Protect the Fold. Preserve the Brain.
We investigate how endoplasmic reticulum protein quality-control systems shape neural development, physiology, aging, and disease.
Our long-term goal is to understand how ER protein quality control and broader ER functions shape brain development, physiology, and disease and to translate these insights into therapeutic strategies for neurological disorders.
Our Goal
We Are Hiring!
We are recruiting a postdoctoral researcher and a research associate to join the Wang Lab at LSU Health Shreveport, with anticipated start dates in spring 2027 or later. Candidates interested in ER biology, protein quality control, neuroscience, or neurological disease are encouraged to contact the PI.
Positions
Launching at LSU Health Shreveport in 2027
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Approximately one-third of cellular proteins enter the endoplasmic reticulum (ER) for folding, maturation, or membrane integration. Because these processes are inherently error-prone, ER-associated degradation (ERAD) serves as a central protein quality-control pathway for eliminating aberrant proteins. The SEL1L–HRD1 ERAD complex constitutes a principal mammalian ERAD machinery, directing selected misfolded or improperly assembled ER proteins toward proteasomal degradation and thereby supporting cellular and tissue homeostasis.
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ERAD-associated neurodevelopmental disorder with onset in infancy (ENDI syndrome) is a rare condition caused by hypomorphic variants in the SEL1L–HRD1 ERAD machinery. Affected individuals exhibit developmental delay, intellectual disability, and neurological abnormalities, revealing an essential role for ER protein quality control in human brain development. Our research seeks to understand how impaired ERAD disrupts neural cells and contributes to neurodevelopmental disease.
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Age-related decline in protein quality control may compromise neuronal function and contribute to neurodegenerative diseases, including Alzheimer’s disease. We seek to understand how ERAD protects the aging brain and how its disruption influences disease progression.
Meet the PI
Huilun (Helen) Wang, PhD
Helen is an incoming Assistant Professor at LSU Health Shreveport. Her research bridges ER biology, protein quality control, and neuroscience to understand neurodevelopment and neurodegeneration.
She earned her Bachelor of Medicine from Peking University Health Science Center, completed her PhD training in the laboratory of Dr. Y. Eugene Chen at the University of Michigan, and pursued postdoctoral training under the mentorship of Drs. Ling Qi and Shengyi (Iris) Sun in the Qi-Sun Lab, initially at the University of Michigan and later at the University of Virginia.
Publication
Wang HH*, Wang Z, Lin LL, Verma SK, Gniadzik S, Wang H, Li ZJ, Jiang L, Kuyumcu-Martinez MN, Sun S*, Qi L*. “Functional rescue of a disease-linked ERAD pathway mutation via alternative splicing.” EMBO Journal. 2026 Mar 20. 2026 May;45(9):3230-3251. (*Co-corresponding authors)
Wang HH, Biunno I, Sun S, Qi L. “SEL1L-HRD1-mediated ERAD in mammals.” (Review) Nat Cell Biol. 2025 Jul;27(7):1063-1073.
Wang HH*, Lin LL*, Li JZ*, Wei X, Askander O, Cappuccio G, Hashem MO, Huber L, Munnich A, Alqahtani M, Pang Q, Burmeister M, Lu Y, Poirier K, Besmond C, Sun S, Brunetti-Pierri N, Alkuraya FS, Qi L. “Hypomorphic variants of SEL1L-HRD1 ER-associated degradation are associated with neurodevelopmental disorders.” The Journal of Clinical Investigation. 2024 Jan 16;134(2):e170054. (*Co-first authors)
Highlighted in: Umphred-Wilson K, Adoro S. Hypomorphic human SEL1L and HRD1 variants uncouple multiplayered ER-associated degradation machinery. The Journal of Clinical Investigation. 2024 Jan 16;134(2):e175448.
Media coverage: Molecular Physiology and Biological Physics Researchers Identify Protein Variants Affecting Human Neurodevelopment. Medicine in Motion News (UVA). December 6,2023.
Weis D*, Lin LL*, Wang HH*, Li JZ, Kusikova K, Ciznar P, Wolf HM, Less-Piller A, Wang Z, Wei X, Weis S, Skalicka K, Hrckova G, Danisovic L, Soltysova A, Yang TT, Feichtinger R, Mayr HA, Qi L. “Biallelic Cys141Tyr Variant of SEL1L is associated with neurodevelopmental disorders, agammaglobulinemia, and premature death.” The Journal of Clinical Investigation. 2024 Jan 16;134(2):e170882.(*Co-first authors)
Wang H, Guo Y, Lu H, Luo Y3, Hu W, Liang W, Garcia-Barrio MT, Chang L, Schwendeman A, Zhang J, Chen YE. “Krüppel-like factor 14 deletion in myeloid cells accelerates atherosclerotic lesion development.” Cardiovascular Research. 2022 Jan 29;118(2):475-488.
Funding
NIH Pathway to Independence Awards (K99/R00) 1K99HD118580-01A1 (PI) 2025-2030