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  1. Article ; Online: Senolysis through thrombomodulation.

    Webster, Corey M / van Deursen, Jan M

    Cell research

    2023  Volume 33, Issue 8, Page(s) 575–576

    Language English
    Publishing date 2023-07-05
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-023-00842-y
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  2. Article ; Online: Senolytic therapies for healthy longevity.

    van Deursen, Jan M

    Science (New York, N.Y.)

    2019  Volume 364, Issue 6441, Page(s) 636–637

    MeSH term(s) Animals ; Apoptosis/drug effects ; Atherosclerosis/prevention & control ; Cellular Senescence/drug effects ; Healthy Aging ; Humans ; Longevity ; Mice ; Models, Animal ; Neoplasms/prevention & control ; Neurodegenerative Diseases/prevention & control ; Rejuvenation
    Language English
    Publishing date 2019-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aaw1299
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  3. Article ; Online: Immune checkpoint inhibitors as senolytic agents.

    Singh, Parminder / Kapahi, Pankaj / van Deursen, Jan M

    Cell research

    2022  Volume 33, Issue 3, Page(s) 197–198

    MeSH term(s) Immune Checkpoint Inhibitors/pharmacology ; Senotherapeutics ; Cellular Senescence
    Chemical Substances Immune Checkpoint Inhibitors ; Senotherapeutics
    Language English
    Publishing date 2022-12-05
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-022-00761-4
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  4. Article ; Online: Crystallizing BubR1's kinase activity.

    Limzerwala, Jazeel F / van Deursen, Jan M

    Cell research

    2019  Volume 29, Issue 8, Page(s) 605–606

    MeSH term(s) Microtubules ; Phosphorylation
    Language English
    Publishing date 2019-06-28
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-019-0199-7
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  5. Article ; Online: The role of senescent cells in ageing.

    van Deursen, Jan M

    Nature

    2014  Volume 509, Issue 7501, Page(s) 439–446

    Abstract: Cellular senescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to protect against cancer, but recent discoveries have extended its known role to complex biological processes such as development, tissue repair, ... ...

    Abstract Cellular senescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to protect against cancer, but recent discoveries have extended its known role to complex biological processes such as development, tissue repair, ageing and age-related disorders. New insights indicate that, unlike a static endpoint, senescence represents a series of progressive and phenotypically diverse cellular states acquired after the initial growth arrest. A deeper understanding of the molecular mechanisms underlying the multi-step progression of senescence and the development and function of acute versus chronic senescent cells may lead to new therapeutic strategies for age-related pathologies and extend healthy lifespan.
    MeSH term(s) Aging/pathology ; Animals ; Cellular Senescence/physiology ; Disease ; Humans ; Longevity ; Mitosis ; Models, Biological
    Language English
    Publishing date 2014-05-21
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature13193
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  6. Article ; Online: Senescent cells: a therapeutic target for cardiovascular disease.

    Childs, Bennett G / Li, Hu / van Deursen, Jan M

    The Journal of clinical investigation

    2018  Volume 128, Issue 4, Page(s) 1217–1228

    Abstract: Cellular senescence, a major tumor-suppressive cell fate, has emerged from humble beginnings as an in vitro phenomenon into recognition as a fundamental mechanism of aging. In the process, senescent cells have attracted attention as a therapeutic target ... ...

    Abstract Cellular senescence, a major tumor-suppressive cell fate, has emerged from humble beginnings as an in vitro phenomenon into recognition as a fundamental mechanism of aging. In the process, senescent cells have attracted attention as a therapeutic target for age-related diseases, including cardiovascular disease (CVD), the leading cause of morbidity and mortality in the elderly. Given the aging global population and the inadequacy of current medical management, attenuating the health care burden of CVD would be transformative to clinical practice. Here, we review the evidence that cellular senescence drives CVD in a bimodal fashion by both priming the aged cardiovascular system for disease and driving established disease forward. Hence, the growing field of senotherapy (neutralizing senescent cells for therapeutic benefit) is poised to contribute to both prevention and treatment of CVD.
    MeSH term(s) Aged ; Aging/metabolism ; Aging/pathology ; Animals ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/therapy ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Cellular Senescence ; Humans
    Language English
    Publishing date 2018-04-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI95146
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  7. Article ; Online: Chronic social and psychological stress impact select neuropathologies in the PS19 mouse model of tauopathy.

