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1. ImAge quantitates aging and rejuvenation

Author

Alvarez-Kuglen, Martin, Ninomiya, Kenta, Qin, Haodong, Rodriguez, Delany, Fiengo, Lorenzo, Farhy, Chen, Hsu, Wei-Mien, Kirk, Brian, Havas, Aaron, Feng, Gen-Sheng, Roberts, Amanda J., Anderson, Rozalyn M., Serrano, Manuel, Adams, Peter D., Sharpee, Tatyana O., and Terskikh, Alexey V.

Published
2024
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2. Senescent glia link mitochondrial dysfunction and lipid accumulation

Author

Byrns, China N., Perlegos, Alexandra E., Miller, Karl N., Jin, Zhecheng, Carranza, Faith R., Manchandra, Palak, Beveridge, Connor H., Randolph, Caitlin E., Chaluvadi, V. Sai, Zhang, Shirley L., Srinivasan, Ananth R., Bennett, F. C., Sehgal, Amita, Adams, Peter D., Chopra, Gaurav, and Bonini, Nancy M.

Published
2024
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6. Histone chaperone HIRA, promyelocytic leukemia protein, and p62/SQSTM1 coordinate to regulate inflammation during cell senescence

Author

Dasgupta, Nirmalya, Lei, Xue, Shi, Christina Huan, Arnold, Rouven, Teneche, Marcos G., Miller, Karl N., Rajesh, Adarsh, Davis, Andrew, Anschau, Valesca, Campos, Alexandre R., Gilson, Rebecca, Havas, Aaron, Yin, Shanshan, Chua, Zong Ming, Liu, Tianhui, Proulx, Jessica, Alcaraz, Michael, Rather, Mohammed Iqbal, Baeza, Josue, Schultz, David C., Yip, Kevin Y., Berger, Shelley L., and Adams, Peter D.

Published
2024
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7. Guidelines for minimal information on cellular senescence experimentation in vivo

Author

Ogrodnik, Mikolaj, Carlos Acosta, Juan, Adams, Peter D., d’Adda di Fagagna, Fabrizio, Baker, Darren J., Bishop, Cleo L., Chandra, Tamir, Collado, Manuel, Gil, Jesus, Gorgoulis, Vassilis, Gruber, Florian, Hara, Eiji, Jansen-Dürr, Pidder, Jurk, Diana, Khosla, Sundeep, Kirkland, James L., Krizhanovsky, Valery, Minamino, Tohru, Niedernhofer, Laura J., Passos, João F., Ring, Nadja A.R., Redl, Heinz, Robbins, Paul D., Rodier, Francis, Scharffetter-Kochanek, Karin, Sedivy, John M., Sikora, Ewa, Witwer, Kenneth, von Zglinicki, Thomas, Yun, Maximina H., Grillari, Johannes, and Demaria, Marco

Published
2024
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8. Apoptotic stress causes mtDNA release during senescence and drives the SASP

Author

Victorelli, Stella, Salmonowicz, Hanna, Chapman, James, Martini, Helene, Vizioli, Maria Grazia, Riley, Joel S., Cloix, Catherine, Hall-Younger, Ella, Machado Espindola-Netto, Jair, Jurk, Diana, Lagnado, Anthony B., Sales Gomez, Lilian, Farr, Joshua N., Saul, Dominik, Reed, Rebecca, Kelly, George, Eppard, Madeline, Greaves, Laura C., Dou, Zhixun, Pirius, Nicholas, Szczepanowska, Karolina, Porritt, Rebecca A., Huang, Huijie, Huang, Timothy Y., Mann, Derek A., Masuda, Claudio Akio, Khosla, Sundeep, Dai, Haiming, Kaufmann, Scott H., Zacharioudakis, Emmanouil, Gavathiotis, Evripidis, LeBrasseur, Nathan K., Lei, Xue, Sainz, Alva G., Korolchuk, Viktor I., Adams, Peter D., Shadel, Gerald S., Tait, Stephen W. G., and Passos, João F.

Published
2023
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9. Conserved transcription factors promote cell fate stability and restrict reprogramming potential in differentiated cells

Author

Missinato, Maria A., Murphy, Sean, Lynott, Michaela, Yu, Michael S., Kervadec, Anaïs, Chang, Yu-Ling, Kannan, Suraj, Loreti, Mafalda, Lee, Christopher, Amatya, Prashila, Tanaka, Hiroshi, Huang, Chun-Teng, Puri, Pier Lorenzo, Kwon, Chulan, Adams, Peter D., Qian, Li, Sacco, Alessandra, Andersen, Peter, and Colas, Alexandre R.

