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Article ; Online: A role for CUX1 in the regulation of p16 and senescence.

Chan, Adelyne Sue Li / Narita, Masashi

Nature aging

2023 Volume 2, Issue 2, Page(s) 100–101

MeSH term(s)	Repressor Proteins/genetics ; Up-Regulation
Chemical Substances	Repressor Proteins
Language	English
Publishing date	2023-04-28
Publishing country	United States
Document type	Journal Article ; Comment
ISSN	2662-8465
ISSN (online)	2662-8465
DOI	10.1038/s43587-022-00173-4
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Article ; Online: Crisis management by autophagy.

Narita, Masashi

Nature structural & molecular biology

2019 Volume 26, Issue 3, Page(s) 151–152

MeSH term(s)	Autophagy/physiology ; Carcinogenesis/pathology ; Humans ; Neoplasms/pathology
Language	English
Publishing date	2019-01-18
Publishing country	United States
Document type	News
ZDB-ID	2126708-X
ISSN	1545-9985 ; 1545-9993
ISSN (online)	1545-9985
ISSN	1545-9993
DOI	10.1038/s41594-019-0195-0
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Article ; Online: Determining the Compaction State of Genes Using DNA FISH.

Narita, Masako / Olan, Ioana / Narita, Masashi

Methods in molecular biology (Clifton, N.J.)

2024 Volume 2784, Page(s) 215–225

Abstract: DNA fluorescence in situ hybridization (FISH) enables the visualization of chromatin architecture and the interactions between genomic loci at a single-cell level, complementary to genome-wide methods such as Hi-C. DNA FISH uses fluorescent-labeled DNA ... ...

Abstract	DNA fluorescence in situ hybridization (FISH) enables the visualization of chromatin architecture and the interactions between genomic loci at a single-cell level, complementary to genome-wide methods such as Hi-C. DNA FISH uses fluorescent-labeled DNA probes targeted to the loci of interest, allowing for the analysis of their spatial positioning and proximity with microscopy. Here, we describe an optimized experimental procedure for DNA FISH, from probe design and sample preparation through imaging and image quantification. This protocol can be readily applied to querying the spatial positioning of genomic loci of interest.
MeSH term(s)	In Situ Hybridization, Fluorescence/methods ; DNA/genetics ; Chromatin/genetics ; Chromosomes ; DNA Probes/genetics ; Fluorescent Dyes
Chemical Substances	DNA (9007-49-2) ; Chromatin ; DNA Probes ; Fluorescent Dyes
Language	English
Publishing date	2024-03-19
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3766-1_15
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Article: Driving Behavior during Left-Turn Maneuvers at Intersections on Left-Hand Traffic Roads.

Matsui, Yasuhiro / Narita, Masashi / Oikawa, Shoko

Stapp car crash journal

2024 Volume 67, Page(s) 180–201

Abstract: Understanding left-turn vehicle-pedestrian accident mechanisms is critical for developing accident-prevention systems. This study aims to clarify the features of driver behavior focusing on drivers' gaze, vehicle speed, and time to collision (TTC) during ...

Abstract	Understanding left-turn vehicle-pedestrian accident mechanisms is critical for developing accident-prevention systems. This study aims to clarify the features of driver behavior focusing on drivers' gaze, vehicle speed, and time to collision (TTC) during left turns at intersections on left-hand traffic roads. Herein, experiments with a sedan and light-duty truck (< 7.5 tons GVW) are conducted under four conditions: no pedestrian dummy (No-P), near-side pedestrian dummy (Near-P), far-side pedestrian dummy (Far-P) and near-and-far side pedestrian dummies (NF-P). For NF-P, sedans have a significantly shorter gaze time for left-side mirrors compared with light-duty trucks. The light-duty truck's average speed at the initial line to the intersection (L1) and pedestrian crossing line (L0) is significantly lower than the sedan's under No-P, Near-P, and NF-P conditions, without any significant difference between any two conditions. The TTC for sedans is significantly shorter than that for trucks with near-side pedestrians (Near-P and NF-P) and far-side pedestrians in Far-P. These insights can contribute to the ongoing development of accident-prevention safety systems for left-turning maneuvers at intersections.
Language	English
Publishing date	2024-04-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2037200-0
ISSN	1532-8546 ; 0585-086X
ISSN	1532-8546 ; 0585-086X
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Article ; Online: p53 in senescence – it's a marathon, not a sprint

Sheekey, Eleanor / Narita, Masashi

The FEBS Journal. 2023 Mar., v. 290, no. 5 p.1212-1220

2023

Abstract: The tumour suppressor p53, a stress‐responsive transcription factor, plays a central role in cellular senescence. The role of p53 in senescence‐associated stable proliferative arrest has been extensively studied. However, increasing evidence indicates ... ...

