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1,102 results on '"Hall, Michael N."'

1. Arginine reprograms metabolism in liver cancer via RBM39

Author

Mossmann, Dirk, Müller, Christoph, Park, Sujin, Ryback, Brendan, Colombi, Marco, Ritter, Nathalie, Weißenberger, Diana, Dazert, Eva, Coto-Llerena, Mairene, Nuciforo, Sandro, Blukacz, Lauriane, Ercan, Caner, Jimenez, Veronica, Piscuoglio, Salvatore, Bosch, Fatima, Terracciano, Luigi M., Sauer, Uwe, Heim, Markus H., and Hall, Michael N.

Published
2023
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8. Integrative proteogenomic characterization of hepatocellular carcinoma across etiologies and stages

Author

Ng, Charlotte K. Y., Dazert, Eva, Boldanova, Tuyana, Coto-Llerena, Mairene, Nuciforo, Sandro, Ercan, Caner, Suslov, Aleksei, Meier, Marie-Anne, Bock, Thomas, Schmidt, Alexander, Ketterer, Sylvia, Wang, Xueya, Wieland, Stefan, Matter, Matthias S., Colombi, Marco, Piscuoglio, Salvatore, Terracciano, Luigi M., Hall, Michael N., and Heim, Markus H.

Published
2022
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16. mTORC1 phosphorylates and stabilizes LST2 to negatively regulate EGFR.

Author

Battaglioni, Stefania, Craigie, Louise-Marie, Filippini, Sofia, Maier, Timm, and Hall, Michael N.

Subjects
EPIDERMAL growth factor receptors, AMINO acid sequence, PROTEIN kinases, AMINO acids, CELL growth
Abstract

TORC1 (target of rapamycin complex 1) is a highly conserved protein kinase that plays a central role in regulating cell growth. Given the role of mammalian TORC1 (mTORC1) in metabolism and disease, understanding mTORC1 downstream signaling and feedback loops is important. mTORC1 recognizes some of its substrates via a five amino acid binding sequence called the TOR signaling (TOS) motif. mTORC1 binding to a TOS motif facilitates phosphorylation of a distinct, distal site. Here, we show that LST2, also known as ZFYVE28, contains a TOS motif (amino acids 401 to 405) and is directly phosphorylated by mTORC1 at serine 670 (S670). mTORC1-mediated S670 phosphorylation promotes LST2 monoubiquitination on lysine 87 (K87). Monoubiquitinated LST2 is stable and displays a broad reticular distribution. When mTORC1 is inactive, unphosphorylated LST2 is degraded by the proteasome. The absence of LST2 enhances EGFR (epidermal growth factor receptor) signaling. We propose that mTORC1 negatively feeds back on its upstream receptor EGFR via LST2. [ABSTRACT FROM AUTHOR]

Published
2024
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17. ALK signaling primes the DNA damage response sensitizing ALK-driven neuroblastoma to therapeutic ATR inhibition

Author

Borenäs, Marcus, primary, Umapathy, Ganesh, additional, Lind, Dan E., additional, Lai, Wei-Yun, additional, Guan, Jikui, additional, Johansson, Joel, additional, Jennische, Eva, additional, Schmidt, Alexander, additional, Kurhe, Yeshwant, additional, Gabre, Jonatan L., additional, Aniszewska, Agata, additional, Strömberg, Anneli, additional, Bemark, Mats, additional, Hall, Michael N., additional, Eynden, Jimmy Van den, additional, Hallberg, Bengt, additional, and Palmer, Ruth H., additional

Published
2023
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20. Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8+ T Cells

Author

Bantug, Glenn R., Fischer, Marco, Grählert, Jasmin, Balmer, Maria L., Unterstab, Gunhild, Develioglu, Leyla, Steiner, Rebekah, Zhang, Lianjun, Costa, Ana S.H., Gubser, Patrick M., Burgener, Anne-Valérie, Sauder, Ursula, Löliger, Jordan, Belle, Réka, Dimeloe, Sarah, Lötscher, Jonas, Jauch, Annaïse, Recher, Mike, Hönger, Gideon, Hall, Michael N., Romero, Pedro, Frezza, Christian, and Hess, Christoph

