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218 results on '"Gilmore, Petra"'

3. Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein

Author

Day, Ryan B., Hickman, Julia A., Xu, Ziheng, Katerndahl, Casey D.S., Ferraro, Francesca, Ramakrishnan, Sai Mukund, Erdmann-Gilmore, Petra, Sprung, Robert W., Mi, Yiling, Townsend, R. Reid, Miller, Christopher A., and Ley, Timothy J.

Subjects
Myosin -- Genetic aspects, Genes -- Genetic aspects, Biotin -- Genetic aspects, Muscle proteins -- Genetic aspects, B cells -- Genetic aspects, Ligases -- Genetic aspects, Health care industry
Abstract

Several canonical translocations produce oncofusion genes that can initiate acute myeloid leukemia (AML). Although each translocation is associated with unique features, the mechanisms responsible remain unclear. While proteins interacting with each oncofusion are known to be relevant for how they act, these interactions have not yet been systematically defined. To address this issue in an unbiased fashion, we fused a promiscuous biotin ligase (TurboID) in-frame with 3 favorablerisk AML oncofusion cDNAs (PML::RARA, RUNX1::RUNX1T1, and CBFB::MYH11) and identified their interacting proteins in primary murine hematopoietic cells. The PML::RARA- and RUNX1::RUNX1T1-TurboID fusion proteins labeled common and unique nuclear repressor complexes, implying their nuclear localization. However, CBFB::MYH11-TurboID-interacting proteins were largely cytoplasmic, probably because of an interaction of the MYH11 domain with several cytoplasmic myosin- related proteins. Using a variety of methods, we showed that the CBFB domain of CBFB::MYH11 sequesters RUNX1 in cytoplasmic aggregates; these findings were confirmed in primary human AML cells. Paradoxically, CBFB::MYH11 expression was associated with increased RUNX1/2 expression, suggesting the presence of a sensor for reduced functional RUNX1 protein, and a feedback loop that may attempt to compensate by increasing RUNX1/2 transcription. These findings may have broad implications for AML pathogenesis., Introduction Oncofusion genes exist in a variety of solid tumors and hematopoietic malignancies, and are often predictive of outcomes. Elucidating the mechanism of action of an oncofusion protein presents unique [...]

Published
2024
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4. Targeted Proteomic Quantitation of NRF2 Signaling and Predictive Biomarkers in HNSCC

Author

Wamsley, Nathan T., Wilkerson, Emily M., Guan, Li, LaPak, Kyle M., Schrank, Travis P., Holmes, Brittany J., Sprung, Robert W., Gilmore, Petra Erdmann, Gerndt, Sophie P., Jackson, Ryan S., Paniello, Randal C., Pipkorn, Patrik, Puram, Sidharth V., Rich, Jason T., Townsend, Reid R., Zevallos, José P., Zolkind, Paul, Le, Quynh-Thu, Goldfarb, Dennis, and Major, Michael B.

Published
2023
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8. Diurnal Rhythms Spatially and Temporally Organize Autophagy.

Author

Ryzhikov, Mikhail, Ehlers, Anna, Steinberg, Deborah, Xie, Wenfang, Oberlander, Eitan, Brown, Samuel, Gilmore, Petra, Townsend, Reid, Lane, William, Dolinay, Tamas, Nakahira, Kiichi, Choi, Augustine, and Haspel, Jeffrey

Subjects
autophagy, chaperone-mediated autophagy, circadian rhythm, clock, endotoxin, inflammation, lipopolysaccharide, macroautophagy, proteasome, Autophagy, Circadian Rhythm, Humans, Proteomics
Abstract

Circadian rhythms are a hallmark of physiology, but how such daily rhythms organize cellular catabolism is poorly understood. Here, we used proteomics to map daily oscillations in autophagic flux in mouse liver and related these rhythms to proteasome activity. We also explored how systemic inflammation affects the temporal structure of autophagy. Our data identified a globally harmonized rhythm for basal macroautophagy, chaperone-mediated autophagy, and proteasomal activity, which concentrates liver proteolysis during the daytime. Basal autophagy rhythms could be resolved into two antiphase clusters that were distinguished by the subcellular location of targeted proteins. Inflammation induced by lipopolysaccharide reprogrammed autophagic flux away from a temporal pattern that favors cytosolic targets and toward the turnover of mitochondrial targets. Our data detail how daily biological rhythms connect the temporal, spatial, and metabolic aspects of protein catabolism.