Abstract	The tumour suppressor p53, a stress‐responsive transcription factor, plays a central role in cellular senescence. The role of p53 in senescence‐associated stable proliferative arrest has been extensively studied. However, increasing evidence indicates that p53 also modulates the ability of senescent cells to produce and secrete diverse bioactive factors (collectively called the senescence‐associated secretory phenotype, SASP). Senescence has been linked with both physiological and pathological conditions, the latter including ageing, cancer and other age‐related disorders, in part through the SASP. Cellular functions are generally dictated by the expression profile of lineage‐specific genes. Indeed, expression of SASP factors and their regulators are often biased by cell type. In addition, emerging evidence suggests that p53 contributes to deregulation of more stringent lineage‐specific genes during senescence. P53 itself is also tightly regulated at the protein level. In contrast to the rapid and transient activity of p53 upon stress (‘acute‐p53’), during senescence and other prolonged pathological conditions, p53 activities are sustained and fine‐tuned through a combination of different inputs and outputs (‘chronic‐p53’).
Keywords	cell senescence ; neoplasms ; phenotype ; protein content ; transcription factors
Language	English
Dates of publication	2023-03
Size	p. 1212-1220.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16325
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Juxtacrine regulation of cellular senescence.

Narita, Masashi

BMB reports

2018 Volume 52, Issue 1, Page(s) 3–4

Abstract: Cellular senescence is defined as a state of stable cell cycle exit in response to various stimuli, which include both cytotoxic stress and physiological cues. In addition to the core non-proliferative aspect, senescence is associated with diverse ... ...

Abstract	Cellular senescence is defined as a state of stable cell cycle exit in response to various stimuli, which include both cytotoxic stress and physiological cues. In addition to the core non-proliferative aspect, senescence is associated with diverse functionalities, which contribute to the role of senescence in a wide range of pathological and physiological processes. Such functionality is often mediated by the capability of senescent cells to communicate with their surroundings. Emerging evidence suggests that senescence is not a single entity, but a dynamic and heterogeneous collective phenotype. Understanding the diverse nature of senescence should provide insights into the complexity of tissue homeostasis and its disruption, such as in aging and tumorigenesis. [BMB Reports 2019; 52(1): 3-4].
MeSH term(s)	Aging ; Cell Communication/physiology ; Cellular Senescence/physiology ; Epigenesis, Genetic/genetics ; Epigenomics ; Homeostasis ; Humans ; Intercellular Junctions ; Receptors, Notch/physiology ; Signal Transduction/physiology
Chemical Substances	Receptors, Notch
Language	English
Publishing date	2018-12-11
Publishing country	Korea (South)
Document type	News
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
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Article ; Online: Senescence: An Identity Crisis Originating from Deep Within the Nucleus.

Olan, Ioana / Narita, Masashi

Annual review of cell and developmental biology

2022 Volume 38, Page(s) 219–239

Abstract: Cellular senescence is implicated in a wide range of physiological and pathological conditions throughout an organism's entire lifetime. In particular, it has become evident that senescence plays a causative role in aging and age-associated disorders. ... ...

Abstract	Cellular senescence is implicated in a wide range of physiological and pathological conditions throughout an organism's entire lifetime. In particular, it has become evident that senescence plays a causative role in aging and age-associated disorders. This is not due simply to the loss of function of senescent cells. Instead, the substantial alterations of the cellular activities of senescent cells, especially the array of secretory factors, impact the surrounding tissues or even entire organisms. Such non-cell-autonomous functionality is largely coordinated by tissue-specific genes, constituting a cell fate-determining state. Senescence can be viewed as a gain-of-function phenotype or a process of cell identity shift. Cellular functionality or lineage-specific gene expression is tightly linked to the cell type-specific epigenetic landscape, reinforcing the heterogeneity of senescence across cell types. Here, we aim to define the senescence cellular functionality and epigenetic features that may contribute to the gain-of-function phenotype.
MeSH term(s)	Cell Nucleus ; Cellular Senescence/genetics ; Identity Crisis ; Phenotype
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1293750-2
ISSN	1530-8995 ; 1081-0706
ISSN (online)	1530-8995
ISSN	1081-0706
DOI	10.1146/annurev-cellbio-120420-013537
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Article ; Online: Autophagy at the intersection of aging, senescence, and cancer.

Cassidy, Liam D / Narita, Masashi

Molecular oncology

2022 Volume 16, Issue 18, Page(s) 3259–3275

Abstract: Autophagy is an evolutionarily conserved cellular process in which macromolecules undergo lysosomal degradation. It fulfills essential roles in quality controlling cellular constituents and in energy homeostasis. Basal autophagy is also widely accepted ... ...

