Induction and analysis of oxidative stress-induced premature senescence
Premature senescence was induced by oxidative stress in H[sub]2O[sub]2-treated human RPE cells, as previously described with minor modifications.
of cotton (Gossypium hirsutum L.
ROS-generating oxidases Nox1 and Nox4 contribute to oncogenic Ras-induced premature senescence
," Genes to Cells, vol.
The main objective of this study was to compare various forms of K, mineralogy, and K adsorption characteristics of some cotton soils from fields that were affected by premature senescence
(PS) and normal fields (Non-PS) to gain a better understanding of the K availability in soils in relation to the occurrence of premature senescence
in cotton plants.
Mike Capizzi, vice-president and general manager of The COLLOQUY Group, reminds us to avoid premature senescence
and to remember that we're in the business of customer information.
showed that mouse melanocytes lacking the autophagy protein Atg7 undergo premature senescence
in vitro and accumulate products of oxidative damage, despite activation of the redox response .
The studies show that premature senescence
driven by these pathogens is inhibited in Senesco plants relative to control plants.
Replicative senescence," which is provoked by endogenous stimuli, is distinct from "stress-induced premature senescence
," which is provoked by exogenous stimuli.
The Company believes that Senesco's technology can be used to develop superior strains of crops by delaying natural plant senescence and reducing the incidence of premature senescence
due to environmental stress.
Internal DNA damage (telomere shortening) as well as multiple stress signals, including ROS, aberrant oncogene activation, and chemotherapeutic drugs, are able to induce premature senescence
via activation of the p53-p21 and/or p16 Ink4a pathway .
The cellular premature senescence
is characterized by G1 cell cycle arrest, activation of cyclin-dependent kinase inhibitors including p53 and [p21.
Senesco's new research and development initiative, which was announced in the Company's October 2, 2000 press release, focuses on reducing the harmful effects of premature senescence
induced by environmental stress.