Published
2019

9. Proteomic and phosphoproteomic landscapes of acute myeloid leukemia

Author

Kramer, Michael H., Zhang, Qiang, Sprung, Robert, Day, Ryan B., Erdmann-Gilmore, Petra, Li, Yang, Xu, Ziheng, Helton, Nichole M., George, Daniel R., Mi, Yiling, Westervelt, Peter, Payton, Jacqueline E., Ramakrishnan, Sai M., Miller, Christopher A., Link, Daniel C., DiPersio, John F., Walter, Matthew J., Townsend, R. Reid, and Ley, Timothy J.

Published
2022
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10. Missense mutations in Myc Box I influence nucleocytoplasmic transport to promote leukemogenesis.

Author

Arthur, Nancy BJ., primary, Christensen, Keegan A., additional, Mannino, Kathleen, additional, Ruzinova, Marianna B., additional, Kumar, Ashutosh, additional, Gruszczynska, Agata, additional, Day, Ryan B., additional, Erdmann-Gilmore, Petra, additional, Mi, Yiling, additional, Sprung, Robert, additional, York, Conner R., additional, Townsend, R. Reid., additional, Spencer, David H., additional, Sykes, Stephen M., additional, and Ferraro, Francesca, additional

Published
2024
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11. Functional characterization of the dural sinuses as a neuroimmune interface

Author

Rustenhoven, Justin, Drieu, Antoine, Mamuladze, Tornike, de Lima, Kalil Alves, Dykstra, Taitea, Wall, Morgan, Papadopoulos, Zachary, Kanamori, Mitsuhiro, Salvador, Andrea Francesca, Baker, Wendy, Lemieux, Mackenzie, Da Mesquita, Sandro, Cugurra, Andrea, Fitzpatrick, James, Sviben, Sanja, Kossina, Ross, Bayguinov, Peter, Townsend, Reid R., Zhang, Qiang, Erdmann-Gilmore, Petra, Smirnov, Igor, Lopes, Maria-Beatriz, Herz, Jasmin, and Kipnis, Jonathan

Published
2021
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12. HTLV‐1 infected T cells cause bone loss via small extracellular vesicles.

Author

Pokhrel, Nitin Kumar, Panfil, Amanda R., Habib, Haniya, Seeniraj, Shamreethaa, Joseph, Ancy, Rauch, Daniel, Cox, Linda, Sprung, Robert, Gilmore, Petra Erdmann, Zhang, Qiang, Townsend, Robert Reid, Yu, Lianbo, Yilmaz, Ayse Selen, Aurora, Rajeev, Park, William, Ratner, Lee, Weilbaecher, Katherine N., and Veis, Deborah J.

Subjects
VIRAL proteins, SYNTAXINS, T cells, CYTOKINE receptors, BONE cells, BONE resorption
Abstract

Adult T cell leukaemia (ATL), caused by infection with human T‐ lymphotropic virus type 1 (HTLV‐1), is often complicated by hypercalcemia and osteolytic lesions. Therefore, we studied the communication between patient‐derived ATL cells (ATL‐PDX) and HTLV‐1 immortalized CD4+ T cell lines (HTLV/T) with osteoclasts and their effects on bone mass in mice. Intratibial inoculation of some HTLV/T leads to a profound local decrease in bone mass similar to marrow‐replacing ATL‐PDX, despite the fact that few HTLV/T cells persisted in the bone. To study the direct effect of HTLV/T and ATL‐PDX on osteoclasts, supernatants were added to murine and human osteoclast precursors. ATL‐PDX supernatants from hypercalcemic patients promoted the formation of mature osteoclasts, while those from HTLV/T were variably stimulatory, but had largely consistent effects between human and murine cultures. Interestingly, this osteoclastic activity did not correlate with expression of osteoclastogenic cytokine receptor activator of nuclear factor kappa‐B ligand (RANKL), suggesting an alternative mechanism. HTLV/T and ATL‐PDX produce small extracellular vesicles (sEV), known to facilitate HTLV‐1 infection. We hypothesized that these sEV also mediate bone loss by targeting osteoclasts. We isolated sEV from both HTLV/T and ATL‐PDX, and found they carried most of the activity found in supernatants. In contrast, sEV from uninfected activated T cells had little effect. Analysis of sEV (both active and inactive) by mass spectrometry and electron microscopy confirmed absence of RANKL and intact virus. Viral proteins Tax and Env were only present in sEV from the active, osteoclast‐stimulatory group, along with increased representation of proteins involved in osteoclastogenesis and bone resorption. sEV from osteoclast‐active HTLV/T injected over mouse calvaria in the presence of low‐dose RANKL caused more osteolysis than osteoclast‐inactive sEV or RANKL alone. Thus, HTLV‐1 infection of T cells can cause release of sEV with strong osteolytic potential, providing a mechanism beyond RANKL production that modifies the bone microenvironment, even in the absence of overt leukaemia. [ABSTRACT FROM AUTHOR]

