We are interested in identifying novel pathways that enable cellular and organismal adaptation to metabolic stress and changes in environmental conditions. We also study how these pathways go awry in human diseases such as cancer, neurodegeneration and metabolic syndrome, in order to engineer new therapeutic modalities.
To address these questions, our lab uses a multidisciplinary approach to study the biochemical functions of the lysosome in vitro and in vivo. Lysosomes are membrane-bound compartments that degrade macromolecules and clear damaged organelles to enable cellular adaptation to various metabolic states. Lysosomal function is critical for organismal homeostasis—mutations in genes encoding lysosomal proteins cause severe human disorders known as lysosomal storage diseases, and lysosome dysfunction is implicated in age-associated diseases including cancer, neurodegeneration and metabolic syndrome.
By developing novel tools and harnessing the power of metabolomics, proteomics and functional genomics, our lab will define 1) how the lysosome communicates with other cellular compartments to fulfill the metabolic demands of the cell under various metabolic states, 2) and how its dysfunction leads to rare and common human diseases. Using insights from our research, we will engineer novel therapies to modulate the pathways that govern human disease.
Monther Abu-Remaileh, Ph.D.
ChEM-H Institute Scholar
Assistant Professor of Chemical Engineering
Assistant Professor of Genetics (by courtesy)
Email: monther (at) stanford.edu
Nouf Laqtom, Ph.D.
Email: nlaqtom (at) stanford.edu
Email: clin5 (at) stanford.edu
Wentao Dong, Ph.D.
Email: wdong5 (at) stanford.edu
Email: austinmu (at) stanford.edu
Ali Ghoochani, Ph.D.
Email: aligh (at) stanford.edu
Email: uchemed (at) stanford.edu
1. Weber RA, Yen FS, Nicholson SPV, Alwaseem H, Bayraktar EC, Alam M, Timson RC, La K, Abu-Remaileh M, Molina H, Birsoy K. (2020) Maintaining Iron Homeostasis Is the Key Role of Lysosomal Acidity for Cell Proliferation. Mol Cell. 77(3):645-655.e7. doi: 10.1016/j.molcel.2020.01.003
2. Rogala KB, Gu X, Kedir JF, Abu-Remaileh M, Bianchi LF, Bottino AMS, Dueholm R, Niehaus A, Overwijn D, Fils AP, Zhou SX, Leary D, Laqtom NN, Brignole EJ, Sabatini DM. (2019) Structural basis for the docking of mTORC1 on the lysosomal surface. Science. doi: 10.1126/science.aay0166. [Epub ahead of print]
3. Bayraktar EC, Baudrier L, Özerdem C, Lewis CA, Chan SH, Kunchok T, Abu-Remaileh M, Cangelosi AL, Sabatini DM, Birsoy K, Chen WW. (2019) MITO-Tag Mice enable rapid isolation and multimodal profiling of mitochondria from specific cell types in vivo. Proc Natl Acad Sci U S A. 116 (1): 303-312 doi: 10.1073/pnas.1816656115
4. Kanarek N, Keys HR, Cantor JR, Lewis CA, Chan SH, Kunchok T, Abu-Remaileh M, Freinkman E, Schweitzer LD, Sabatini DM. (2018) Histidine catabolism is a major determinant of methotrexate sensitivity. Nature. 559 (7715): 632-636 doi: 10.1038/s41586-018-0316-7
5. Wyant GA#, Abu-Remaileh M#, Frenkel EM, Laqtom N, Dharamdasani V, Lewis CA, Chan SH, Heinze I, Ori A, Sabatini DM. (2018) NUFIP1 is a ribosome receptor for starvation-induced ribophagy. Science. 360 (6390): 751-758 doi: 10.1126/science.aar2663
6. Abu-Remaileh M#, Wyant GA#, Kim C, Laqtom N, Abbasi M, Chan SH, Freinkman E, Sabatini DM. (2017) Lysosomal metabolomics reveals V-ATPase- and mTOR-dependent mechanisms for the efflux of amino acids from lysosomes. Science. 358 (6364): 807-813 doi: 10.1126/science.aan6298
7. Wyant GA#, Abu-Remaileh M#, Wolfson RL, Chen WW, Freinkman E, Danai LV, Vander Heiden M, Sabatini DM. (2017) mTORC1 activator SLC38A9 is required to efflux essential amino acids from lysosomes and use protein as a nutrient. Cell. 171 (3): 642-654 doi: 10.1016/j.cell.2017.09.046
8. Cantor JR, Abu-Remaileh M, Kanarek N, Freinkman E, Gao X, Louissaint A Jr, Lewis CA, Sabatini DM. (2017) Physiologic Medium Rewires Cellular Metabolism and Reveals Uric Acid as an Endogenous Inhibitor of UMP Synthase. Cell. 169 (2): 258-272 doi: 10.1016/j.cell.2017.03.023
9. Wolfson RL, Chantranupong L, Wyant GA, Gu X, Orozco JM, Shen K, Condon KJ, Petri S, Kedir J, Scaria SM, Abu-Remaileh M, Frankel WN, Sabatini DM. (2017) KICSTOR recruits GATOR1 to the lysosome and is necessary for nutrients to regulate mTORC1. Nature. 543 (7645): 438-442 doi: 10.1038/nature21423.
For full list visti Google Scholar.
Current Stanford graduate students from all programs (PhD, MD, PhD/MD) who are interested in joining our lab are welcome to contact Monther directly. Please send a current CV in pdf format.
Postdocs and Clinical Fellows:
Motivated postdocs and clinical fellows with expertise in biochemistry, molecular biology, metabolism, mouse physiology or neurobiology are encouraged to apply. Please email a cover letter, your CV, and contact information for three references to Monther.
Students who are interested in conducting biomedical research and being part of our multidisciplinary team are welcome to email Monther for opportunities.
Current masters students who are enrolled in national or international programs and hoping to join our lab as visiting students (6-12 month duration) to complete their thesis are welcome. Research experience in biology, biochemistry or chemistry is an advantage. Please email a cover letter, your CV, and contacts of two references to Monther.
ChEM-H Building, Room: N227
290 Jane Stanford Way
Stanford, CA 94305
Our Lab is located at the new building that hosts both ChEM-H and Wu Tsai Neuroscience Research Center.