Published
2023
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10. Spatial mapping of cellular senescence: emerging challenges and opportunities

Author

Gurkar, Aditi U., Gerencser, Akos A., Mora, Ana L., Nelson, Andrew C., Zhang, Anru R., Lagnado, Anthony B., Enninful, Archibald, Benz, Christopher, Furman, David, Beaulieu, Delphine, Jurk, Diana, Thompson, Elizabeth L., Wu, Fei, Rodriguez, Fernanda, Barthel, Grant, Chen, Hao, Phatnani, Hemali, Heckenbach, Indra, Chuang, Jeffrey H., Horrell, Jeremy, Petrescu, Joana, Alder, Jonathan K., Lee, Jun Hee, Niedernhofer, Laura J., Kumar, Manoj, Königshoff, Melanie, Bueno, Marta, Sokka, Miiko, Scheibye-Knudsen, Morten, Neretti, Nicola, Eickelberg, Oliver, Adams, Peter D., Hu, Qianjiang, Zhu, Quan, Porritt, Rebecca A., Dong, Runze, Peters, Samuel, Victorelli, Stella, Pengo, Thomas, Khaliullin, Timur, Suryadevara, Vidyani, Fu, Xiaonan, Bar-Joseph, Ziv, Ji, Zhicheng, and Passos, João F.

Published
2023
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11. Transcriptional control of leukemogenesis by the chromatin reader SGF29

Author

Barbosa, Karina, Deshpande, Anagha, Perales, Marlenne, Xiang, Ping, Murad, Rabi, Pramod, Akula Bala, Minkina, Anna, Robertson, Neil, Schischlik, Fiorella, Lei, Xue, Sun, Younguk, Brown, Adam, Amend, Diana, Jeremias, Irmela, Doench, John G., Humphries, R. Keith, Ruppin, Eytan, Shendure, Jay, Mali, Prashant, Adams, Peter D., and Deshpande, Aniruddha J.

Published
2024
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12. The San Diego Nathan Shock Center: tackling the heterogeneity of aging

Author

Shadel, Gerald S, Adams, Peter D, Berggren, W Travis, Diedrich, Jolene K, Diffenderfer, Kenneth E, Gage, Fred H, Hah, Nasun, Hansen, Malene, Hetzer, Martin W, Molina, Anthony JA, Manor, Uri, Marek, Kurt, O’Keefe, David D, Pinto, Antonio FM, Sacco, Alessandra, Sharpee, Tatyana O, Shokriev, Maxim N, and Zambetti, Stefania

Subjects
Stem Cell Research - Nonembryonic - Non-Human, Aging, Biotechnology, Stem Cell Research, 1.1 Normal biological development and functioning, Underpinning research, Good Health and Well Being, Frailty, Geroscience, Humans, Heterogeneity, Organoids, Human cohort, Single-cell analysis, Machine learning
Abstract

Understanding basic mechanisms of aging holds great promise for developing interventions that prevent or delay many age-related declines and diseases simultaneously to increase human healthspan. However, a major confounding factor in aging research is the heterogeneity of the aging process itself. At the organismal level, it is clear that chronological age does not always predict biological age or susceptibility to frailty or pathology. While genetics and environment are major factors driving variable rates of aging, additional complexity arises because different organs, tissues, and cell types are intrinsically heterogeneous and exhibit different aging trajectories normally or in response to the stresses of the aging process (e.g., damage accumulation). Tackling the heterogeneity of aging requires new and specialized tools (e.g., single-cell analyses, mass spectrometry-based approaches, and advanced imaging) to identify novel signatures of aging across scales. Cutting-edge computational approaches are then needed to integrate these disparate datasets and elucidate network interactions between known aging hallmarks. There is also a need for improved, human cell-based models of aging to ensure that basic research findings are relevant to human aging and healthspan interventions. The San Diego Nathan Shock Center (SD-NSC) provides access to cutting-edge scientific resources to facilitate the study of the heterogeneity of aging in general and to promote the use of novel human cell models of aging. The center also has a robust Research Development Core that funds pilot projects on the heterogeneity of aging and organizes innovative training activities, including workshops and a personalized mentoring program, to help investigators new to the aging field succeed. Finally, the SD-NSC participates in outreach activities to educate the general community about the importance of aging research and promote the need for basic biology of aging research in particular.