Published
2024
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13. HTLV-1 infected T cells cause bone loss via small extracellular vesicles

Author

Pokhrel, Nitin Kumar, primary, Panfil, Amanda, additional, Habib, Haniya, additional, Seeniraj, Sham, additional, Joseph, Ancy, additional, Rauch, Daniel, additional, Cox, Linda, additional, Sprung, Robert, additional, Gilmore, Petra Erdmann, additional, Zhang, Qiang, additional, Townsend, R Reid, additional, Yu, Lianbo, additional, Yilmaz, Ayse Selen, additional, Aurora, Rajeev, additional, Park, William, additional, Ratner, Lee, additional, Weilbaecher, Katherine N, additional, and Veis, Deborah J, additional

Published
2024
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14. Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia–initiating CBFB::MYH11 oncofusion protein

Author

Day, Ryan B., primary, Hickman, Julia A., additional, Xu, Ziheng, additional, Katerndahl, Casey D.S., additional, Ferraro, Francesca, additional, Ramakrishnan, Sai Mukund, additional, Erdmann-Gilmore, Petra, additional, Sprung, Robert W., additional, Mi, Yiling, additional, Townsend, R. Reid, additional, Miller, Christopher A., additional, and Ley, Timothy J., additional

Published
2023
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16. Human Experimental Challenge With Enterotoxigenic Escherichia coli Elicits Immune Responses to Canonical and Novel Antigens Relevant to Vaccine Development

Author

Chakraborty, Subhra, Randall, Arlo, Vickers, Tim J., Molina, Doug, Harro, Clayton D., DeNearing, Barbara, Brubaker, Jessica, Sack, David A., Bourgeois, A. Louis, Felgner, Philip. L., Liang, Xiaowu, Mani, Sachin, Wenzel, Heather, Townsend, R. Reid, Gilmore, Petra E., Darsley, Michael J., Rasko, David A., and Fleckenstein, James M.

Published
2018

17. Missense mutations in Myc Box I influence MYC cellular localization, mRNA partitioning and turnover to promote leukemogenesis

Author

Arthur, Nancy, primary, Christensen, Keegan A, additional, Mannino, Kathleen, additional, Ruzinova, Marianna, additional, Kumar, Ashutosh, additional, Gruszczynska, Agata, additional, Day, Ryan B., additional, Erdmann-Gilmore, Petra, additional, Mi, Yiling, additional, Sprung, Robert, additional, York, Conner R., additional, Spencer, David H., additional, Townsend, Reid, additional, Sykes, Stephen M., additional, and Ferraro, Francesca, additional

Published
2023
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19. An Analysis of the Sensitivity of Proteogenomic Mapping of Somatic Mutations and Novel Splicing Events in Cancer

Author

Ruggles, Kelly V., Tang, Zuojian, Wang, Xuya, Grover, Himanshu, Askenazi, Manor, Teubl, Jennifer, Cao, Song, McLellan, Michael D., Clauser, Karl R., Tabb, David L., Mertins, Philipp, Slebos, Robbert, Erdmann-Gilmore, Petra, Li, Shunqiang, Gunawardena, Harsha P., Xie, Ling, Liu, Tao, Zhou, Jian-Ying, Sun, Shisheng, Hoadley, Katherine A., Perou, Charles M., Chen, Xian, Davies, Sherri R., Maher, Christopher A., Kinsinger, Christopher R., Rodland, Karen D., Zhang, Hui, Zhang, Zhen, Ding, Li, Townsend, R. Reid, Rodriguez, Henry, Chan, Daniel, Smith, Richard D., Liebler, Daniel C., Carr, Steven A., Payne, Samuel, Ellis, Matthew J., and Fenyő, David

Published
2016
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21. Interrogation of a live-attenuated enterotoxigenic Escherichia coli vaccine highlights features unique to wild-type infection

Author

Chakraborty, Subhra, Randall, Arlo, Vickers, Tim J., Molina, Doug, Harro, Clayton D., DeNearing, Barbara, Brubaker, Jessica, Sack, David A., Bourgeois, A. Louis, Felgner, Philip L., Liang, Xiaowu, Mani, Sachin, Wenzel, Heather, Townsend, R. Reid, Gilmore, Petra E., Darsley, Michael J., Rasko, David A., and Fleckenstein, James M.

