Sentences with phrase «in cellular senescence»

An enzyme called SETD8 appears to play a critical role in cellular senescence onset Senescent cells may have stopped dividing, but they continue to remain active — churning out a specific cocktail of factors that increases inflammation and breaks down tissue among other things.

Excitingly, our study points out that condensin plays an important role in cellular senescence, a major tumor suppression mechanism.

The Cang lab is interested in developing novel biophotonics tools to understand chromatin modifications in cellular senescence.

Some of the leading folk in the cellular senescence research community today published the results from a very encouraging life span study, extending life in mice via a method of removing senescent cells.

Not exact matches

Through the mTOR signalling pathway, it is involved in the regulation of many cellular processes, including cell survival, metabolism, proliferation, differentiation, and senescence.

When researchers suppressed the ARF gene in mole - rat cells during the reprogramming process to iPSCs, the cells stopped proliferation with sign of cellular senescence, while the opposite happens with mouse cells.

Intermittent dosing with rapamycin selectively breaks the cascade of inflammatory events that follow cellular senescence, a phenomena in which cells cease to divide in response to DNA damaging agents, including many chemotherapies.

They focused in on genes known to regulate a cellular state called senescence.

«Understanding the cellular and molecular events of senescence might help in finding preventive measures that are useful to improve the quality of life of millions of people,» said Silvia Bradamante, a researcher involved in the work from the CNR - ISTM, Institute of Molecular Science and Technologies in Milan, Italy.

This series addresses the contribution of cellular senescence to cardiovascular, neurodegenerative, and arthritic disorders as well as the senescent phenotypes in various tissues and cell types.

The breast cancer drug palbociclib arrests cells in G1 phase by CDK4 / 6 inhibition, but also causes cellular senescence.

Busulfan selectively induces cellular senescence but not apoptosis in WI38 fibroblasts via a p53 - independent but extracellular signal - regulated kinase - p38 mitogen - activated protein kinase - dependent mechanism.

As an assistant professor at the Boston University Medical School, she became interested in the control of cellular senescence and its role in tumor suppression and aging.

But then, upon reading the article mentionned by Deleo, I spotted the following: «So 20 - employee Unity now has a potential drug that David [the CEO] said could land in human clinical trials within two years, venture cash, respected executives, intellectual property blanketing cellular senescence -LRB-...)»

Again, then, there is significant evidence consistent with a role of cellular senescence in age - related lipodystrophy and lipoatrophy, and for the benefits observed in treated mice in these studies to translate into aging humans.

This project seeks to explore cellular senescence in ILDs.

Part of this is a pathological redistribution of adipose from the subcutaneous to the visceral depot, but it now emerges that the subcutaneous depot becomes qualitative as well as quantitatively abnormal in the degenerative aging process also suffers genuine age - related lipoatrophy and lipodystrophy — and that p16Ink4a - driven cellular senescence is at the heart of it.

This project has the potential to uncover clinically relevant mechanisms of cellular senescence in fibrosing ILDs and identify new therapeutic targets

In recent years, cellular senescence has been proposed as a mechanism that may be involved in lung fibrosiIn recent years, cellular senescence has been proposed as a mechanism that may be involved in lung fibrosiin lung fibrosis.

There is only the most tentative of evidence suggesting a link between cellular senescence and cataract in «normal» aging.

In particular, they are focused on studying the functional role and molecular mechanisms of cellular senescence in both of these events, and how a deregulation of normal epithelial stem cell proliferation is involveIn particular, they are focused on studying the functional role and molecular mechanisms of cellular senescence in both of these events, and how a deregulation of normal epithelial stem cell proliferation is involvein both of these events, and how a deregulation of normal epithelial stem cell proliferation is involved.

The damage that it will repair is the one that is causal in senenscence of DNA pathway (such x-ray radiation causing senescence) and oncogenic activated senescence; but not of the type of replicative senescence (that's the domain of telomeres / telomerase / sub-telomeres and epigenetics) and cellular replication / proliferation.

What is particularly interesting is that AGEs have been shown to induce premature cellular senescence, suggesting that high glucose levels associated with diabetes likely accelerates ageing in other tissues that consequently manifest as disease.

A number of recent articles, however, have reported that hiPSCs are, in fact, notably distinct from human embryonic stem cells in terms of their gene expression, epigenetic profile, proliferative capacity and the susceptibility of their differentiated progeny to cellular senescence and apoptosis [3 — 6].

Using replicative senescence as a cellular model, we will dissect the functions of ATR and ATM in the process of aging and in premature aging diseases.

We investigated telomere dysfunction, a recently discovered biomarker of cellular senescence, and found that the number of senescent fibroblasts increases exponentially in the skin of aging baboons, reaching > 15 % of all cells in very old individuals.

These data indicate that cellular senescence is causally implicated in generating age - related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.

Only in the last 10 years, with increasing knowledge of the senescent phenotype and the ability to detect senescent cells in human tissues, have biologists been able to investigate the relationship between cellular senescence and disease.

It has recently been proposed that the primary role of cellular senescence is in mitotic compartments of fixed size in which spatial considerations dictate that a deleted cell is replaced by a neighboring cell.

p53 also plays important and complex roles in regulating cellular senescence and animal aging, and can exert both pro-aging and pro-longevity effects in mice.

The ability to measure the degree of cellular senescence is important in understanding the biological processes regulating cell aging and immortalization.

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

Passos JF, Saretzki G, von Zglinicki T. DNA damage in telomeres and mitochondria during cellular senescence: is there a connection?

We have shown that the human condensin complex functions in global 3D genome reorganization during the important process of cellular senescence (Yokoyama et al..

In the figure: Condensin triggers cellular senescence and its associated genome organization.

The aim of WICT is the removal from the organismal environment of accumulated cellular and intracellular damage present in the patient's endogenous cells, including telomere depletion, nuclear DNA damage and mutations, mitochondrial DNA damage and mutations, replicative senescence, functionally - deleterious age - related changes in gene expression and accumulated cellular and intracellular aggregates.

In addition to LOX - 1 mediated vascular inflammation, oxLDL / LOX -1 internalization triggers endothelial / vascular smooth muscle cell dysfunction, apoptosis, cellular senescence, or osteoblastic differentiation.

However, there is a scenario in which cellular senescence is desirable.

An anti-cancer diet also needs to be low or moderate in complete protein and high - insulemic index foods (to reduce growth promoting IGF - 1), and perhaps low in methionine specifically while high in fiber, phytochemical hormetics (to induce endogenous antioxidant responses and toxin removal), epigenetically active compunds (to reexpress tumor suppressor genes for induce cellular senescence or apoptosis), inflammation inhibitors, and antiangiogenetic compounds.