Published
2021

14. Author Correction: Apoptotic stress causes mtDNA release during senescence and drives the SASP

Author

Victorelli, Stella, Salmonowicz, Hanna, Chapman, James, Martini, Helene, Vizioli, Maria Grazia, Riley, Joel S., Cloix, Catherine, Hall-Younger, Ella, Machado Espindola-Netto, Jair, Jurk, Diana, Lagnado, Anthony B., Sales Gomez, Lilian, Farr, Joshua N., Saul, Dominik, Reed, Rebecca, Kelly, George, Eppard, Madeline, Greaves, Laura C., Dou, Zhixun, Pirius, Nicholas, Szczepanowska, Karolina, Porritt, Rebecca A., Huang, Huijie, Huang, Timothy Y., Mann, Derek A., Masuda, Claudio Akio, Khosla, Sundeep, Dai, Haiming, Kaufmann, Scott H., Zacharioudakis, Emmanouil, Gavathiotis, Evripidis, LeBrasseur, Nathan K., Lei, Xue, Sainz, Alva G., Korolchuk, Viktor I., Adams, Peter D., Shadel, Gerald S., Tait, Stephen W. G., and Passos, João F.

Published
2024
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15. PSGL-1 attenuates early TCR signaling to suppress CD8+ T cell progenitor differentiation and elicit terminal CD8+ T cell exhaustion

Author

Hope, Jennifer L., Otero, Dennis C., Bae, Eun-Ah, Stairiker, Christopher J., Palete, Ashley B., Faso, Hannah A., Lin, Michelle, Henriquez, Monique L., Roy, Sreeja, Seo, Hyungseok, Lei, Xue, Wang, Eric S., Chow, Savio, Tinoco, Roberto, Daniels, Gregory A., Yip, Kevin, Campos, Alexandre Rosa, Yin, Jun, Adams, Peter D., Rao, Anjana, and Bradley, Linda M.

Published
2023
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16. SIRT1 is downregulated by autophagy in senescence and ageing

Author

Xu, Caiyue, Wang, Lu, Fozouni, Parinaz, Evjen, Gry, Chandra, Vemika, Jiang, Jing, Lu, Congcong, Nicastri, Michael, Bretz, Corey, Winkler, Jeffrey D, Amaravadi, Ravi, Garcia, Benjamin A, Adams, Peter D, Ott, Melanie, Tong, Wei, Johansen, Terje, Dou, Zhixun, and Berger, Shelley L

Subjects
Stem Cell Research, Stem Cell Research - Nonembryonic - Human, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Animals, Autophagosomes, Autophagy, Cell Nucleus, Cell Proliferation, Cell Survival, Cellular Senescence, Female, Humans, Lysosomes, Male, Mice, Mice, Inbred C57BL, Microtubule-Associated Proteins, Middle Aged, Sirtuin 1, Stem Cells, T-Lymphocytes, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

SIRT1 (Sir2) is an NAD+-dependent deacetylase that plays critical roles in a broad range of biological events, including metabolism, the immune response and ageing1-5. Although there is strong interest in stimulating SIRT1 catalytic activity, the homeostasis of SIRT1 at the protein level is poorly understood. Here we report that macroautophagy (hereafter referred to as autophagy), a catabolic membrane trafficking pathway that degrades cellular components through autophagosomes and lysosomes, mediates the downregulation of mammalian SIRT1 protein during senescence and in vivo ageing. In senescence, nuclear SIRT1 is recognized as an autophagy substrate and is subjected to cytoplasmic autophagosome-lysosome degradation, via the autophagy protein LC3. Importantly, the autophagy-lysosome pathway contributes to the loss of SIRT1 during ageing of several tissues related to the immune and haematopoietic system in mice, including the spleen, thymus, and haematopoietic stem and progenitor cells, as well as in CD8+CD28- T cells from aged human donors. Our study reveals a mechanism in the regulation of the protein homeostasis of SIRT1 and suggests a potential strategy to stabilize SIRT1 to promote productive ageing.

Published
2020

17. Quantitative Translation of Dog-to-Human Aging by Conserved Remodeling of the DNA Methylome

Author

Wang, Tina, Ma, Jianzhu, Hogan, Andrew N, Fong, Samson, Licon, Katherine, Tsui, Brian, Kreisberg, Jason F, Adams, Peter D, Carvunis, Anne-Ruxandra, Bannasch, Danika L, Ostrander, Elaine A, and Ideker, Trey

Subjects
Biological Sciences, Genetics, Aging, Human Genome, Underpinning research, 1.1 Normal biological development and functioning, Animals, DNA Methylation, Dogs, Humans, aging, canine, dog, epigenetic aging, epigenetic clock, epigenetics, epigenome, evolution, methylation, methylome, Biochemistry and Cell Biology, Biochemistry and cell biology
Abstract

All mammals progress through similar physiological stages throughout life, from early development to puberty, aging, and death. Yet, the extent to which this conserved physiology reflects underlying genomic events is unclear. Here, we map the common methylation changes experienced by mammalian genomes as they age, focusing on comparison of humans with dogs, an emerging model of aging. Using oligo-capture sequencing, we characterize methylomes of 104 Labrador retrievers spanning a 16-year age range, achieving >150× coverage within mammalian syntenic blocks. Comparison with human methylomes reveals a nonlinear relationship that translates dog-to-human years and aligns the timing of major physiological milestones between the two species, with extension to mice. Conserved changes center on developmental gene networks, which are sufficient to translate age and the effects of anti-aging interventions across multiple mammals. These results establish methylation not only as a diagnostic age readout but also as a cross-species translator of physiological aging milestones.