    Lyons, Carey E / Graves, Sara I / Razzoli, Maria / Jeganathan, Karthik / Mansk, Rachel P / McGonigle, Seth / Sabarinathan, Nivedita / van Deursen, Jan M / Baker, Darren J / Bartolomucci, Alessandro

    Psychosomatic medicine

    2023  

    Abstract: Objective: Despite advances toward understanding the etiology of Alzheimer's disease (AD), it remains unclear which aspects of this disease are affected by environmental factors. Chronic life stress increases risk for aging-related diseases including AD. ...

    Abstract Objective: Despite advances toward understanding the etiology of Alzheimer's disease (AD), it remains unclear which aspects of this disease are affected by environmental factors. Chronic life stress increases risk for aging-related diseases including AD. The impact of stress on tauopathies remains understudied. We examined the effects of stress elicited by social (chronic subordination stress, CSS) or psychological/physical (chronic restraint stress, CRS) factors - on the PS19 mouse model of tauopathy.
    Methods: Male PS19 mice (average age 6.3 months) were randomized to receive CSS, CRS, or to remain as singly-housed controls. Behavioral tests were used to assess anxiety-like behaviors and cognitive functions. Immunofluorescence staining and western blotting analysis were used to measure levels of astrogliosis, microgliosis and tau burden. Immunohistochemistry was used to assess glucocorticoid receptor expression.
    Results: PS19 mice exhibit neuroinflammation (GFAP, t-tests; p = 0.0297; Iba1, t-tests; p = 0.006) and tau hyperphosphorylation (t-test, p = 0.0446) in the hippocampus, reduced anxiety (post hoc, p = 0.046), and cognitive deficits, when compared to wild type mice. Surprisingly, CRS reduced hippocampal levels of both total tau and phospho-tauS404 (t-test, p = 0.0116), and attenuated some aspects of both astrogliosis and microgliosis in PS19 mice (t-tests, p = 0.068 to p = 0.0003); however, this was not associated with significant changes in neurodegeneration or cognitive function. Anxiety-like behaviors were increased by CRS (post hoc, p = 0.046). Conversely, CSS impaired spatial learning in Barnes Maze without impacting tau phosphorylation or neurodegeneration and having a minimal impact on gliosis.
    Conclusions: Our results demonstrate that social or psychological stress can differentially impact anxiety-like behavior, select cognitive functions, and some aspects of tau-dependent pathology in PS19 male mice, providing entry points for the development of experimental approaches designed to slow AD progression.
    Language English
    Publishing date 2023-10-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3469-1
    ISSN 1534-7796 ; 0033-3174
    ISSN (online) 1534-7796
    ISSN 0033-3174
    DOI 10.1097/PSY.0000000000001256
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    Ui I Zs.181: Show issues Location:
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  8. Article ; Online: Hyperphosphorylated PTEN exerts oncogenic properties.

    van Ree, Janine H / Jeganathan, Karthik B / Fierro Velasco, Raul O / Zhang, Cheng / Can, Ismail / Hamada, Masakazu / Li, Hu / Baker, Darren J / van Deursen, Jan M

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 2983

    Abstract: PTEN is a multifaceted tumor suppressor that is highly sensitive to alterations in expression or function. The PTEN C-tail domain, which is rich in phosphorylation sites, has been implicated in PTEN stability, localization, catalytic activity, and ... ...

