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Understanding organelle-associated disorders requires us to look not further, but deeper—into the subcellular compartments where dysfunction quietly begins. 

Program Affiliations

Center of Excellence

Biography

Professor Nouf Laqtom is an Ibn Rushd Assistant Professor at KAUST, where she leads the Subcellular Metabolism and Disease Lab. Her research focuses on how organelle dysfunction — particularly within lysosomes and the endoplasmic reticulum — drives rare neurodegenerative diseases. By integrating advanced multi-omics, CRISPR screens, and organelle purification techniques, her lab investigates how subcellular disruptions impair cellular function and homeostasis, with an emphasis on lysosomal storage disorders like Batten disease. 

 

In 2023, prior to joining KAUST, Professor Laqtom conducted postdoctoral research at the Whitehead Institute for Biomedical Research at MIT and in the Department of Chemical Engineering at Stanford University, U.S. During this time, she co-developed the LysoTag mouse model and contributed to several pioneering studies in lysosomal and lipid metabolism. She earned her M.S. and Ph.D. in Biomedical Sciences from the University of Edinburgh, following a B.S. in Biology from King Abdulaziz University in Saudi Arabia. 

 

Professor Laqtom is the recipient of competitive research funding and has published in leading journals such as Nature and Cell Chemical Biology. She plays an active role on institutional research committees and fosters interdisciplinary collaboration. Her lab is dedicated to building a diverse, inclusive, and high-performing team with a strong commitment to translational impact in human disease research. 

Research Interests

Professor Nouf Laqtom’s research focuses on how dysfunction at the subcellular level — particularly within lysosomes and the endoplasmic reticulum — drives the onset and progression of rare neurodegenerative and metabolic diseases. 

To investigate these mechanisms, the Laqtom Lab integrates multi-omics profiling (including metabolomics, lipidomics, and proteomics), CRISPR-based genetic screening, and advanced organelle isolation techniques, such as Lyso-IP and ER-IP. These tools enable precise characterization of disrupted metabolic reactions within purified organelles and help identify molecular drivers of disease. 

Her team employs human iPSC-derived neuronal models and transgenic mouse models to examine how subcellular dysfunction impacts neuronal homeostasis, survival, and therapeutic response. Their work aims to elucidate disease mechanisms, identify diagnostic biomarkers, and uncover novel therapeutic targets with translational relevance. 

Keyword tag icon
Lysosomal Biology Subcellular Metabolism Metabolic Diseases Batten Disease Neurodegeneration iPSC-derived Neurons Organelle Isolation Multi-omics CRISPR Screening Metabolomics Lipidomics Proteomics Therapeutic Target Discovery

Education Profile

  • Postdoctoral Fellow, Department of Chemical Engineering, Stanford University, 2022

  • Postdoctoral Fellow, Department of Biology, Whitehead Institute-Massachusetts Institute of Technology, 2019

  • Lecturer, Division of Genomics and Biotechnology, King Abdulaziz University, 2016

  • M.Sc. and Ph.D. in Genomics and Pathway Biology, University of Edinburgh, 2013

Awards and Recognitions

  • KAUST Competitive Research Grant, 2025–2028 

  • Hevolution Foundation Award for Applications in Saudi Arabia, 2025–2027 

  • KAUST Smart Health Initiative Seed Grant, KAUST, 2023–2025 

Publications

  • Laqtom, N. N., Dong, W., Medoh, U. N., Cangelosi, A. L., Dharamdasani, V., Chan, S. H., Kunchok, T., Lewis, C. A., Heinze, I., Tang, R., Grimm, C., Do, A. N. D., Porter, F. D., Ori, A., Sabatini, D. M., & Abu-Remaileh, M. (2022). CLN3 is required for the clearance of glycerophosphodiesters from lysosomes. Nature, 609, 1005–1011. https://doi.org/10.1038/s41586-022-05221-y 

  • Armenta, D., Laqtom, N. N., Alchemy, G., Dong, W., Morrow, D., Poltorack, C., Nathanson, D., Abu-Remaileh, M., & Dixon, S. J. (2022). Ferroptosis inhibition by lysosomal protein catabolism. Cell Chemical Biology, 29(12), 1902–1913.e6. https://doi.org/10.1016/j.chembiol.2022.10.006 

  • Pedram, K., Laqtom, N. N., Shon, D. J., Di Spiezio, A., Riley, N. M., Saftig, P., Abu-Remaileh, M., & Bertozzi, C. R. (2022). Discovery of a pathway for endogenous mucin glycodomain catabolism in mammals. Proceedings of the National Academy of Sciences, 119(39), e2117105119. https://doi.org/10.1073/pnas.2117105119 

Research Areas

  • Chemical and Biological Engineering