Published
2020

18. DNA methylation aging clocks: challenges and recommendations

Author

Bell, Christopher G, Lowe, Robert, Adams, Peter D, Baccarelli, Andrea A, Beck, Stephan, Bell, Jordana T, Christensen, Brock C, Gladyshev, Vadim N, Heijmans, Bastiaan T, Horvath, Steve, Ideker, Trey, Issa, Jean-Pierre J, Kelsey, Karl T, Marioni, Riccardo E, Reik, Wolf, Relton, Caroline L, Schalkwyk, Leonard C, Teschendorff, Andrew E, Wagner, Wolfgang, Zhang, Kang, and Rakyan, Vardhman K

Subjects
Human Genome, Genetics, Aging, Generic health relevance, Animals, Biological Clocks, DNA Methylation, Epigenesis, Genetic, Genome, Human, Genome-Wide Association Study, Humans, Environmental Sciences, Biological Sciences, Information and Computing Sciences, Bioinformatics
Abstract

Epigenetic clocks comprise a set of CpG sites whose DNA methylation levels measure subject age. These clocks are acknowledged as a highly accurate molecular correlate of chronological age in humans and other vertebrates. Also, extensive research is aimed at their potential to quantify biological aging rates and test longevity or rejuvenating interventions. Here, we discuss key challenges to understand clock mechanisms and biomarker utility. This requires dissecting the drivers and regulators of age-related changes in single-cell, tissue- and disease-specific models, as well as exploring other epigenomic marks, longitudinal and diverse population studies, and non-human models. We also highlight important ethical issues in forensic age determination and predicting the trajectory of biological aging in an individual.

Published
2019

21. A Multiscale Map of the Stem Cell State in Pancreatic Adenocarcinoma

Author

Lytle, Nikki K, Ferguson, L Paige, Rajbhandari, Nirakar, Gilroy, Kathryn, Fox, Raymond G, Deshpande, Anagha, Schürch, Christian M, Hamilton, Michael, Robertson, Neil, Lin, Wei, Noel, Pawan, Wartenberg, Martin, Zlobec, Inti, Eichmann, Micha, Galván, José A, Karamitopoulou, Eva, Gilderman, Tami, Esparza, Lourdes Adriana, Shima, Yutaka, Spahn, Philipp, French, Randall, Lewis, Nathan E, Fisch, Kathleen M, Sasik, Roman, Rosenthal, Sara Brin, Kritzik, Marcie, Von Hoff, Daniel, Han, Haiyong, Ideker, Trey, Deshpande, Aniruddha J, Lowy, Andrew M, Adams, Peter D, and Reya, Tannishtha

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Bioinformatics and Computational Biology, Genetics, Oncology and Carcinogenesis, Pancreatic Cancer, Biotechnology, Human Genome, Stem Cell Research, Regenerative Medicine, Orphan Drug, Stem Cell Research - Nonembryonic - Human, Rare Diseases, Stem Cell Research - Nonembryonic - Non-Human, Digestive Diseases, Cancer, 2.1 Biological and endogenous factors, Aetiology, Adenocarcinoma, Animals, Cell Adhesion Molecules, Cell Differentiation, Epigenesis, Genetic, Gene Library, Humans, Mice, Mice, Knockout, Mice, SCID, Neoplastic Stem Cells, Nuclear Receptor Subfamily 1, Group F, Member 3, Pancreatic Neoplasms, RNA Interference, RNA, Small Interfering, Receptors, G-Protein-Coupled, Receptors, Interleukin-10, T-Lymphocytes, Transcriptome, Tumor Cells, Cultured, Msi, Musashi, PDAC, RORg, cancer, cancer stem cells, cytokines, immune, pancreatic cancer, stem cells, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Drug resistance and relapse remain key challenges in pancreatic cancer. Here, we have used RNA sequencing (RNA-seq), chromatin immunoprecipitation (ChIP)-seq, and genome-wide CRISPR analysis to map the molecular dependencies of pancreatic cancer stem cells, highly therapy-resistant cells that preferentially drive tumorigenesis and progression. This integrated genomic approach revealed an unexpected utilization of immuno-regulatory signals by pancreatic cancer epithelial cells. In particular, the nuclear hormone receptor retinoic-acid-receptor-related orphan receptor gamma (RORγ), known to drive inflammation and T cell differentiation, was upregulated during pancreatic cancer progression, and its genetic or pharmacologic inhibition led to a striking defect in pancreatic cancer growth and a marked improvement in survival. Further, a large-scale retrospective analysis in patients revealed that RORγ expression may predict pancreatic cancer aggressiveness, as it positively correlated with advanced disease and metastasis. Collectively, these data identify an orthogonal co-option of immuno-regulatory signals by pancreatic cancer stem cells, suggesting that autoimmune drugs should be evaluated as novel treatment strategies for pancreatic cancer patients.

Published
2019

22. Aberrant chromatin landscape following loss of the H3.3 chaperone Daxx in haematopoietic precursors leads to Pu.1-mediated neutrophilia and inflammation

Author

Gerber, Julia P., Russ, Jenny, Chandrasekar, Vijay, Offermann, Nina, Lee, Hang-Mao, Spear, Sarah, Guzzi, Nicola, Maida, Simona, Pattabiraman, Sundararaghavan, Zhang, Ruoyu, Kayvanjoo, Amir H., Datta, Preeta, Kasturiarachchi, Jagath, Sposito, Teresa, Izotova, Natalia, Händler, Kristian, Adams, Peter D., Marafioti, Teresa, Enver, Tariq, Wenzel, Jörg, Beyer, Marc, Mass, Elvira, Bellodi, Cristian, Schultze, Joachim L., Capasso, Melania, Nimmo, Rachael, and Salomoni, Paolo

Published
2021
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23. Epigenetic aging signatures in mice livers are slowed by dwarfism, calorie restriction and rapamycin treatment

Author

Wang, Tina, Tsui, Brian, Kreisberg, Jason F, Robertson, Neil A, Gross, Andrew M, Yu, Michael Ku, Carter, Hannah, Brown-Borg, Holly M, Adams, Peter D, and Ideker, Trey

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Digestive Diseases, Aging, Genetics, Animals, Caloric Restriction, Cluster Analysis, CpG Islands, DNA Methylation, Dwarfism, Epigenesis, Genetic, Epigenomics, Female, Gene Expression Profiling, Humans, Liver, Longevity, Male, Mice, Sirolimus, DNA methylation, Epigenetic aging, Environmental Sciences, Biological Sciences, Information and Computing Sciences, Bioinformatics
Abstract

BackgroundGlobal but predictable changes impact the DNA methylome as we age, acting as a type of molecular clock. This clock can be hastened by conditions that decrease lifespan, raising the question of whether it can also be slowed, for example, by conditions that increase lifespan. Mice are particularly appealing organisms for studies of mammalian aging; however, epigenetic clocks have thus far been formulated only in humans.ResultsWe first examined whether mice and humans experience similar patterns of change in the methylome with age. We found moderate conservation of CpG sites for which methylation is altered with age, with both species showing an increase in methylome disorder during aging. Based on this analysis, we formulated an epigenetic-aging model in mice using the liver methylomes of 107 mice from 0.2 to 26.0 months old. To examine whether epigenetic aging signatures are slowed by longevity-promoting interventions, we analyzed 28 additional methylomes from mice subjected to lifespan-extending conditions, including Prop1df/df dwarfism, calorie restriction or dietary rapamycin. We found that mice treated with these lifespan-extending interventions were significantly younger in epigenetic age than their untreated, wild-type age-matched controls.ConclusionsThis study shows that lifespan-extending conditions can slow molecular changes associated with an epigenetic clock in mice livers.

