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221 results on '"Bartom, Elizabeth T."'

1. Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer’s disease and aging

Author

Paudel, Bidur, Jeong, Si-Yeon, Martinez, Carolina Pena, Rickman, Alexis, Haluck-Kangas, Ashley, Bartom, Elizabeth T., Fredriksen, Kristina, Affaneh, Amira, Kessler, John A., Mazzulli, Joseph R., Murmann, Andrea E., Rogalski, Emily, Geula, Changiz, Ferreira, Adriana, Heckmann, Bradlee L., Green, Douglas R., Sadleir, Katherine R., Vassar, Robert, and Peter, Marcus E.

Published
2024
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3. Iron drives anabolic metabolism through active histone demethylation and mTORC1

Author

Shapiro, Jason S., Chang, Hsiang-Chun, Tatekoshi, Yuki, Zhao, Zibo, Waxali, Zohra Sattar, Hong, Bong Jin, Chen, Haimei, Geier, Justin A., Bartom, Elizabeth T., De Jesus, Adam, Nejad, Farnaz K., Mahmoodzadeh, Amir, Sato, Tatsuya, Ramos-Alonso, Lucia, Romero, Antonia Maria, Martinez-Pastor, Maria Teresa, Jiang, Shang-Chuan, Sah-Teli, Shiv K., Li, Liming, Bentrem, David, Lopaschuk, Gary, Ben-Sahra, Issam, O’Halloran, Thomas V., Shilatifard, Ali, Puig, Sergi, Bergelson, Joy, Koivunen, Peppi, and Ardehali, Hossein

Published
2023
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10. Therapeutic targeting of metabolic vulnerabilities in cancers with MLL3/4-COMPASS epigenetic regulator mutations

Author

Zhao, Zibo, Cao, Kaixiang, Watanabe, Jun, Philips, Cassandra N., Zeidner, Jacob M., Ishi, Yukitomo, Wang, Qixuan, Gold, Sarah R., Junkins, Katherine, Bartom, Elizabeth T., Yue, Feng, Chandel, Navdeep S., Hashizume, Rintaro, Ben-Sahra, Issam, and Shilatifard, Ali

Subjects
Cancer -- Care and treatment -- Development and progression -- Genetic aspects, Methyltransferases -- Physiological aspects -- Health aspects -- Genetic aspects, Epigenetic inheritance -- Health aspects, Health care industry
Abstract

Epigenetic status-altering mutations in chromatin-modifying enzymes are a feature of human diseases, including many cancers. However, the functional outcomes and cellular dependencies arising from these mutations remain unresolved. In this study, we investigated cellular dependencies, or vulnerabilities, that arise when enhancer function is compromised by loss of the frequently mutated COMPASS family members MLL3 and MLL4. CRISPR dropout screens in MLL3/4-depleted mouse embryonic stem cells (mESCs) revealed synthetic lethality upon suppression of purine and pyrimidine nucleotide synthesis pathways. Consistently, we observed a shift in metabolic activity toward increased purine synthesis in MLL3/4-KO mESCs. These cells also exhibited enhanced sensitivity to the purine synthesis inhibitor lometrexol, which induced a unique gene expression signature. RNA-Seq identified the top MLL3/4 target genes coinciding with suppression of purine metabolism, and tandem mass tag proteomic profiling further confirmed upregulation of purine synthesis in MLL3/4-KO cells. Mechanistically, we demonstrated that compensation by MLL1/COMPASS was underlying these effects. Finally, we demonstrated that tumors with MLL3 and/or MLL4 mutations were highly sensitive to lometrexol in vitro and in vivo, both in culture and in animal models of cancer. Our results depicted a targetable metabolic dependency arising from epigenetic factor deficiency, providing molecular insight to inform therapy for cancers with epigenetic alterations secondary to MLL3/4 COMPASS dysfunction., Introduction The COMplex of Proteins Associated with Setl (COMPASS) family members MLL3 and MLL4 are the major H3K4 histone lysine mono-methyltransferases functioning at enhancers (1-3). Their roles in the regulation [...]

