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Your search keyword '"Machida, Yuichi J."' showing total 32 results
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32 results on '"Machida, Yuichi J."'

2. Dimerization-dependent serine protease activity of FAM111A prevents replication fork stalling at topoisomerase 1 cleavage complexes

Author

Palani, Sowmiya, primary, Machida, Yuka, additional, Alvey, Julia R., additional, Mishra, Vandana, additional, Welter, Allison L., additional, Cui, Gaofeng, additional, Bragantini, Benoît, additional, Botuyan, Maria Victoria, additional, Cong, Anh T. Q., additional, Mer, Georges, additional, Schellenberg, Matthew J., additional, and Machida, Yuichi J., additional

Published
2024
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3. Cell Cycle Machinery and Its Alterations in Pancreatic Cancer

Author

Kojima, Yusuke, Maskey, Reeja S., Machida, Yuichi J., Urrutia, Raul, Section Editor, Büchler, M. W., Section Editor, Neoptolemos, John P., Section Editor, Hackert, Th., Section Editor, Neoptolemos, John P., editor, Urrutia, Raul, editor, Abbruzzese, James L., editor, and Büchler, Markus W., editor

Published
2018
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8. MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor-1.

Author

Popay, Tessa M., Wang, Jing, Adams, Clare M., Howard, Gregory Caleb, Codreanu, Simona G., Sherrod, Stacy D., McLean, John A., Thomas, Lance R., Lorey, Shelly L., Machida, Yuichi J., Weissmiller, April M., Eischen, Christine M., Liu, Qi, Tansey, William P., Popay, Tessa M., Wang, Jing, Adams, Clare M., Howard, Gregory Caleb, Codreanu, Simona G., Sherrod, Stacy D., McLean, John A., Thomas, Lance R., Lorey, Shelly L., Machida, Yuichi J., Weissmiller, April M., Eischen, Christine M., Liu, Qi, and Tansey, William P.

Abstract

The oncoprotein transcription factor MYC is a major driver of malignancy and a highly validated but challenging target for the development of anticancer therapies. Novel strategies to inhibit MYC may come from understanding the co-factors it uses to drive pro-tumorigenic gene expression programs, providing their role in MYC activity is understood. Here we interrogate how one MYC co-factor, host cell factor (HCF)-1, contributes to MYC activity in a human Burkitt lymphoma setting. We identify genes connected to mitochondrial function and ribosome biogenesis as direct MYC/HCF-1 targets and demonstrate how modulation of the MYC-HCF-1 interaction influences cell growth, metabolite profiles, global gene expression patterns, and tumor growth in vivo. This work defines HCF-1 as a critical MYC co-factor, places the MYC-HCF-1 interaction in biological context, and highlights HCF-1 as a focal point for development of novel anti-MYC therapies.

Published
2021

9. MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor–1

Author

Popay, Tessa M, primary, Wang, Jing, additional, Adams, Clare M, additional, Howard, Gregory Caleb, additional, Codreanu, Simona G, additional, Sherrod, Stacy D, additional, McLean, John A, additional, Thomas, Lance R, additional, Lorey, Shelly L, additional, Machida, Yuichi J, additional, Weissmiller, April M, additional, Eischen, Christine M, additional, Liu, Qi, additional, and Tansey, William P, additional

Published
2021
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10. Right Place, Right Time, and Only Once: Replication Initiation in Metazoans

Author

Machida, Yuichi J., Hamlin, Joyce L., and Dutta, Anindya

Subjects
DNA replication, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.09.019 Byline: Yuichi J. Machida, Joyce L. Hamlin, Anindya Dutta Abstract: DNA replication is tightly regulated at the initiation step by both the cell cycle machinery and checkpoint pathways. Here, we discuss recent advances in understanding how replication is initiated in metazoans at the correct chromosome positions, at the appropriate time, and only once per cell cycle. Author Affiliation: Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, Virginia 22908

Published
2005

11. Author response: MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor–1

Author

Popay, Tessa M, primary, Wang, Jing, additional, Adams, Clare M, additional, Howard, Gregory Caleb, additional, Codreanu, Simona G, additional, Sherrod, Stacy D, additional, McLean, John A, additional, Thomas, Lance R, additional, Lorey, Shelly L, additional, Machida, Yuichi J, additional, Weissmiller, April M, additional, Eischen, Christine M, additional, Liu, Qi, additional, and Tansey, William P, additional

Published
2020
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14. MYC regulates ribosome biogenesis and mitochondrial gene expression programs through interaction with Host Cell Factor-1

Author

Popay, Tessa M., primary, Wang, Jing, additional, Adams, Clare M., additional, Codreanu, Simona G., additional, Sherrod, Stacy, additional, McClean, John A., additional, Thomas, Lance R., additional, Lorey, Shelly L., additional, Machida, Yuichi J., additional, Weissmiller, April M., additional, Eischen, Christine M., additional, Liu, Qi, additional, and Tansey, William. P., additional

Published
2020
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16. APC/C – the master controller of origin licensing?

Author

Dutta Anindya, Machida Yuichi J, and Sivaprasad Umasundari

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671
Abstract

Abstract DNA replication must be tightly controlled to prevent initiation of a second round of replication until mitosis is complete. So far, components of the pre-replicative complex (Cdt1, Cdc6 and geminin) were considered key players in this regulation. In a new study, Machida and Dutta have shown that depletion of Emi1 caused cells to replicate their DNA more than once per cell cycle 1. This effect was dependent on the ability of Emi1 to inhibit the APC/C. In addition to its role in regulating entry into mitosis, oscillation of APC/C activity regulates pre-RC formation: high APC/C activity in late M/G1 allows pre-RC formation and low APC/C activity in S/G2 prevents pre-RC formation for a second time thereby preventing rereplication. Each redundant pathway to prevent rereplication is dependent on regulating one of the pre-RC components, and all of the pathways are co-regulated by Emi1 through the APC/C. In this commentary we discuss how this new role of Emi1 adds to our understanding of the regulation of replication initiation. We also review the literature to analyze whether APC/C has a role in regulating endoreduplication (a normal state of polyploidy in some differentiated cells). Similarly a role of premature APC/C activation in genomic instability of tumors is discussed.

Published
2007
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17. The APC/C inhibitor, Emil, is essential for prevention of rereplication

Author

Machida, Yuichi J. and Dutta, Anindya

Subjects
Cell cycle -- Research, Cell proliferation -- Research, Biological sciences
Abstract

Study is conducted to show that early mitotic inhibitor (Emil) plays an important function in cell proliferation by preventing rereplication. Results suggest that an essential function of Emil in S and G2 cells is to prevent rereplication via stabilization of inhibitors of rereplication of such as cyclin A and geminin.

Published
2007

18. Spartan deficiency causes accumulation of Topoisomerase 1 cleavage complexes and tumorigenesis

Author

Maskey, Reeja S., primary, Flatten, Karen S., additional, Sieben, Cynthia J., additional, Peterson, Kevin L., additional, Baker, Darren J., additional, Nam, Hyun-Ja, additional, Kim, Myoung Shin, additional, Smyrk, Thomas C., additional, Kojima, Yusuke, additional, Machida, Yuka, additional, Santiago, Annyoceli, additional, van Deursen, Jan M., additional, Kaufmann, Scott H., additional, and Machida, Yuichi J., additional

Published
2017
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