Published
2017

27. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Author

Klionsky, Daniel J, Abdelmohsen, Kotb, Abe, Akihisa, Abedin, Md Joynal, Abeliovich, Hagai, Acevedo Arozena, Abraham, Adachi, Hiroaki, Adams, Christopher M, Adams, Peter D, Adeli, Khosrow, Adhihetty, Peter J, Adler, Sharon G, Agam, Galila, Agarwal, Rajesh, Aghi, Manish K, Agnello, Maria, Agostinis, Patrizia, Aguilar, Patricia V, Aguirre-Ghiso, Julio, Airoldi, Edoardo M, Ait-Si-Ali, Slimane, Akematsu, Takahiko, Akporiaye, Emmanuel T, Al-Rubeai, Mohamed, Albaiceta, Guillermo M, Albanese, Chris, Albani, Diego, Albert, Matthew L, Aldudo, Jesus, Algül, Hana, Alirezaei, Mehrdad, Alloza, Iraide, Almasan, Alexandru, Almonte-Beceril, Maylin, Alnemri, Emad S, Alonso, Covadonga, Altan-Bonnet, Nihal, Altieri, Dario C, Alvarez, Silvia, Alvarez-Erviti, Lydia, Alves, Sandro, Amadoro, Giuseppina, Amano, Atsuo, Amantini, Consuelo, Ambrosio, Santiago, Amelio, Ivano, Amer, Amal O, Amessou, Mohamed, Amon, Angelika, An, Zhenyi, Anania, Frank A, Andersen, Stig U, Andley, Usha P, Andreadi, Catherine K, Andrieu-Abadie, Nathalie, Anel, Alberto, Ann, David K, Anoopkumar-Dukie, Shailendra, Antonioli, Manuela, Aoki, Hiroshi, Apostolova, Nadezda, Aquila, Saveria, Aquilano, Katia, Araki, Koichi, Arama, Eli, Aranda, Agustin, Araya, Jun, Arcaro, Alexandre, Arias, Esperanza, Arimoto, Hirokazu, Ariosa, Aileen R, Armstrong, Jane L, Arnould, Thierry, Arsov, Ivica, Asanuma, Katsuhiko, Askanas, Valerie, Asselin, Eric, Atarashi, Ryuichiro, Atherton, Sally S, Atkin, Julie D, Attardi, Laura D, Auberger, Patrick, Auburger, Georg, Aurelian, Laure, Autelli, Riccardo, Avagliano, Laura, Avantaggiati, Maria Laura, Avrahami, Limor, Awale, Suresh, Azad, Neelam, Bachetti, Tiziana, Backer, Jonathan M, Bae, Dong-Hun, Bae, Jae-Sung, Bae, Ok-Nam, Bae, Soo Han, Baehrecke, Eric H, Baek, Seung-Hoon, Baghdiguian, Stephen, and Bagniewska-Zadworna, Agnieszka

Subjects
Biochemistry and Cell Biology, Biological Sciences, Animals, Autophagy, Biological Assay, Computer Simulation, Humans, autolysosome, autophagosome, chaperone-mediated autophagy, flux, LC3, lysosome, macroautophagy, phagophore, stress, vacuole, Biochemistry & Molecular Biology, Biochemistry and cell biology
Published
2016

28. A mitochondria-regulated p53-CCF circuit integrates genome integrity with inflammation

Author

Miller, Karl N, primary, Li, Brightany, additional, Pierce-Hoffman, Hannah R, additional, Lei, Xue, additional, Havas, Aaron P, additional, Patel, Shreeya, additional, Cano Macip, Carolina, additional, Victorelli, Stella G, additional, Woo, Seung-Hwa, additional, Lagnado, Anthony B, additional, Liu, Tianhui, additional, Dasgupta, Nirmalya, additional, Lyu, Jun, additional, Altman, Yoav, additional, Porritt, Rebecca A, additional, Garcia, Guillermina, additional, Mogler, Carolin, additional, Dou, Zhixun, additional, Chen, Chongyi, additional, Passos, Joao F, additional, and Adams, Peter D, additional

Published
2023
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29. BRD4-mediated repression of p53 is a target for combination therapy in AML

Author

Latif, Anne-Louise, Newcombe, Ashley, Li, Sha, Gilroy, Kathryn, Robertson, Neil A., Lei, Xue, Stewart, Helen J. S., Cole, John, Terradas, Maria Terradas, Rishi, Loveena, McGarry, Lynn, McKeeve, Claire, Reid, Claire, Clark, William, Campos, Joana, Kirschner, Kristina, Davis, Andrew, Lopez, Jonathan, Sakamaki, Jun-ichi, Morton, Jennifer P., Ryan, Kevin M., Tait, Stephen W. G., Abraham, Sheela A., Holyoake, Tessa, Higgins, Brian, Huang, Xu, Blyth, Karen, Copland, Mhairi, Chevassut, Timothy J. T., Keeshan, Karen, and Adams, Peter D.

Published
2021
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30. MYC regulates fatty acid metabolism through a multigenic program in claudin-low triple negative breast cancer

Author

Casciano, Jessica C., Perry, Caroline, Cohen-Nowak, Adam J., Miller, Katelyn D., Vande Voorde, Johan, Zhang, Qifeng, Chalmers, Susan, Sandison, Mairi E., Liu, Qin, Hedley, Ann, McBryan, Tony, Tang, Hsin-Yao, Gorman, Nicole, Beer, Thomas, Speicher, David W., Adams, Peter D., Liu, Xuefeng, Schlegel, Richard, McCarron, John G., Wakelam, Michael J. O., Gottlieb, Eyal, Kossenkov, Andrew V., and Schug, Zachary T.