Published
2023
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12. Mitochondria regulate proliferation in adult cardiac myocytes

Author

Waypa, Gregory B., primary, Smith, Kimberly A., additional, Mungai, Paul T., additional, Dudley, Vincent J., additional, Helmin, Kathryn A., additional, Singer, Benjamin D., additional, Peek, Clara Bien, additional, Bass, Joseph, additional, Beussink-Nelson, Lauren, additional, Shah, Sanjiv J., additional, Ofman, Gaston, additional, Wasserstrom, J. Andrew, additional, Muller, William A., additional, Misharin, Alexander V., additional, Budinger, G.R. Scott, additional, Abdala-Valencia, Hiam, additional, Chandel, Navdeep S., additional, Dokic, Danijela, additional, Bartom, Elizabeth T., additional, Zhang, Shuang, additional, Tatekoshi, Yuki, additional, Mahmoodzadeh, Amir, additional, Ardehali, Hossein, additional, Thorp, Edward B., additional, and Schumacker, Paul T., additional

Published
2024
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13. Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span

Author

Misharin, Alexander V, Morales-Nebreda, Luisa, Reyfman, Paul A, Cuda, Carla M, Walter, James M, McQuattie-Pimentel, Alexandra C, Chen, Ching-I, Anekalla, Kishore R, Joshi, Nikita, Williams, Kinola JN, Abdala-Valencia, Hiam, Yacoub, Tyrone J, Chi, Monica, Chiu, Stephen, Gonzalez-Gonzalez, Francisco J, Gates, Khalilah, Lam, Anna P, Nicholson, Trevor T, Homan, Philip J, Soberanes, Saul, Dominguez, Salina, Morgan, Vince K, Saber, Rana, Shaffer, Alexander, Hinchcliff, Monique, Marshall, Stacy A, Bharat, Ankit, Berdnikovs, Sergejs, Bhorade, Sangeeta M, Bartom, Elizabeth T, Morimoto, Richard I, Balch, William E, Sznajder, Jacob I, Chandel, Navdeep S, Mutlu, Gökhan M, Jain, Manu, Gottardi, Cara J, Singer, Benjamin D, Ridge, Karen M, Bagheri, Neda, Shilatifard, Ali, Budinger, GR Scott, and Perlman, Harris

Subjects
Biomedical and Clinical Sciences, Lung, Biotechnology, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Animals, Cell Differentiation, Fibrosis, Humans, Macrophages, Alveolar, Mice, Monocytes, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Little is known about the relative importance of monocyte and tissue-resident macrophages in the development of lung fibrosis. We show that specific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis. Using transcriptomic profiling of flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously over the course of fibrosis and its resolution. During the fibrotic phase, monocyte-derived alveolar macrophages differ significantly from tissue-resident alveolar macrophages in their expression of profibrotic genes. A population of monocyte-derived alveolar macrophages persisted in the lung for one year after the resolution of fibrosis, where they became increasingly similar to tissue-resident alveolar macrophages. Human homologues of profibrotic genes expressed by mouse monocyte-derived alveolar macrophages during fibrosis were up-regulated in human alveolar macrophages from fibrotic compared with normal lungs. Our findings suggest that selectively targeting alveolar macrophage differentiation within the lung may ameliorate fibrosis without the adverse consequences associated with global monocyte or tissue-resident alveolar macrophage depletion.

Published
2017

14. An HSF1-JMJD6-HSP feedback circuit promotes cell adaptation to proteotoxic stress.

Author

Alasady, Milad J., Koeva, Martina, Takagishi, Seesha R., Segal, Dmitri, Amici, David R., Smith, Roger S., Ansel, Daniel J., Lindquist, Susan, Whitesell, Luke, Bartom, Elizabeth T., Taipale, Mikko, and Mendillo, Marc L.