Published
2018
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21. Impact papers on aging in 2009

Author

Blagosklonny, Mikhail V, Campisi, Judy, Sinclair, David A, Bartke, Andrzej, Blasco, Maria A, Bonner, William M, Bohr, Vilhelm A, Jr, Robert M Brosh, Brunet, Anne, DePinho, Ronald A, Donehower, Lawrence A, Finch, Caleb E, Finkel, Toren, Gorospe, Myriam, Gudkov, Andrei V, Hall, Michael N, Hekimi, Siegfried, Helfand, Stephen L, Karlseder, Jan, Kenyon, Cynthia, Kroemer, Guido, Longo, Valter, Nussenzweig, Andre, Osiewacz, Heinz D, Peeper, Daniel S, Rando, Thomas A, Rudolph, K Lenhard, Sassone-Corsi, Paolo, Serrano, Manuel, Sharpless, Norman E, Skulachev, Vladimir P, Tilly, Jonathan L, Tower, John, Verdin, Eric, and Vijg, Jan

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Aging, 1.1 Normal biological development and functioning, Underpinning research, Good Health and Well Being, Adult Stem Cells, Animals, Autophagy, Caloric Restriction, Cellular Reprogramming, Circadian Rhythm, DNA Damage, Humans, Mitochondria, Neoplasms, Oxidative Stress, RNA Processing, Post-Transcriptional, Telomere, aging, senescence, signal transduction, genes for longevity, Biochemistry and cell biology, Clinical sciences
Abstract

The Editorial Board of Aging reviews research papers published in 2009, which they believe have or will have significant impact on aging research. Among many others, the topics include genes that accelerate aging or in contrast promote longevity in model organisms, DNA damage responses and telomeres, molecular mechanisms of life span extension by calorie restriction and pharmacological interventions into aging. The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically.

Published
2010

27. Evolution of TOR and Translation Control

Author

Fonseca, Bruno D., Graber, Tyson E., Hoang, Huy-Dung, González, Asier, Soukas, Alexander A., Hernández, Greco, Alain, Tommy, Swift, Stephanie L., Weisman, Ronit, Meyer, Christian, Robaglia, Christophe, Avruch, Joseph, Hall, Michael N., Hernández, Greco, editor, and Jagus, Rosemary, editor

Published
2016
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28. Insulin resistance causes inflammation in adipose tissue

Author

Shimobayashi, Mitsugu, Albert, Verena, Woelnerhanssen, Bettina, Frei, Irina C., Weissenberger, Diana, Meyer-Gerspach, Anne Christin, Clement, Nicolas, Moes, Suzette, Colombi, Marco, Meier, Jerome A., Swierczynska, Marta M., Jeno, Paul, Beglinger, Christoph, Peterli, Ralph, and Hall, Michael N.

Subjects
Physiological aspects, Complications and side effects, Development and progression, Risk factors, Health aspects, Causes of, Obesity -- Complications and side effects, Inflammation -- Causes of -- Development and progression, Insulin resistance -- Complications and side effects -- Risk factors, Adipose tissue -- Health aspects -- Physiological aspects
Abstract

