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RESEARCH INTEREST

Cellular metabolic processes are catalyzed within specific compartments consisting of cytosol and different subcellular organelles. Many inherited metabolic diseases are caused by defects in genes that encode organellar proteins (commonly enzymes or transporters). These defects lead to the accumulation of metabolites that cannot be further processed or transported. The accumulation of a metabolite eventually results in organelle dysfunction, perturbation of cellular homeostasis, and organ damage. The brain is often impacted by organelle-associated metabolic disorders, including lysosomal and peroxisomal storage diseases and mitochondrial disorders.

 

Our laboratory is devoted to understanding the molecular and biochemical basis of organelle-associated metabolic disorders with a special focus on lysosomal storage diseases. Our goals include characterizing these metabolic disorders, understanding the impact of metabolic perturbations on organellar function and cellular homeostasis, developing tools to monitor organellar metabolism, searching for biomarkers, and designing therapies to restore normal metabolism.

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We conduct our experiments using cell cultures and transgenic mouse models, employing several subcellular multi-omics, high-throughput functional genomics, and biochemical techniques. Moreover, we collaborate with clinical geneticists and scientists at prestigious hospitals and institutions (such as Johns Hopkins Aramco Healthcare, King Faisal Specialist Hospital & Research Centre, and Stanford University). This provides us with valuable opportunities to access patient samples and cells as well as engage in hands-on training utilizing state-of-the-art technologies. Our research will offer novel insights into organellar metabolism and inform the development of future therapeutics of human diseases in which organelles are implicated. 

SPECIFIC RESEARCH PROJECTS 

Selected Publications

SELECTED PUBLICATIONS

# Equal contribution

 

1. Laqtom NN. 2023. Studying lysosomal function and dysfunction using LysoIP. Nat Rev Mol Cell Biol. doi.org/10.1038/s41580-023-00619-6

 

2. Laqtom NN, Dong W, Medoh UN, Cangelosi AL, Dharamdasani V, Chan SH, Kunchok T, Lewis CA, Heinze I, Tang R, Grimm C, Do AND, Porter FD, Ori A, Sabatini DM, AbuRemaileh M. 2022.  CLN3 is required for the clearance of glycerophosphodiesters from lysosomes. Nature. 609, 1005–11. doi.10.1038/s41586-022-05221-y

 

3. Armenta D, Laqtom NN#, Alchemy G, Dong W, Morrow D, Alchemy G, Poltorack C, Nathanson D, Abu-Remalieh M, Dixon SJ. 2022. Ferroptosis inhibition by lysosomal protein catabolism. Cell Chem Biol. 24:S2451-9456(22)00360-9. doi: 10.1016/j.chembiol.2022.10.006.  

 

4. Pedram K, Laqtom NN, Shon DJ, Di Spiezio A, Riley NM, Saftig P, Abu-Remaileh M, Bertozzi, CR. 2022. Discovery of a pathway for endogenous mucin glycodomain catabolism in mammals. PNAS. 119(39):e2117105119.  

 

5. Vest RT, Chou C-C, Zhang H, Haney MS, Li L, Laqtom NN, Chang B, Shuken S, Nguyen A, Yerra L, Yang AC, Green C, Tanga M, Abu-Remaileh M, Bassik MC, Frydman J, Luo J, WyssCoray T. 2022. Small molecule C381 targets the lysosome to reduce inflammation and ameliorate disease in models of neurodegeneration. PNAS. 119 (11) e2121609119.

 

6. 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. 366(6464): 468–475.

 

7. Abu-Remaileh M, Wyant GA, Kim C, Laqtom NN, 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.  

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