Subjects
HEAT shock factors, HEAT shock proteins, HOMEOSTASIS, PROTEINS
Abstract

Heat Shock Factor 1 (HSF1) is best known as the master transcriptional regulator of the heat-shock response (HSR), a conserved adaptive mechanism critical for protein homeostasis (proteostasis). Combining a genome-wide RNAi library with an HSR reporter, we identified Jumonji domain-containing protein 6 (JMJD6) as an essential mediator of HSF1 activity. In follow-up studies, we found that JMJD6 is itself a noncanonical transcriptional target of HSF1 which acts as a critical regulator of proteostasis. In a positive feedback circuit, HSF1 binds and promotes JMJD6 expression, which in turn reduces heat shock protein 70 (HSP70) R469 monomethylation to disrupt HSP70-HSF1 repressive complexes resulting in enhanced HSF1 activation. Thus, JMJD6 is intricately wired into the proteostasis network where it plays a critical role in cellular adaptation to proteotoxic stress. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Iron drives anabolic metabolism through active histone demethylation and mTORC1

Author

Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Waxali, Zohra Sattar [0000-0003-2615-1221], Geier, Justin A. [0000-0002-1755-1410], Bartom, Elizabeth T. [0000-0002-5618-2582], De Jesus, Adam [0000-0002-7491-4732], Sato, Tatsuya [0000-0001-7876-1772], Martinez-Pastor, Maria Teresa [0000-0002-4128-958X], Jiang, Shang Chuan [0000-0001-7012-5739], Sah-Teli, Shiv K. [0000-0001-7285-8522], Ben-Sahra, Issam [0000-0001-9333-4162], Shilatifard, Ali [0000-0002-7490-2854], Puig, Sergi [0000-0002-1856-490X], Ardehali, Hossein [0000-0002-7662-0551], Shapiro, Jason S., Chang, Hsiang Chun, Tatekoshi, Yuki, Zhao, Zibo, Waxali, Zohra Sattar, Hong, Bong Jin, Chen, Haimei, Geier, Justin A., Bartom, Elizabeth T., De Jesus, Adam, Nejad, Farnaz K., Mahmoodzadeh, Amir, Sato, Tatsuya, Ramos-Alonso, Lucia, Romero, Antonia Maria, Martinez-Pastor, Maria Teresa, Jiang, Shang Chuan, Sah-Teli, Shiv K., Li, Liming, Bentrem, David, Lopaschuk, Gary, Ben-Sahra, Issam, O’Halloran, Thomas V., Shilatifard, Ali, Puig, Sergi, Bergelson, Joy, Koivunen, Peppi, Ardehali, Hossein, Ministerio de Ciencia, Innovación y Universidades (España), European Commission, Waxali, Zohra Sattar [0000-0003-2615-1221], Geier, Justin A. [0000-0002-1755-1410], Bartom, Elizabeth T. [0000-0002-5618-2582], De Jesus, Adam [0000-0002-7491-4732], Sato, Tatsuya [0000-0001-7876-1772], Martinez-Pastor, Maria Teresa [0000-0002-4128-958X], Jiang, Shang Chuan [0000-0001-7012-5739], Sah-Teli, Shiv K. [0000-0001-7285-8522], Ben-Sahra, Issam [0000-0001-9333-4162], Shilatifard, Ali [0000-0002-7490-2854], Puig, Sergi [0000-0002-1856-490X], Ardehali, Hossein [0000-0002-7662-0551], Shapiro, Jason S., Chang, Hsiang Chun, Tatekoshi, Yuki, Zhao, Zibo, Waxali, Zohra Sattar, Hong, Bong Jin, Chen, Haimei, Geier, Justin A., Bartom, Elizabeth T., De Jesus, Adam, Nejad, Farnaz K., Mahmoodzadeh, Amir, Sato, Tatsuya, Ramos-Alonso, Lucia, Romero, Antonia Maria, Martinez-Pastor, Maria Teresa, Jiang, Shang Chuan, Sah-Teli, Shiv K., Li, Liming, Bentrem, David, Lopaschuk, Gary, Ben-Sahra, Issam, O’Halloran, Thomas V., Shilatifard, Ali, Puig, Sergi, Bergelson, Joy, Koivunen, Peppi, and Ardehali, Hossein