Introduction Obesity-induced insulin resistance is a major risk factor for type 2 diabetes, hyperlipidemia, cardiovascular disease, and some types of cancer (1-3). Although the mechanism by which obesity causes insulin [...], Obesity is a major risk factor for insulin resistance and type 2 diabetes. In adipose tissue, obesity-mediated insulin resistance correlates with the accumulation of proinflammatory macrophages and inflammation. However, the causal relationship of these events is unclear. Here, we report that obesity-induced insulin resistance in mice precedes macrophage accumulation and inflammation in adipose tissue. Using a mouse model that combines genetically induced, adipose-specific insulin resistance (mTORC2-knockout) and diet-induced obesity, we found that insulin resistance causes local accumulation of proinflammatory macrophages. Mechanistically, insulin resistance in adipocytes results in production of the chemokine monocyte chemoattractant protein 1 (MCP1), which recruits monocytes and activates proinflammatory macrophages. Finally, insulin resistance (high homeostatic model assessment of insulin resistance [HOMA-IR]) correlated with reduced insulin/ mTORC2 signaling and elevated MCP1 production in visceral adipose tissue from obese human subjects. Our findings suggest that insulin resistance in adipose tissue leads to inflammation rather than vice versa.

Published
2018
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35. LATS1 but not LATS2 represses autophagy by a kinase-independent scaffold function

Author

Tang, Fengyuan, Gao, Ruize, Jeevan-Raj, Beena, Wyss, Christof B., Kalathur, Ravi K. R., Piscuoglio, Salvatore, Ng, Charlotte K. Y., Hindupur, Sravanth K., Nuciforo, Sandro, Dazert, Eva, Bock, Thomas, Song, Shuang, Buechel, David, Morini, Marco F., Hergovich, Alexander, Matthias, Patrick, Lim, Dae-Sik, Terracciano, Luigi M., Heim, Markus H., Hall, Michael N., and Christofori, Gerhard

Published
2019
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37. ALK signaling primes the DNA damage response sensitizing ALK-driven neuroblastoma to therapeutic ATR inhibition.

Author

Borenäs, Marcus, Umapathy, Ganesh, Lind, Dan E., Wei-Yun Lai, Jikui Guan, Johansson, Joel, Jennische, Eva, Schmidt, Alexander, Kurhe, Yeshwant, Gabre, Jonatan L., Aniszewska, Agata, Strömberg, Anneli, Bemark, Mats, Hall, Michael N., Van den Eynden, Jimmy, Hallberg, Bengt, and Palmer, Ruth H.

Subjects
DNA repair, ANAPLASTIC lymphoma kinase, NEUROBLASTOMA, ATAXIA telangiectasia, SCHWANN cells
Abstract

High-risk neuroblastoma (NB) is a significant clinical challenge. MYCN and Anaplastic Lymphoma Kinase (ALK), which are often involved in high-risk NB, lead to increased replication stress in cancer cells, suggesting therapeutic strategies. We previously identified an ATR (ataxia telangiectasia and Rad3-related)/ALK inhibitor (ATRi/ALKi) combination as such a strategy in two independent genetically modified mouse NB models. Here, we identify an underlying molecular mechanism, in which ALK signaling leads to phosphorylation of ATR and CHK1, supporting an effective DNA damage response. The importance of ALK inhibition is supported by mouse data, in which ATRi monotreatment resulted in a robust initial response, but subsequent relapse, in contrast to a 14-d ALKi/ATRi combination treatment that resulted in a robust and sustained response. Finally, we show that the remarkable response to the 14-d combined ATR/ALK inhibition protocol reflects a robust differentiation response, reprogramming tumor cells to a neuronal/Schwann cell lineage identity. Our results identify an ability of ATR inhibition to promote NB differentiation and underscore the importance of further exploring combined ALK/ATR inhibition in NB, particularly in high-risk patient groups with oncogene-induced replication stress. [ABSTRACT FROM AUTHOR]

Published
2024
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39. Data from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer

Author

Driscoll, David R., primary, Karim, Saadia A, primary, Sano, Makoto, primary, Gay, David M., primary, Jacob, Wright, primary, Yu, Jun, primary, Mizukami, Yusuke, primary, Gopinathan, Aarthi, primary, Jodrell, Duncan I., primary, Evans, T.R. Jeffry, primary, Bardeesy, Nabeel, primary, Hall, Michael N., primary, Quattrochi, Brian J., primary, Klimstra, David S., primary, Barry, Simon T., primary, Sansom, Owen J., primary, Lewis, Brian C., primary, and Morton, Jennifer P., primary