Abstract	Autophagy is an evolutionarily conserved cellular process in which macromolecules undergo lysosomal degradation. It fulfills essential roles in quality controlling cellular constituents and in energy homeostasis. Basal autophagy is also widely accepted to provide a protective role in aging and aging-related disorders, and its decline with age might precipitate the onset of a variety of diseases. In this review, we discuss the role of basal autophagy in maintaining homeostasis, in part through the maintenance of stem cell populations and the prevention of cellular senescence. We also consider how stress-induced senescence, for example, during oncogene activation and in premalignant disease, might rely on autophagy, and the possibility that the age-associated decline in autophagy might promote tumour development through a variety of mechanisms. Ultimately, evidence suggests that autophagy is required for malignant cancer progression in a number of settings. Thus, autophagy appears to be tumour-suppressive during the early stages of tumorigenesis and tumour-promoting at later stages.
MeSH term(s)	Aging/metabolism ; Autophagy/physiology ; Cellular Senescence ; Humans ; Lysosomes/metabolism ; Neoplasms/pathology
Language	English
Publishing date	2022-07-09
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.13269
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Article ; Online: Cellular senescence: beneficial, harmful, and highly complex.

Baker, Darren J / Narita, Masashi / Muñoz-Cánoves, Pura

The FEBS journal

2023 Volume 290, Issue 5, Page(s) 1156–1160

Abstract: The contribution of cellular senescence to a diverse range of biological processes, including normal physiology, ageing, and pathology were long overlooked but have now taken centre stage. In this Editorial, we will briefly outline the review and ... ...

Abstract	The contribution of cellular senescence to a diverse range of biological processes, including normal physiology, ageing, and pathology were long overlooked but have now taken centre stage. In this Editorial, we will briefly outline the review and original work articles contained in The FEBS Journal's Special Issue on Senescence in Ageing and Disease. It is beginning to be appreciated that senescent cells can exert both beneficial and adverse effects following tissue injury. Additionally, while these cells play critical roles for maintaining a healthy physiology, they also promote ageing and certain pathological conditions (including developmental disorders). Progress has been made in re-defining and identifying senescent cells, especially in slow-proliferating or terminally differentiated tissues, such as the brain and cardiovascular system. Novel approaches and techniques for isolating senescent cells will greatly increase our appreciation for senescent properties in tissues. The inter-organ communication between senescent cells and other residents of the tissue microenvironment, via the senescence-associated secretory phenotype (SASP), is a focus of several reviews in this Special Issue. The importance of the SASP in promoting tumour development and the evolution of SARS CoV-2 variants is also highlighted. In one of the two original articles included in the issue, the impact of dietary macronutrients and the presence of senescent cells in mice is investigated. Lastly, we continue to deepen our understanding on the use of senolytics and senomorphics to specifically target senescent cells or their secreted components, respectively, which is discussed in several of the reviews included here.
MeSH term(s)	Animals ; Mice ; COVID-19 ; Cellular Senescence ; Aging ; Cell Differentiation ; Brain
Language	English
Publishing date	2023-02-28
Publishing country	England
Document type	Editorial
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16735
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Article ; Online: Beyond SAHF: An integrative view of chromatin compartmentalization during senescence.

Olan, Ioana / Handa, Tetsuya / Narita, Masashi

Current opinion in cell biology

2023 Volume 83, Page(s) 102206

Abstract: Cellular senescence, a persistent form of cell cycle arrest, has been linked to the formation of heterochromatic foci, accompanied by additional concentric epigenetic layers. However, senescence is a highly heterogeneous phenotype, and the formation of ... ...

Abstract	Cellular senescence, a persistent form of cell cycle arrest, has been linked to the formation of heterochromatic foci, accompanied by additional concentric epigenetic layers. However, senescence is a highly heterogeneous phenotype, and the formation of these structures is context dependent. Recent developments in the understanding of the high-order chromatin organization have opened new avenues for contextualizing the nuclear and chromatin phenotypes of senescence. Oncogene-induced senescence displays prominent foci and typically exhibits increased chromatin compartmentalization, based on the chromosome conformation assays, as marked by increased transcompaction and segregation of the heterochromatin and euchromatin. However, other types of senescence (e.g., replicative senescence) exhibit comparatively lower levels of compartmentalization. Thus, a more integrative view of the global rearrangement of the chromatin architecture that occurs during senescence is emerging, with potential functional implications for the heterogeneity of the senescence phenotype.
MeSH term(s)	Chromatin/metabolism ; Heterochromatin/metabolism ; Cell Nucleus/metabolism ; Cellular Senescence/genetics
Chemical Substances	Chromatin ; Heterochromatin
Language	English
Publishing date	2023-07-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2023.102206
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