Abstract

All eukaryotic cells require a minimal iron threshold to sustain anabolic metabolism. However, the mechanisms by which cells sense iron to regulate anabolic processes are unclear. Here we report a previously undescribed eukaryotic pathway for iron sensing in which molecular iron is required to sustain active histone demethylation and maintain the expression of critical components of the pro-anabolic mTORC1 pathway. Specifically, we identify the iron-binding histone-demethylase KDM3B as an intrinsic iron sensor that regulates mTORC1 activity by demethylating H3K9me2 at enhancers of a high-affinity leucine transporter, LAT3, and RPTOR. By directly suppressing leucine availability and RAPTOR levels, iron deficiency supersedes other nutrient inputs into mTORC1. This process occurs in vivo and is not an indirect effect by canonical iron-utilizing pathways. Because ancestral eukaryotes share homologues of KDMs and mTORC1 core components, this pathway probably pre-dated the emergence of the other kingdom-specific nutrient sensors for mTORC1.

Published
2023

23. Supplementary Table 1 from Targeting ULK1 Decreases IFNγ-Mediated Resistance to Immune Checkpoint Inhibitors

Author

Fenton, Sarah E., primary, Zannikou, Markella, primary, Ilut, Liliana, primary, Fischietti, Mariafausta, primary, Ji, Chunni, primary, Oku, Chidera V., primary, Horvath, Curt M., primary, Le Poole, I. Caroline, primary, Bosenberg, Marcus, primary, Bartom, Elizabeth T., primary, Kocherginsky, Masha, primary, Platanias, Leonidas C., primary, and Saleiro, Diana, primary

Published
2023
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24. Supplementary Figures and Supplementary Materials and Methods with References from Targeting ULK1 Decreases IFNγ-Mediated Resistance to Immune Checkpoint Inhibitors

Author

Fenton, Sarah E., primary, Zannikou, Markella, primary, Ilut, Liliana, primary, Fischietti, Mariafausta, primary, Ji, Chunni, primary, Oku, Chidera V., primary, Horvath, Curt M., primary, Le Poole, I. Caroline, primary, Bosenberg, Marcus, primary, Bartom, Elizabeth T., primary, Kocherginsky, Masha, primary, Platanias, Leonidas C., primary, and Saleiro, Diana, primary

Published
2023
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25. Supplementary Table 2 from USP7 Cooperates with NOTCH1 to Drive the Oncogenic Transcriptional Program in T-Cell Leukemia

Author

Jin, Qi, primary, Martinez, Carlos A., primary, Arcipowski, Kelly M., primary, Zhu, Yixing, primary, Gutierrez-Diaz, Blanca T., primary, Wang, Kenneth K., primary, Johnson, Megan R., primary, Volk, Andrew G., primary, Wang, Feng, primary, Wu, Jian, primary, Grove, Charles, primary, Wang, Hui, primary, Sokirniy, Ivan, primary, Thomas, Paul M., primary, Goo, Young Ah, primary, Abshiru, Nebiyu A., primary, Hijiya, Nobuko, primary, Peirs, Sofie, primary, Vandamme, Niels, primary, Berx, Geert, primary, Goosens, Steven, primary, Marshall, Stacy A., primary, Rendleman, Emily J., primary, Takahashi, Yoh-hei, primary, Wang, Lu, primary, Rawat, Radhika, primary, Bartom, Elizabeth T., primary, Collings, Clayton K., primary, Van Vlierberghe, Pieter, primary, Strikoudis, Alexandros, primary, Kelly, Stephen, primary, Ueberheide, Beatrix, primary, Mantis, Christine, primary, Kandela, Irawati, primary, Bourquin, Jean-Pierre, primary, Bornhauser, Beat, primary, Serafin, Valentina, primary, Bresolin, Silvia, primary, Paganin, Maddalena, primary, Accordi, Benedetta, primary, Basso, Giuseppe, primary, Kelleher, Neil L., primary, Weinstock, Joseph, primary, Kumar, Suresh, primary, Crispino, John D., primary, Shilatifard, Ali, primary, and Ntziachristos, Panagiotis, primary