Published
2020
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35. Author Correction: Aberrant chromatin landscape following loss of the H3.3 chaperone Daxx in haematopoietic precursors leads to Pu.1-mediated neutrophilia and inflammation

Author

Gerber, Julia P., Russ, Jenny, Chandrasekar, Vijay, Offermann, Nina, Lee, Hang-Mao, Spear, Sarah, Guzzi, Nicola, Maida, Simona, Pattabiraman, Sundararaghavan, Zhang, Ruoyu, Kayvanjoo, Amir H., Datta, Preeta, Kasturiarachchi, Jagath, Sposito, Teresa, Izotova, Natalia, Händler, Kristian, Adams, Peter D., Marafioti, Teresa, Enver, Tariq, Wenzel, Jörg, Beyer, Marc, Mass, Elvira, Bellodi, Cristian, Schultze, Joachim L., Capasso, Melania, Nimmo, Rachael, and Salomoni, Paolo

Published
2022
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36. Histone chaperone HIRA, Promyelocytic Leukemia (PML) protein and p62/SQSTM1 coordinate to regulate inflammation during cell senescence and aging

Author

Dasgupta, Nirmalya, primary, Lei, Xue, additional, Arnold, Rouven, additional, Teneche, Marcos Garcia, additional, Miller, Karl N., additional, Rajesh, Adarsh, additional, Davis, Andrew, additional, Anschau, Valesca, additional, Campos, Alexandre R., additional, Gilson, Rebecca, additional, Havas, Aaron, additional, Yin, Shanshan, additional, Chua, Zong Ming, additional, Proulx, Jessica, additional, Alcaraz, Michael, additional, Rather, Mohammed Iqbal, additional, Baeza, Josue, additional, Schultz, David C., additional, Berger, Shelley L., additional, and Adams, Peter D., additional

Published
2023
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37. Dynamic enhancer interactome promotes senescence and aging

Author

Wang, Lu, primary, Donahue, Gregory, additional, Zhang, Chen, additional, Havas, Aaron, additional, Lei, Xue, additional, Xu, Caiyue, additional, Wang, Wenliang, additional, Vahedi, Golnaz, additional, Adams, Peter D, additional, and Berger, Shelley L, additional

Published
2023
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42. Supplementary Table from Dual G9A/EZH2 Inhibition Stimulates Antitumor Immune Response in Ovarian High-Grade Serous Carcinoma

Author

Spiliopoulou, Pavlina, primary, Spear, Sarah, primary, Mirza, Hasan, primary, Garner, Ian, primary, McGarry, Lynn, primary, Grundland-Freile, Fabio, primary, Cheng, Zhao, primary, Ennis, Darren P., primary, Iyer, Nayana, primary, McNamara, Sophie, primary, Natoli, Marina, primary, Mason, Susan, primary, Blyth, Karen, primary, Adams, Peter D., primary, Roxburgh, Patricia, primary, Fuchter, Matthew J., primary, Brown, Bob, primary, and McNeish, Iain A., primary

Published
2023
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43. Supplementary Data from Dual G9A/EZH2 Inhibition Stimulates Antitumor Immune Response in Ovarian High-Grade Serous Carcinoma

Author

Spiliopoulou, Pavlina, primary, Spear, Sarah, primary, Mirza, Hasan, primary, Garner, Ian, primary, McGarry, Lynn, primary, Grundland-Freile, Fabio, primary, Cheng, Zhao, primary, Ennis, Darren P., primary, Iyer, Nayana, primary, McNamara, Sophie, primary, Natoli, Marina, primary, Mason, Susan, primary, Blyth, Karen, primary, Adams, Peter D., primary, Roxburgh, Patricia, primary, Fuchter, Matthew J., primary, Brown, Bob, primary, and McNeish, Iain A., primary

Published
2023
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44. Supplementary Figure from Dual G9A/EZH2 Inhibition Stimulates Antitumor Immune Response in Ovarian High-Grade Serous Carcinoma

Author

Spiliopoulou, Pavlina, primary, Spear, Sarah, primary, Mirza, Hasan, primary, Garner, Ian, primary, McGarry, Lynn, primary, Grundland-Freile, Fabio, primary, Cheng, Zhao, primary, Ennis, Darren P., primary, Iyer, Nayana, primary, McNamara, Sophie, primary, Natoli, Marina, primary, Mason, Susan, primary, Blyth, Karen, primary, Adams, Peter D., primary, Roxburgh, Patricia, primary, Fuchter, Matthew J., primary, Brown, Bob, primary, and McNeish, Iain A., primary

Published
2023
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46. SenNet recommendations for detecting senescent cells in different tissues