Published
2023
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40. Supplemental Tables 1 through 3 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer

Author

Driscoll, David R., primary, Karim, Saadia A, primary, Sano, Makoto, primary, Gay, David M., primary, Jacob, Wright, primary, Yu, Jun, primary, Mizukami, Yusuke, primary, Gopinathan, Aarthi, primary, Jodrell, Duncan I., primary, Evans, T.R. Jeffry, primary, Bardeesy, Nabeel, primary, Hall, Michael N., primary, Quattrochi, Brian J., primary, Klimstra, David S., primary, Barry, Simon T., primary, Sansom, Owen J., primary, Lewis, Brian C., primary, and Morton, Jennifer P., primary

Published
2023
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41. Supplemental Figures 1 through 8 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer

Author

Driscoll, David R., primary, Karim, Saadia A, primary, Sano, Makoto, primary, Gay, David M., primary, Jacob, Wright, primary, Yu, Jun, primary, Mizukami, Yusuke, primary, Gopinathan, Aarthi, primary, Jodrell, Duncan I., primary, Evans, T.R. Jeffry, primary, Bardeesy, Nabeel, primary, Hall, Michael N., primary, Quattrochi, Brian J., primary, Klimstra, David S., primary, Barry, Simon T., primary, Sansom, Owen J., primary, Lewis, Brian C., primary, and Morton, Jennifer P., primary

Published
2023
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42. Supplemental Figure Legends from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer

Author

Driscoll, David R., primary, Karim, Saadia A, primary, Sano, Makoto, primary, Gay, David M., primary, Jacob, Wright, primary, Yu, Jun, primary, Mizukami, Yusuke, primary, Gopinathan, Aarthi, primary, Jodrell, Duncan I., primary, Evans, T.R. Jeffry, primary, Bardeesy, Nabeel, primary, Hall, Michael N., primary, Quattrochi, Brian J., primary, Klimstra, David S., primary, Barry, Simon T., primary, Sansom, Owen J., primary, Lewis, Brian C., primary, and Morton, Jennifer P., primary

Published
2023
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43. Supplemental Methods from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer

Author

Driscoll, David R., primary, Karim, Saadia A, primary, Sano, Makoto, primary, Gay, David M., primary, Jacob, Wright, primary, Yu, Jun, primary, Mizukami, Yusuke, primary, Gopinathan, Aarthi, primary, Jodrell, Duncan I., primary, Evans, T.R. Jeffry, primary, Bardeesy, Nabeel, primary, Hall, Michael N., primary, Quattrochi, Brian J., primary, Klimstra, David S., primary, Barry, Simon T., primary, Sansom, Owen J., primary, Lewis, Brian C., primary, and Morton, Jennifer P., primary

Published
2023
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44. Supplementary Figure 5 from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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45. Supplementary Figure Legends from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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46. Supplementary Figure 2 from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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47. Supplementary Figure 9 from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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48. Supplementary Figure 6 from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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49. Supplementary Figure 7 from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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50. Data from Maximizing the Efficacy of MAPK-Targeted Treatment in PTENLOF/BRAFMUT Melanoma through PI3K and IGF1R Inhibition

Author

Herkert, Barbara, primary, Kauffmann, Audrey, primary, Mollé, Sandra, primary, Schnell, Christian, primary, Ferrat, Thomas, primary, Voshol, Hans, primary, Juengert, Janina, primary, Erasimus, Hélène, primary, Marszalek, Grégory, primary, Kazic-Legueux, Malika, primary, Billy, Eric, primary, Ruddy, David, primary, Stump, Mark, primary, Guthy, Daniel, primary, Ristov, Mitko, primary, Calkins, Keith, primary, Maira, Sauveur-Michel, primary, Sellers, William R., primary, Hofmann, Francesco, primary, Hall, Michael N., primary, and Brachmann, Saskia M., primary

Published
2023
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