Published
2023
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26. Figures S1-17 plus legends from USP7 Cooperates with NOTCH1 to Drive the Oncogenic Transcriptional Program in T-Cell Leukemia

Author

Jin, Qi, primary, Martinez, Carlos A., primary, Arcipowski, Kelly M., primary, Zhu, Yixing, primary, Gutierrez-Diaz, Blanca T., primary, Wang, Kenneth K., primary, Johnson, Megan R., primary, Volk, Andrew G., primary, Wang, Feng, primary, Wu, Jian, primary, Grove, Charles, primary, Wang, Hui, primary, Sokirniy, Ivan, primary, Thomas, Paul M., primary, Goo, Young Ah, primary, Abshiru, Nebiyu A., primary, Hijiya, Nobuko, primary, Peirs, Sofie, primary, Vandamme, Niels, primary, Berx, Geert, primary, Goosens, Steven, primary, Marshall, Stacy A., primary, Rendleman, Emily J., primary, Takahashi, Yoh-hei, primary, Wang, Lu, primary, Rawat, Radhika, primary, Bartom, Elizabeth T., primary, Collings, Clayton K., primary, Van Vlierberghe, Pieter, primary, Strikoudis, Alexandros, primary, Kelly, Stephen, primary, Ueberheide, Beatrix, primary, Mantis, Christine, primary, Kandela, Irawati, primary, Bourquin, Jean-Pierre, primary, Bornhauser, Beat, primary, Serafin, Valentina, primary, Bresolin, Silvia, primary, Paganin, Maddalena, primary, Accordi, Benedetta, primary, Basso, Giuseppe, primary, Kelleher, Neil L., primary, Weinstock, Joseph, primary, Kumar, Suresh, primary, Crispino, John D., primary, Shilatifard, Ali, primary, and Ntziachristos, Panagiotis, primary

Published
2023
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27. Supplementary Table 1 from USP7 Cooperates with NOTCH1 to Drive the Oncogenic Transcriptional Program in T-Cell Leukemia

Author

Jin, Qi, primary, Martinez, Carlos A., primary, Arcipowski, Kelly M., primary, Zhu, Yixing, primary, Gutierrez-Diaz, Blanca T., primary, Wang, Kenneth K., primary, Johnson, Megan R., primary, Volk, Andrew G., primary, Wang, Feng, primary, Wu, Jian, primary, Grove, Charles, primary, Wang, Hui, primary, Sokirniy, Ivan, primary, Thomas, Paul M., primary, Goo, Young Ah, primary, Abshiru, Nebiyu A., primary, Hijiya, Nobuko, primary, Peirs, Sofie, primary, Vandamme, Niels, primary, Berx, Geert, primary, Goosens, Steven, primary, Marshall, Stacy A., primary, Rendleman, Emily J., primary, Takahashi, Yoh-hei, primary, Wang, Lu, primary, Rawat, Radhika, primary, Bartom, Elizabeth T., primary, Collings, Clayton K., primary, Van Vlierberghe, Pieter, primary, Strikoudis, Alexandros, primary, Kelly, Stephen, primary, Ueberheide, Beatrix, primary, Mantis, Christine, primary, Kandela, Irawati, primary, Bourquin, Jean-Pierre, primary, Bornhauser, Beat, primary, Serafin, Valentina, primary, Bresolin, Silvia, primary, Paganin, Maddalena, primary, Accordi, Benedetta, primary, Basso, Giuseppe, primary, Kelleher, Neil L., primary, Weinstock, Joseph, primary, Kumar, Suresh, primary, Crispino, John D., primary, Shilatifard, Ali, primary, and Ntziachristos, Panagiotis, primary