    Abstract PTEN is a multifaceted tumor suppressor that is highly sensitive to alterations in expression or function. The PTEN C-tail domain, which is rich in phosphorylation sites, has been implicated in PTEN stability, localization, catalytic activity, and protein interactions, but its role in tumorigenesis remains unclear. To address this, we utilized several mouse strains with nonlethal C-tail mutations. Mice homozygous for a deletion that includes S370, S380, T382 and T383 contain low PTEN levels and hyperactive AKT but are not tumor prone. Analysis of mice containing nonphosphorylatable or phosphomimetic versions of S380, a residue hyperphosphorylated in human gastric cancers, reveal that PTEN stability and ability to inhibit PI3K-AKT depends on dynamic phosphorylation-dephosphorylation of this residue. While phosphomimetic S380 drives neoplastic growth in prostate by promoting nuclear accumulation of β-catenin, nonphosphorylatable S380 is not tumorigenic. These data suggest that C-tail hyperphosphorylation creates oncogenic PTEN and is a potential target for anti-cancer therapy.
    MeSH term(s) Animals ; Humans ; Male ; Mice ; Carcinogenesis/genetics ; Homozygote ; Mutation ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; PTEN Phosphohydrolase/genetics ; Phosphorylation
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
    Language English
    Publishing date 2023-05-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-38740-x
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  9. Article ; Online: Singling Out Chromosome Gains in Tumor Evolution.

    Naylor, Ryan M / van Deursen, Jan M

    Cancer cell

    2017  Volume 31, Issue 2, Page(s) 165–166

    Abstract: In this issue of Cancer Cell, Sheltzer et al. shed new light on Theodor Boveri's century-old hypothesis by demonstrating that aneuploidy characterized by single-chromosome gains acts to suppress tumorigenesis and that aneuploidy itself is a nidus for ... ...

    Abstract In this issue of Cancer Cell, Sheltzer et al. shed new light on Theodor Boveri's century-old hypothesis by demonstrating that aneuploidy characterized by single-chromosome gains acts to suppress tumorigenesis and that aneuploidy itself is a nidus for genomic instability.
    MeSH term(s) Aneuploidy ; Chromosome Aberrations ; Chromosomes ; Genomic Instability ; Humans ; Neoplasms/genetics
    Language English
    Publishing date 2017-02-15
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2017.01.011
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  10. Article ; Online: Aneuploidy in Cancer and Aging.

    Naylor, Ryan M / van Deursen, Jan M

    Annual review of genetics

    2016  Volume 50, Page(s) 45–66

    Abstract: Chromosomal instability (CIN), the persistent inability of a cell to faithfully segregate its genome, is a feature of many cancer cells. It stands to reason that CIN enables the acquisition of multiple cancer hallmarks; however, there is a growing body ... ...

    Abstract Chromosomal instability (CIN), the persistent inability of a cell to faithfully segregate its genome, is a feature of many cancer cells. It stands to reason that CIN enables the acquisition of multiple cancer hallmarks; however, there is a growing body of evidence suggesting that CIN impairs cellular fitness and prevents neoplastic transformation. Here, we suggest a new perspective to reconcile this apparent paradox and share an unexpected link between aneuploidy and aging that was discovered through attempts to investigate the CIN-cancer relationship. Additionally, we provide a comprehensive overview of the function and regulation of the anaphase-promoting complex, an E3 ubiquitin ligase that mediates high-fidelity chromosome segregation, and describe the mechanisms that lead to whole-chromosome gain or loss. With this review, we aim to expand our understanding of the role of CIN in cancer and aging with the long-term objective of harnessing this information for the advancement of patient care.
    MeSH term(s) Aging/genetics ; Anaphase-Promoting Complex-Cyclosome/genetics ; Anaphase-Promoting Complex-Cyclosome/metabolism ; Aneuploidy ; Chromatids ; Chromosomal Instability ; Humans ; Neoplasms/genetics
    Chemical Substances Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27)
    Language English
    Publishing date 2016-11-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 207928-8
    ISSN 1545-2948 ; 0066-4170 ; 0066-4197
    ISSN (online) 1545-2948
    ISSN 0066-4170 ; 0066-4197
    DOI 10.1146/annurev-genet-120215-035303
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