Author

Suryadevara, Vidyani, Hudgins, Adam D., Rajesh, Adarsh, Pappalardo, Alberto, Karpova, Alla, Dey, Amit K., Hertzel, Ann, Agudelo, Anthony, Rocha, Azucena, Soygur, Bikem, Schilling, Birgit, Carver, Chase M., Aguayo-Mazzucato, Cristina, Baker, Darren J., Bernlohr, David A., Jurk, Diana, Mangarova, Dilyana B., Quardokus, Ellen M., Enninga, Elizabeth Ann L., Schmidt, Elizabeth L., Chen, Feng, Duncan, Francesca E., Cambuli, Francesco, Kaur, Gagandeep, Kuchel, George A., Lee, Gung, Daldrup-Link, Heike E., Martini, Helene, Phatnani, Hemali, Al-Naggar, Iman M., Rahman, Irfan, Nie, Jia, Passos, João F., Silverstein, Jonathan C., Campisi, Judith, Wang, Julia, Iwasaki, Kanako, Barbosa, Karina, Metis, Kay, Nernekli, Kerem, Niedernhofer, Laura J., Ding, Li, Wang, Lichao, Adams, Lisa C., Ruiyang, Liu, Doolittle, Madison L., Teneche, Marcos G., Schafer, Marissa J., Xu, Ming, Hajipour, Mohammadjavad, Boroumand, Mozhgan, Basisty, Nathan, Sloan, Nicholas, Slavov, Nikolai, Kuksenko, Olena, Robson, Paul, Gomez, Paul T., Vasilikos, Periklis, Adams, Peter D., Carapeto, Priscila, Zhu, Quan, Ramasamy, Ramalakshmi, Perez-Lorenzo, Rolando, Fan, Rong, Dong, Runze, Montgomery, Ruth R., Shaikh, Sadiya, Vickovic, Sanja, Yin, Shanshan, Kang, Shoukai, Suvakov, Sonja, Khosla, Sundeep, Garovic, Vesna D., Menon, Vilas, Xu, Yanxin, Song, Yizhe, Suh, Yousin, Dou, Zhixun, and Neretti, Nicola

Abstract

Once considered a tissue culture-specific phenomenon, cellular senescence has now been linked to various biological processes with both beneficial and detrimental roles in humans, rodents and other species. Much of our understanding of senescent cell biology still originates from tissue culture studies, where each cell in the culture is driven to an irreversible cell cycle arrest. By contrast, in tissues, these cells are relatively rare and difficult to characterize, and it is now established that fully differentiated, postmitotic cells can also acquire a senescence phenotype. The SenNet Biomarkers Working Group was formed to provide recommendations for the use of cellular senescence markers to identify and characterize senescent cells in tissues. Here, we provide recommendations for detecting senescent cells in different tissues based on a comprehensive analysis of existing literature reporting senescence markers in 14 tissues in mice and humans. We discuss some of the recent advances in detecting and characterizing cellular senescence, including molecular senescence signatures and morphological features, and the use of circulating markers. We aim for this work to be a valuable resource for both seasoned investigators in senescence-related studies and newcomers to the field.

Published
2024
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47. PAK4 suppresses RELB to prevent senescence-like growth arrest in breast cancer

Author

Costa, Tânia D. F., Zhuang, Ting, Lorent, Julie, Turco, Emilia, Olofsson, Helene, Masia-Balague, Miriam, Zhao, Miao, Rabieifar, Parisa, Robertson, Neil, Kuiper, Raoul, Sjölund, Jonas, Spiess, Matthias, Hernández-Varas, Pablo, Rabenhorst, Uta, Roswall, Pernilla, Ma, Ran, Gong, Xiaowei, Hartman, Johan, Pietras, Kristian, Adams, Peter D., Defilippi, Paola, and Strömblad, Staffan

Published
2019
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50. Cytoplasmic chromatin triggers inflammation in senescence and cancer

Author

Dou, Zhixun, Ghosh, Kanad, Vizioli, Maria Grazia, Zhu, Jiajun, Sen, Payel, Wangensteen, Kirk J., Simithy, Johayra, Lan, Yemin, Lin, Yanping, Zhou, Zhuo, Capell, Brian C., Xu, Caiyue, Xu, Mingang, Kieckhaefer, Julia E., Jiang, Tianying, Shoshkes-Carmel, Michal, Tanim, K. M. Ahasan Al, Barber, Glen N., Seykora, John T., Millar, Sarah E., Kaestner, Klaus H., Garcia, Benjamin A., Adams, Peter D., and Berger, Shelley L.

Subjects
Inflammation -- Physiological aspects, Aging (Biology) -- Health aspects, Chromatin -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Zhixun Dou [1]; Kanad Ghosh [1]; Maria Grazia Vizioli [2, 3]; Jiajun Zhu [1]; Payel Sen [1]; Kirk J. Wangensteen [4]; Johayra Simithy [1, 5]; Yemin Lan [1]; Yanping [...]

Published
2017
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