Published
2023
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35. Targeting ULK1 Decreases IFNγ-Mediated Resistance to Immune Checkpoint Inhibitors

Author

Fenton, Sarah E., primary, Zannikou, Markella, additional, Ilut, Liliana, additional, Fischietti, Mariafausta, additional, Ji, Chunni, additional, Oku, Chidera V., additional, Horvath, Curt M., additional, Le Poole, I. Caroline, additional, Bosenberg, Marcus, additional, Bartom, Elizabeth T., additional, Kocherginsky, Masha, additional, Platanias, Leonidas C., additional, and Saleiro, Diana, additional

Published
2023
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38. Death induced by survival gene elimination (DISE) contributes to neurotoxicity in Alzheimer’s disease

Author

Paudel, Bidur, primary, Jeong, Si-Yeon, additional, Martinez, Carolina Pena, additional, Rickman, Alexis, additional, Haluck-Kangas, Ashley, additional, Bartom, Elizabeth T., additional, Fredriksen, Kristina, additional, Affaneh, Amira, additional, Kessler, John A., additional, Mazzulli, Joseph R., additional, Murmann, Andrea E., additional, Rogalski, Emily, additional, Geula, Changiz, additional, Ferreira, Adriana, additional, Heckmann, Bradlee L., additional, Green, Douglas R., additional, Sadleir, Katherine R., additional, Vassar, Robert, additional, and Peter, Marcus E., additional

Published
2022
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42. SPOROS: A pipeline to analyze DISE/6mer seed toxicity

Author

Bartom, Elizabeth T., primary, Kocherginsky, Masha, additional, Paudel, Bidur, additional, Vaidyanathan, Aparajitha, additional, Haluck-Kangas, Ashley, additional, Patel, Monal, additional, O’Shea, Kaitlyn L., additional, Murmann, Andrea E., additional, and Peter, Marcus E., additional

Published
2022
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46. SPOROS: A pipeline to analyze DISE/6mer seed toxicity

Author

Bartom, Elizabeth T., primary, Kocherginsky, Masha, additional, Paudel, Bidur, additional, Vaidyanathan, Aparajitha, additional, Haluck-Kangas, Ashley, additional, Patel, Monal, additional, O’Shea, Kaitlyn L., additional, Murmann, Andrea E., additional, and Peter, Marcus E., additional

Published
2021
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48. The transcriptional repressor ID2 supports natural killer cell maturation by controlling TCF1 amplitude

Author

Li, Zhong-Yin, Morman, Rosemary E., Hegermiller, Emma, Sun, Mengxi, Bartom, Elizabeth T., Maienschein-Cline, Mark, Sigvardsson, Mikael, Kee, Barbara L., Li, Zhong-Yin, Morman, Rosemary E., Hegermiller, Emma, Sun, Mengxi, Bartom, Elizabeth T., Maienschein-Cline, Mark, Sigvardsson, Mikael, and Kee, Barbara L.

Abstract

Gaining a mechanistic understanding of the expansion and maturation program of natural killer (NK) cells will provide opportunities for harnessing their inflammation-inducing and oncolytic capacity for therapeutic purposes. Here, we demonstrated that ID2, a transcriptional regulatory protein constitutively expressed in NK cells, supports NK cell effector maturation by controlling the amplitude and temporal dynamics of the transcription factor TCF1. TCF1 promotes immature NK cell expansion and restrains differentiation. The increased TCF1 expression in ID2-deficient NK cells arrests their maturation and alters cell surface receptor expression. Moreover, TCF1 limits NK cell functions, such as cytokine-induced IFN-gamma production and the ability to clear metastatic melanoma in ID2-deficient NK cells. Our data demonstrate that ID2 sets a threshold for TCF1 during NK cell development, thus controlling the balance of immature and terminally differentiated cells that support future NK cell responses., Funding Agencies|National Institutes of Allergy and Infectious DiseasesUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Allergy & Infectious Diseases (NIAID) [R01 AI106352]; National Cancer InstituteUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [P30 CA014599]

Published
2021
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