Published
2019
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22. Sleep deprivation exacerbates microglial reactivity and Aβ deposition in a TREM2 -dependent manner in mice

Author

Parhizkar, Samira, primary, Gent, Grace, additional, Chen, Yun, additional, Rensing, Nicholas, additional, Gratuze, Maud, additional, Strout, Gregory, additional, Sviben, Sanja, additional, Tycksen, Eric, additional, Zhang, Qiang, additional, Gilmore, Petra Erdmann, additional, Sprung, Robert, additional, Malone, Jim, additional, Chen, Wei, additional, Remolina Serrano, Javier, additional, Bao, Xin, additional, Lee, Choonghee, additional, Wang, Chanung, additional, Landsness, Eric, additional, Fitzpatrick, James, additional, Wong, Michael, additional, Townsend, Reid, additional, Colonna, Marco, additional, Schmidt, Robert E., additional, and Holtzman, David M., additional

Published
2023
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23. Supplementary File 5 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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24. Supplementary File 1 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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25. Supplementary File 2 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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26. Extended Methods from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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27. Supplementary File 3 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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28. Supplementary Figures from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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29. Supplementary tables 1 and 2 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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30. Data from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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31. Supplementary File 4 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers

Author

Mundt, Filip, primary, Rajput, Sandeep, primary, Li, Shunqiang, primary, Ruggles, Kelly V., primary, Mooradian, Arshag D., primary, Mertins, Philipp, primary, Gillette, Michael A., primary, Krug, Karsten, primary, Guo, Zhanfang, primary, Hoog, Jeremy, primary, Erdmann-Gilmore, Petra, primary, Primeau, Tina, primary, Huang, Shixia, primary, Edwards, Dean P., primary, Wang, Xiaowei, primary, Wang, Xuya, primary, Kawaler, Emily, primary, Mani, D.R., primary, Clauser, Karl R., primary, Gao, Feng, primary, Luo, Jingqin, primary, Davies, Sherri R., primary, Johnson, Gary L., primary, Huang, Kuan-lin, primary, Yoon, Christopher J., primary, Ding, Li, primary, Fenyö, David, primary, Ellis, Matthew J., primary, Townsend, R. Reid, primary, Held, Jason M., primary, Carr, Steven A., primary, and Ma, Cynthia X., primary

Published
2023
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32. Targeted proteomic quantitation of NRF2 signaling and predictive biomarkers in HNSCC

Author

Wamsley, Nathan, primary, Wilkerson, Emily, additional, Guan, Li, additional, LaPak, Kyle, additional, Schrank, Travis, additional, Holmes, Brittany, additional, Sprung, Robert, additional, Gilmore, Petra Erdmann, additional, Gerndt, Sophie, additional, Jackson, Ryan, additional, Paniello, Randal, additional, Pipkorn, Patrik, additional, Puram, Sidarth V, additional, Rich, Jason, additional, Townsend, R Reid, additional, Zevallos, Jose, additional, Zolkind, Paul, additional, Le, Quynh-Thu, additional, Goldfarb, Dennis, additional, and Major, Michael B, additional

Published
2023
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35. Type IV Pili Are a Critical Virulence Factor in Clinical Isolates of Paenibacillus thiaminolyticus

Author

Hehnly, Christine, primary, Shi, Aiqin, additional, Ssentongo, Paddy, additional, Zhang, Lijun, additional, Isaacs, Albert, additional, Morton, Sarah U., additional, Streck, Nicholas, additional, Erdmann-Gilmore, Petra, additional, Tolstoy, Igor, additional, Townsend, R. Reid, additional, Limbrick, David D., additional, Paulson, Joseph N., additional, Ericson, Jessica E., additional, Galperin, Michael Y., additional, Schiff, Steven J., additional, and Broach, James R., additional

