12 research outputs found
Susceptibility profile of Brazilian Rhodococcus equi isolates against azithromycin, clarithromycin and erythromycin
Perfil de suscetibilidade antimicrobiana e presença do gene vapA em Rhodococcus equi de origem humana, ambiental e equina
Antimicrobial activity of a porcine myeloperoxidase against plant pathogenic bacteria and fungi
The Activity of Differentiation Factors Induces Apoptosis in Polyomavirus Large T-Expressing Myoblasts
DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis*
Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senescence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving âsensorâ proteins that sense the damage, and transmit signals to âtransducerâ proteins, which, in turn, convey the signals to numerous âeffectorâ proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among the most crucial regulators of apoptosis and performs vital functions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation