Results 51 to 60 of about 26,014 (255)

Cytoplasmic chromatin triggers inflammation in senescence and cancer [PDF]

open access: yes, 2017
Chromatin is traditionally viewed as a nuclear entity that regulates gene expression and silencing. However, we recently discovered the presence of cytoplasmic chromatin fragments that pinch off from intact nuclei of primary cells during senescence, a ...
Adams, Peter D.   +23 more
core   +2 more sources

Cellular senescence and the tumour microenvironment

open access: yesMolecular Oncology, 2022
The senescence‐associated secretory phenotype (SASP), where senescent cells produce a variety of secreted proteins including inflammatory cytokines, chemokines, matrix remodelling factors, growth factors and so on, plays pivotal but varying roles in the ...
Masaki Takasugi   +2 more
doaj   +1 more source

Paracrine Senescence of Mesenchymal Stromal Cells Involves Inflammatory Cytokines and the NF-κB Pathway

open access: yesCells, 2022
It has been known that senescence-associated secretory phenotype (SASP) triggers senescence of the surrounding normal cells. However, SASP signaling regarding mesenchymal stromal cell aging remains to be fully elucidated.
Lun-Yin Chou   +2 more
doaj   +1 more source

Cells exhibiting strong p16INK4a promoter activation in vivo display features of senescence [PDF]

open access: yes, 2019
The activation of cellular senescence throughout the lifespan promotes tumor suppression, whereas the persistence of senescent cells contributes to aspects of aging.
Diekman, Brian O.   +9 more
core   +3 more sources

N-Acetyltransferase 10 Promotes Micronuclei Formation to Activate the Senescence-Associated Secretory Phenotype Machinery in Colorectal Cancer Cells

open access: yesTranslational Oncology, 2020
The formation of micronuclei (MN) is prevalent in human cancer cells and its role in activating the senescence-associated secretory phenotype (SASP) machinery has been identified recently.
Yanan Cao   +5 more
doaj   +1 more source

Loss of MECP2 Leads to Activation of P53 and Neuronal Senescence. [PDF]

open access: yes, 2018
To determine the role for mutations of MECP2 in Rett syndrome, we generated isogenic lines of human induced pluripotent stem cells, neural progenitor cells, and neurons from patient fibroblasts with and without MECP2 expression in an attempt to ...
Allen, Denise   +17 more
core   +2 more sources

Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4+CD25+FoxP3+ regulatory T cells activation [PDF]

open access: yes, 2020
Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive
Drovakova A.   +11 more
core   +1 more source

Downregulation of cytoplasmic DNases is implicated in cytoplasmic DNA accumulation and SASP in senescent cells

open access: yesNature Communications, 2018
Activation of DNA damage response induces the acquisition of senescence-associated secretory phenotype (SASP) in senescent cells, but precise mechanisms remain unclear.
Akiko Takahashi   +11 more
doaj   +1 more source

Inside and out: the activities of senescence in cancer. [PDF]

open access: yes, 2014
The core aspect of the senescent phenotype is a stable state of cell cycle arrest. However, this is a disguise that conceals a highly active metabolic cell state with diverse functionality.
A Alimonti   +162 more
core   +1 more source

Suppression of the senescence-associated secretory phenotype (SASP) in human fibroblasts using small molecule inhibitors of p38 MAP kinase and MK2

open access: yesBiogerontology (Dordrecht), 2015
Senescent cells show an altered secretome profile termed the senescence-associated secretory phenotype (SASP). There is an increasing body of evidence that suggests that the accumulation of SASP-positive senescent cells in humans is partially causal in ...
Dauren S. Alimbetov   +7 more
semanticscholar   +1 more source

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