Published
2022
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38. Ischemia in Tumors Induces Early and Sustained Phosphorylation Changes in Stress Kinase Pathways but Does Not Affect Global Protein Levels

Author

Mertins, Philipp, Yang, Feng, Liu, Tao, Mani, D.R., Petyuk, Vladislav A., Gillette, Michael A., Clauser, Karl R., Qiao, Jana W., Gritsenko, Marina A., Moore, Ronald J., Levine, Douglas A., Townsend, Reid, Erdmann-Gilmore, Petra, Snider, Jacqueline E., Davies, Sherri R., Ruggles, Kelly V., Fenyo, David, Kitchens, R. Thomas, Li, Shunqiang, Olvera, Narciso, Dao, Fanny, Rodriguez, Henry, Chan, Daniel W., Liebler, Daniel, White, Forest, Rodland, Karin D., Mills, Gordon B., Smith, Richard D., Paulovich, Amanda G., Ellis, Matthew, and Carr, Steven A.

Published
2014
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43. Correction: Corrigendum: Proteogenomic integration reveals therapeutic targets in breast cancer xenografts

Author

Huang, Kuan-lin, Li, Shunqiang, Mertins, Philipp, Cao, Song, Gunawardena, Harsha P., Ruggles, Kelly V., Mani, D. R., Clauser, Karl R., Tanioka, Maki, Usary, Jerry, Kavuri, Shyam M., Xie, Ling, Yoon, Christopher, Qiao, Jana W., Wrobel, John, Wyczalkowski, Matthew A., Erdmann-Gilmore, Petra, Snider, Jacqueline E., Hoog, Jeremy, Singh, Purba, Niu, Beifang, Guo, Zhanfang, Sun, Sam Qiancheng, Sanati, Souzan, Kawaler, Emily, Wang, Xuya, Scott, Adam, Ye, Kai, McLellan, Michael D., Wendl, Michael C., Malovannaya, Anna, Held, Jason M., Gillette, Michael A., Fenyö, David, Kinsinger, Christopher R., Mesri, Mehdi, Rodriguez, Henry, Davies, Sherri R., Perou, Charles M., Ma, Cynthia, Townsend, R. Reid, Chen, Xian, Carr, Steven A., Ellis, Matthew J., and Ding, Li

Published
2017
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44. Type IV pili is a critical virulence factor in clinical isolates of Paenibacillus thiaminolyticus

Author

Hehnly, Christine, primary, Shi, Aiqin, additional, Ssentongo, Paddy, additional, Zhang, Lijun, additional, Isaacs, Albert, additional, Morton, Sarah U., additional, Streck, Nicholas, additional, Erdmann-Gilmore, Petra, additional, Tolstoy, Igor, additional, Townsend, R Reid, additional, Limbrick, David D., additional, Paulson, Joseph N., additional, Ericson, Jessica E., additional, Galperin, Michael Y., additional, Schiff, Steven J., additional, and Broach, James R, additional

Published
2022
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45. Analysis of the Proteomes of Primary, De Novo Acute Myeloid Leukemia Cells from Adults

Author

Kramer, Michael H, primary, Zhang, Qiang, additional, Sprung, Robert W., additional, Erdmann-Gilmore, Petra, additional, George, Daniel R, additional, Helton, Nichole M, additional, Heath, Sharon E, additional, Payton, Jacqueline E., additional, Westervelt, Peter, additional, Miller, Christopher A, additional, Walter, Matthew J., additional, Link, Daniel C., additional, DiPersio, John F., additional, Townsend, R Reid, additional, and Ley, Timothy J, additional

Published
2021
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46. Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification

Author

Maurya, Shailendra, Yang, Wei, Tamai, Minori, Zhang, Qiang, Erdmann-Gilmore, Petra, Bystry, Amelia, Rodrigues, Fernanda Martins, Valentine, Mark C., Wong, Wing H, Townsend, Reid, and Druley, Todd E.

Abstract

Germline or somatic variation in the family of KMT2 lysine methyltransferases have been associated with a variety of congenital disorders and cancers. Notably, KMT2A-fusions are prevalent in 70% of infant leukaemias but fail to phenocopy short latency leukaemogenesis in mammalian models, suggesting additional factors are necessary for transformation. Given the lack of additional somatic mutation, the role of epigenetic regulation in cell specification, and our prior results of germline KMT2C variation in infant leukaemia patients, we hypothesized that germline dysfunction of KMT2C altered haematopoietic specification. In isogenic KMT2C KO hPSCs, we found genome-wide differences in histone modifications at active and poised enhancers, leading to gene expression profiles akin to mesendoderm rather than mesoderm highlighted by a significant increase in NODAL expression and WNT inhibition, ultimately resulting in a lack of in vitro hemogenic endothelium specification. These unbiased multi-omic results provide new evidence for germline mechanisms increasing risk of early leukaemogenesis.

