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John van Tuyn
University of Glasgow
CardiologyMesenchymal stem cellMyocyteBiologyCell biology
25Publications
18H-index
1,255Citations
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Publications 26
Newest
#1John van Tuyn (Glas.: University of Glasgow)H-Index: 18
#2Farah Jaber-Hijazi (Glas.: University of Glasgow)H-Index: 5
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 14 authors...
On acquisition of an oncogenic mutation, primary human and mouse cells can enter oncogene-induced senescence (OIS). OIS is characterized by a stable proliferation arrest and secretion of proinflammatory cytokines and chemokines, the senescence-associated secretory phenotype. Proliferation arrest and the senescence-associated secretory phenotype collaborate to enact tumor suppression, the former by blocking cell proliferation and the latter by recruiting immune cells to clear damaged cells. Howev...
7 CitationsSource
#1Dina Dikovskaya (Glas.: University of Glasgow)H-Index: 3
#2John J. Cole (Glas.: University of Glasgow)H-Index: 7
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 21 authors...
Oncogene-induced senescence (OIS) is a tumor suppression mechanism that blocks cell proliferation in response to oncogenic signaling. OIS is frequently accompanied by multinucleation; however, the origin of this is unknown. Here, we show that multinucleate OIS cells originate mostly from failed mitosis. Prior to senescence, mutant H-RasV12 activation in primary human fibroblasts compromised mitosis, concordant with abnormal expression of mitotic genes functionally linked to the observed mitotic ...
19 CitationsSource
#1Taranjit Singh Rai (Glas.: University of Glasgow)H-Index: 18
#2John J. Cole (Glas.: University of Glasgow)H-Index: 7
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 23 authors...
Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Cellular senescence and associated tumor suppression depend on control of chromatin. Histone chaperone HIRA deposits variant histone H3.3 and histone H4 into chromatin in a DNA replication-independent manner. Appropriately for a DNA replication-independent chaperone, HIRA is involved in control of chromatin in nonproliferating senescent cells, although its role is poorly defined. Here, we show that nonproliferati...
46 CitationsSource
#1Taranjit Singh Rai (Glas.: University of Glasgow)H-Index: 18
#2John C. Cole (Glas.: University of Glasgow)H-Index: 1
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 18 authors...
1 Citations
#1Hazel A. Cruickshanks (Glas.: University of Glasgow)H-Index: 8
#2Tony McBryan (Glas.: University of Glasgow)H-Index: 15
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 15 authors...
Altered DNA methylation and associated destabilization of genome integrity and function is a hallmark of cancer. Replicative senescence is a tumour suppressor process that imposes a limit on the proliferative potential of normal cells that all cancer cells must bypass. Here we show by whole-genome single-nucleotide bisulfite sequencing that replicative senescent human cells exhibit widespread DNA hypomethylation and focal hypermethylation. Hypomethylation occurs preferentially at gene-poor, late...
137 CitationsSource
#1Jeff S. Pawlikowski (Glas.: University of Glasgow)H-Index: 9
#2Tony McBryan (Glas.: University of Glasgow)H-Index: 15
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 10 authors...
Cellular senescence is a stable proliferation arrest associated with an altered secretory pathway (senescence-associated secretory phenotype). Cellular senescence is also a tumor suppressor mechanism, to which both proliferation arrest and senescence-associated secretory phenotype are thought to contribute. The melanocytes within benign human nevi are a paradigm for tumor-suppressive senescent cells in a premalignant neoplasm. Here a comparison of proliferating and senescent melanocytes and mela...
29 CitationsSource
#1Andre Ivanov (Glas.: University of Glasgow)H-Index: 3
#2Jeff S. Pawlikowski (Glas.: University of Glasgow)H-Index: 9
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 13 authors...
Cellular senescence is a stable proliferation arrest, a potent tumor suppressor mechanism, and a likely contributor to tissue aging. Cellular senescence involves extensive cellular remodeling, including of chromatin structure. Autophagy and lysosomes are important for recycling of cellular constituents and cell remodeling. Here we show that an autophagy/lysosomal pathway processes chromatin in senescent cells. In senescent cells, lamin A/C–negative, but strongly γ-H2AX–positive and H3K27me3-posi...
170 CitationsSource
#1Nikolay A. Pchelintsev (Glas.: University of Glasgow)H-Index: 14
#2Tony McBryan (Glas.: University of Glasgow)H-Index: 15
Last. Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
view all 7 authors...
The HIRA chaperone complex, comprised of HIRA, UBN1, and CABIN1, collaborates with histone-binding protein ASF1a to incorporate histone variant H3.3 into chromatin in a DNA replication-independent manner. To better understand HIRA’s function and mechanism, we integrated HIRA, UBN1, ASF1a, and histone H3.3 chromatin immunoprecipitation sequencing and gene expression analyses. Most HIRA-binding sites colocalize with UBN1, ASF1a, and H3.3 at active promoters and active and weak/poised enhancers. At...
64 CitationsSource
#1Melina C. den Haan (LUMC: Leiden University Medical Center)H-Index: 4
#2Robert W. Grauss (LUMC: Leiden University Medical Center)H-Index: 10
Last. Douwe E. Atsma (LUMC: Leiden University Medical Center)H-Index: 44
view all 15 authors...
We previously showed that human cardiomyocyte progenitor cells (hCMPCs) injected after myocardial infarction (MI) had differentiated into cardiomyocytes in vivo 3 months after MI. Here, we investigated the short-term (2 weeks) effects of hCMPCs on the infarcted mouse myocardium. MI was induced in immunocompromised (NOD/scid) mice, immediately followed by intramyocardial injection of hCMPCs labelled with enhanced green fluorescent protein (hCMPC group) or vehicle only (control group). Sham-operat...
31 CitationsSource
#1John van Tuyn (Glas.: University of Glasgow)H-Index: 18
#2Peter D. Adams (Glas.: University of Glasgow)H-Index: 43
Cellular senescence is a stable proliferation arrest induced by triggers such as short telomeres, activated oncogenes and genotoxic stress. Two studies show that cellular senescence induced by genotoxic stress depends on chronic DNA-damage signalling from irreparable damage to telomeres. Hence, dysfunctional or damaged telomeres are the initiators of multiple modes of senescence.
9 CitationsSource
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