein inclusions.
Dr. Yu grew up in Chengde, China. He received his bachelor’s degree summa cum laude in Biological Sciences from Nankai University, where he started his research in cell biology. He earned his Ph.D. in Molecular Cell Biology from Washington University in St. Louis, where he focused on how the actin cytoskeleton is regulated by Rho family small GTPases.
As a postdoctoral fellow mentored by Dr. Don Cleveland, Dr. Yu focused on TDP-43, a nuclear RNA-binding protein essential for neuronal health, which forms cytoplasmic aggregates during neurodegenerative disease. He and his colleagues found that TDP-43 de-mixes into complex liquid-crystal droplets when it loses its ability to bind RNA. These droplets, which they named anisosomes, form in neurons in vivo when proteasome activity is inhibited. For this work, he received an NIH postdoctoral fellowship (F32) and a Pathway to Independence award (K99/R00).
Dr. Yu joined the UT Southwestern faculty in 2021 as an Assistant Professor in the Center for Alzheimer’s and Neurodegenerative Diseases, with a secondary appointment in the Department of Molecular Biology. He is also an investigator in the Peter O’Donnell Jr. Brain Institute.
- Membraneless organelles
- Neurodegenerative Diseases
- Protein phase separation
- Protein quality control and degradation pathways
- HSP70 chaperones RNA-free TDP-43 into anisotropic intranuclear liquid spherical shells.
- Yu H, Lu S, Gasior K, Singh D, Vazquez-Sanchez S, Tapia O, Toprani D, Beccari MS, Yates JR, Da Cruz S, Newby JM, Lafarga M, Gladfelter AS, Villa E, Cleveland DW, Science 2021 02 371 6529
- Cytoplasmic TDP-43 De-mixing Independent of Stress Granules Drives Inhibition of Nuclear Import, Loss of Nuclear TDP-43, and Cell Death.
- Gasset-Rosa F, Lu S, Yu H, Chen C, Melamed Z, Guo L, Shorter J, Da Cruz S, Cleveland DW, Neuron 2019 Apr 102 2 339-357.e7
- A role for genetic susceptibility in sporadic focal segmental glomerulosclerosis.
- Yu H, Artomov M, Brähler S, Stander MC, Shamsan G, Sampson MG, White JM, Kretzler M, Miner JH, Jain S, Winkler CA, Mitra RD, Kopp JB, Daly MJ, Shaw AS J. Clin. Invest. 2016 Mar 126 3 1067-78
- Membralin deficiency dysregulates astrocytic glutamate homeostasis leading to ALS-like impairment.
- Jiang LL, Zhu B, Zhao Y, Li X, Liu T, Pina-Crespo J, Zhou L, Xu W, Rodriguez MJ, Yu H, Cleveland DW, Ravits J, Da Cruz S, Long T, Huang TY, Xu H, J. Clin. Invest. 2019 May 130
- Tuning Apoptosis and Neuroinflammation: TBK1 Restrains RIPK1.
- Yu H, Cleveland DW Cell 2018 Sep 174 6 1339-1341
- Intravital and Kidney Slice Imaging of Podocyte Membrane Dynamics.
- Brähler S, Yu H, Suleiman H, Krishnan GM, Saunders BT, Kopp JB, Miner JH, Zinselmeyer BH, Shaw AS J. Am. Soc. Nephrol. 2016 Apr
- Rac1 activation in podocytes induces rapid foot process effacement and proteinuria.
- Yu H, Suleiman H, Kim AH, Miner JH, Dani A, Shaw AS, Akilesh S Mol. Cell. Biol. 2013 Dec 33 23 4755-64
- Allosteric activation of functionally asymmetric RAF kinase dimers.
- Hu J, Stites EC, Yu H, Germino EA, Meharena HS, Stork PJS, Kornev AP, Taylor SS, Shaw AS, Cell 2013 Aug 154 5 1036-1046
- Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosis.
- Akilesh S, Suleiman H, Yu H, Stander MC, Lavin P, Gbadegesin R, Antignac C, Pollak M, Kopp JB, Winn MP, Shaw AS, J Clin Invest 2011 Oct 121 10 4127-37
- Mutation that blocks ATP binding creates a pseudokinase stabilizing the scaffolding function of kinase suppressor of Ras, CRAF and BRAF.
- Hu J, Yu H, Kornev AP, Zhao J, Filbert EL, Taylor SS, Shaw AS, Proc Natl Acad Sci U S A 2011 Apr 108 15 6067-72