Published
2021
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47. Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification

Author

Maurya, Shailendra, primary, Yang, Wei, additional, Tamai, Minori, additional, Zhang, Qiang, additional, Erdmann-Gilmore, Petra, additional, Bystry, Amelia, additional, Martins Rodrigues, Fernanda, additional, Valentine, Mark C., additional, Wong, Wing H, additional, Townsend, Reid, additional, and Druley, Todd E., additional

Published
2021
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49. Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification.

Author

Maurya, Shailendra, Yang, Wei, Tamai, Minori, Zhang, Qiang, Erdmann-Gilmore, Petra, Bystry, Amelia, Martins Rodrigues, Fernanda, Valentine, Mark C., Wong, Wing H, Townsend, Reid, and Druley, Todd E.

Subjects
HEMODILUTION, ENDOTHELIUM, GENE expression profiling, CELL differentiation, GENETIC overexpression, CELLULAR control mechanisms
Abstract

Germline or somatic variation in the family of KMT2 lysine methyltransferases have been associated with a variety of congenital disorders and cancers. Notably, KMT2A-fusions are prevalent in 70% of infant leukaemias but fail to phenocopy short latency leukaemogenesis in mammalian models, suggesting additional factors are necessary for transformation. Given the lack of additional somatic mutation, the role of epigenetic regulation in cell specification, and our prior results of germline KMT2C variation in infant leukaemia patients, we hypothesized that germline dysfunction of KMT2C altered haematopoietic specification. In isogenic KMT2C KO hPSCs, we found genome-wide differences in histone modifications at active and poised enhancers, leading to gene expression profiles akin to mesendoderm rather than mesoderm highlighted by a significant increase in NODAL expression and WNT inhibition, ultimately resulting in a lack of in vitro hemogenic endothelium specification. These unbiased multi-omic results provide new evidence for germline mechanisms increasing risk of early leukaemogenesis. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
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50. Breast tumors educate stromal tissue with individualized but coordinated proteomic signatures

Author

Wang, Xuya, Mooradian, Arshag D., Erdmann-Gilmore, Petra, Zhang, Qiang, Viner, Rosa, Davies, Sherri R., Huang, Kuan-lin, Bomgarden, Ryan, Van Tine, Brian A., Shao, Jieya, Ding, Li, Li, Shunqiang, Ellis, Matthew J., Rogers, John C., Townsend, R. Reid, Fenyö, David, and Held, Jason M.

Subjects
Male, Proteomics, Proteome, Breast Neoplasms, Xenograft Model Antitumor Assays, Article, Gene Expression Regulation, Neoplastic, Mice, Mice, Inbred NOD, Tumor Microenvironment, Animals, Humans, Female, Neoplasm Invasiveness, Neoplasm Metastasis, Stromal Cells
Abstract

Cancer forms specialized microenvironmental niches that promote local invasion and colonization. Engrafted patient-derived xenografts (PDXs) locally invade and colonize naïve stroma in mice while enabling unambiguous molecular discrimination of human proteins in the tumor from mouse proteins in the microenvironment. To characterize how patient breast tumors form a niche and educate naïve stroma, subcutaneous breast cancer PDXs were globally profiled by species-specific quantitative proteomics. Regulation of PDX stromal proteins by breast tumors was extensive, with 35% of the stromal proteome altered by tumors consistently across different animals and passages. Differentially regulated proteins in the stroma clustered into six signatures, which included both known and previously unappreciated contributors to tumor invasion and colonization. Stromal proteomes were coordinately regulated; however, the sets of proteins altered by each tumor were highly distinct. Integrated analysis of tumor and stromal proteins, a comparison made possible in these xenograft models, indicated that the known hallmarks of cancer contribute pleiotropically to establishing and maintaining the microenvironmental niche of the tumor. Education of the stroma by the tumor is therefore an intrinsic property of breast tumors that is highly individualized, yet proceeds by consistent, nonrandom, and defined tumor-promoting molecular alterations.

Published
2017

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