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Your search keyword '"Jia, Yuemeng"' showing total 18 results
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18 results on '"Jia, Yuemeng"'

1. Tryptophan fuels MYC-dependent liver tumorigenesis through indole 3-pyruvate synthesis

Author

Venkateswaran, Niranjan, Garcia, Roy, Lafita-Navarro, M. Carmen, Hao, Yi-Heng, Perez-Castro, Lizbeth, Nogueira, Pedro A. S., Solmonson, Ashley, Mender, Ilgen, Kilgore, Jessica A., Fang, Shun, Brown, Isabella N., Li, Li, Parks, Emily, Lopes dos Santos, Igor, Bhaskar, Mahima, Kim, Jiwoong, Jia, Yuemeng, Lemoff, Andrew, Grishin, Nick V., Kinch, Lisa, Xu, Lin, Williams, Noelle S., Shay, Jerry W., DeBerardinis, Ralph J., Zhu, Hao, and Conacci-Sorrell, Maralice

Published
2024
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8. A mechanosensitive peri-arteriolar niche for osteogenesis and lymphopoiesis

Author

Shen, Bo, Tasdogan, Alpaslan, Ubellacker, Jessalyn M., Zhang, Jingzhu, Nosyreva, Elena D., Du, Liming, Murphy, Malea M., Hu, Shuiqing, Yi, Yating, Kara, Nergis, Liu, Xin, Guela, Shay, Jia, Yuemeng, Ramesh, Vijayashree, Embree, Claire, Mitchell, Evann C., Zhao, Yunduo C., Ju, Lining A., Hu, Zhao, Crane, Genevieve M., Zhao, Zhiyu, Syeda, Ruhma, and Morrison, Sean J.

Published
2021
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11. Arid1a Has Context-Dependent Oncogenic and Tumor Suppressor Functions in Liver Cancer

Author

Sun, Xuxu, Wang, Sam C., Wei, Yonglong, Luo, Xin, Jia, Yuemeng, Li, Lin, Gopal, Purva, Zhu, Min, Nassour, Ibrahim, Chuang, Jen-Chieh, Maples, Thomas, Celen, Cemre, Nguyen, Liem H., Wu, Linwei, Fu, Shunjun, Li, Weiping, Hui, Lijian, Tian, Feng, Ji, Yuan, Zhang, Shuyuan, Sorouri, Mahsa, Hwang, Tae Hyun, Letzig, Lynda, James, Laura, Wang, Zixi, Yopp, Adam C., Singal, Amit G., and Zhu, Hao

Published
2017
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15. Human hematopoietic stem cell vulnerability to ferroptosis.

Author

Zhao, Jiawei, Jia, Yuemeng, Mahmut, Dilnar, Deik, Amy A., Jeanfavre, Sarah, Clish, Clary B., and Sankaran, Vijay G.

Subjects
*HEMATOPOIETIC stem cells, *HUMAN stem cells, *PROTEIN synthesis, *SOMATIC cells, *CELL populations
Abstract

Hematopoietic stem cells (HSCs) have a number of unique physiologic adaptations that enable lifelong maintenance of blood cell production, including a highly regulated rate of protein synthesis. Yet, the precise vulnerabilities that arise from such adaptations have not been fully characterized. Here, inspired by a bone marrow failure disorder due to the loss of the histone deubiquitinase MYSM1, characterized by selectively disadvantaged HSCs, we show how reduced protein synthesis in HSCs results in increased ferroptosis. HSC maintenance can be fully rescued by blocking ferroptosis, despite no alteration in protein synthesis rates. Importantly, this selective vulnerability to ferroptosis not only underlies HSC loss in MYSM1 deficiency but also characterizes a broader liability of human HSCs. Increasing protein synthesis rates via MYSM1 overexpression makes HSCs less susceptible to ferroptosis, more broadly illustrating the selective vulnerabilities that arise in somatic stem cell populations as a result of physiologic adaptations. [Display omitted] • MYSM1 deficiency causes human HSC loss by ferroptosis • MYSM1-deficient HSCs have reduced translation of ferroptosis-protective mRNAs • Human HSCs, but not progenitors, are vulnerable to ferroptosis • Human HSC vulnerability to ferroptosis arises due to low rates of protein synthesis Hematopoietic stem cells have a low rate of protein synthesis that makes them selectively vulnerable to ferroptosis. [ABSTRACT FROM AUTHOR]

Published
2023
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18. A mitofusin 2/HIF1α axis sets a maturation checkpoint in regenerating skeletal muscle.

Author

Xun Wang, Yuemeng Jia, Jiawei Zhao, Lesner, Nicholas P., Menezes, Cameron J., Shelton, Spencer D., Krishna Venigalla, Siva Sai, Jian Xu, Chunyu Cai, Mishra, Prashant, Wang, Xun, Jia, Yuemeng, Zhao, Jiawei, Venigalla, Siva Sai Krishna, Xu, Jian, and Cai, Chunyu

Subjects
*SKELETAL muscle, *MUSCLE regeneration, *MITOFUSIN 2, *MITOCHONDRIAL proteins, *REGENERATIVE medicine, *MUSCLE proteins, *REGENERATION (Biology), *CELLULAR signal transduction
Abstract

A fundamental issue in regenerative medicine is whether there exist endogenous regulatory mechanisms that limit the speed and efficiency of the repair process. We report the existence of a maturation checkpoint during muscle regeneration that pauses myofibers at a neonatal stage. This checkpoint is regulated by the mitochondrial protein mitofusin 2 (Mfn2), the expression of which is activated in response to muscle injury. Mfn2 is required for growth and maturation of regenerating myofibers; in the absence of Mfn2, new myofibers arrested at a neonatal stage, characterized by centrally nucleated myofibers and loss of H3K27me3 repressive marks at the neonatal myosin heavy chain gene. A similar arrest at the neonatal stage was observed in infantile cases of human centronuclear myopathy. Mechanistically, Mfn2 upregulation suppressed expression of hypoxia-induced factor 1α (HIF1α), which is induced in the setting of muscle damage. Sustained HIF1α signaling blocked maturation of new myofibers at the neonatal-to-adult fate transition, revealing the existence of a checkpoint that delays muscle regeneration. Correspondingly, inhibition of HIF1α allowed myofibers to bypass the checkpoint, thereby accelerating the repair process. We conclude that skeletal muscle contains a regenerative checkpoint that regulates the speed of myofiber maturation in response to Mfn2 and HIF1α activity. [ABSTRACT FROM AUTHOR]

Published
2022
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