In conclusion, our studies have revealed that bacterial death involves DNA fragmentation, Phosphatidylserine exposure and expression of a protein with caspase-like substrate specificity.
We carried out PCR purification using the DNA Amplification Clean-Up Kit (Clontech), and probe fragmentation (brief exposure to DNase), biotin-labeling and hybridization as described in the Affymetrix protocol.
LIF deprivation led to a 6.5-fold increase in DNA fragmentation; the exposure to 2 10 μM DETA-NO conferred protection against this action.
Hallmarks of apoptosis include cell shrinkage, chromatin condensation, nuclear fragmentation and exposure of phosphatidylserine on the surface of cells at the early stages [reviewed in [ 31]].
Blocking of DNA fragmentation by exposure of Jurkat E6.1 cells to curcumin and to the JNK inhibitor SP600125 before gal-1 stimulation suggests a pivotal role of the JNK/c-Jun/AP-1 pathway for apoptosis.
Consistent with inducing excessive mitochondrial fragmentation, Cd exposure significantly increased protein levels of Drp1 and promoted the recruitment of Drp1 into mitochondria, which was tightly associated with the disturbance of calcium homeostasis.
At pH 7.5, propionibacterial SCFA were shown to induce cell-cycle arrest in the G2/M phase and morphological characteristics of apoptotic cell death, like membrane blebbing, chromatin condensation and fragmentation, phosphatidylserine exposure and formation of apoptotic bodies.
Observation of apoptotic features such as chromatin condensation, DNA fragmentation, phosphatidylserine exposure, apoptotic body formation and caspase activity have been shown by Al-Olayan et al. in the mosquito midgut stage of P. berghei.
We found that whereas 56% of vector transfectants undergo sub-G1 DNA fragmentation after STS exposure, only 7.1% of PRELI cells exhibited DNA fragments.
Results: Significant sperm deoxyribonucleic acid fragmentation occurred after exposure to deoxyribonucleic acid of human papillomavirus types 16 and 31.
