The TERT promoter mutation does not generate enough telomerase to immortalize the pre-cancerous cells, but does delay
normal cellular aging, Hockemeyer said, allowing more time for additional changes that turns telomerase up.
Not exact matches
«What we're seeing is a
normal process —
cellular aging — augmented and accelerated once a cell becomes cancerous.
While changes in insulin secretion are unlikely to play a major role in the acute effects of SD,
cellular stress in pancreatic tissue suggests that chronic SD may contribute to the loss or dysfunction of endocrine cells, and that these effects may be exacerbated by
normal aging, say the researchers.
Danny Hatters, a molecular biologist at the University of Melbourne, says the study is a convincing demonstration that the Huntington's mutation begins disrupting
normal cellular events «very early in
age and long before clinical diagnosis», he says.
While
normal RNA regulation involves regulated and reversible assembly of RNA - protein particles, both increased
cellular age and mutation push the process towards hyperassembly, which leads to altered pools of RNA or RNA regulatory proteins in neurons that contribute to their eventual death.
DNA damaging agents can promote
ageing, disease and cancer and are widespread in the environment as well as being produced within human cells as
normal cellular metabolites
For setting cancer in the context of
ageing tissue, study of
normal adult homeostasis is important — we are studying mutational processes, clonal dynamics and
cellular competition in thousands of non-cancerous cells and samples from a range of tissue types, in health and disease.
There is only the most tentative of evidence suggesting a link between
cellular senescence and cataract in «
normal»
aging.
(9) Indeed, the degenerative
aging process is by definition one in which the organism progressively accumulates damage to its
cellular and molecular components over time, so any genetic or environmental factor that leads to a greater burden of such damage will bear some resemblance to the
aging phenotype, irrespective of the causal origin of the defect or its relationship to «
normal»
aging.
Topics such as the mechanisms of cell injury in
normal and dystrophic muscle, compensatory muscle regeneration and hypertrophy, and the effects of various therapies or voluntary exercise on muscle repair, satellite cell activation, muscle growth, bone density and
age - related atrophy are examined using a large variety of
cellular, molecular and whole - animal in vivo assays of function.
Our goal is to understand how ATM and ATR contribute to
normal and premature
cellular aging.
This in turn reduces the supply of metabolic enzymes available for
normal cellular functions and is a root cause of many health problems associated with
aging.
It is usually an excess of
cellular damage that isn't all that relevant in
normal aging - any sort of global dysfunction in cells will tend to share high level similarities with
aging, even if the damage is different.