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The implication of ellagic acid on apoptosis was further checked by testing the apoptotic enzyme caspase-3.
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We also investigated if the balance between pro-apoptotic and anti-apoptotic proteins was associated with DSS by testing the impact of Bcl-2/Bax and Bcl-XL/Bax ratios on survival outcome.
Therefore, we tested whether the apoptotic response to radiation was retained by the epithelial outgrowths that originate from E+P-treated or parous tissue.
To evaluate the mechanism by which CML-exosomes are able to sustain tumor growth, we tested the expression of different molecules involved in the apoptotic machinery.
Osmotin by itself affected some but not all of the tested downstream apoptotic markers.
This fungal taxol also had strong anticancer activity against some cancer cells viz., BT 220, H116, Int 407, HL 251, and HLK 210 tested by Apoptotic assay, and it is indicated that with the increase of taxol concentration from 0.005 0.05 M, the taxol induced increased cell death through apoptosis.
We tested the effect of caspase-2, -8 and -10 loss on the apoptotic response, as determined by the NBI1/erlotinib-induced activation of caspase activity in cellular extracts.
After establishing this cellular model, we next wanted to test the recruitment of known downstream mediators of non-apoptotic CD95 signals.
The three tested extracts induced apoptotic effect by the activation of the extrinsic apoptotic pathway.
We calculated apoptotic indices by counting the apoptotic figures per 5,000 hepatocytes on tumor sections from 10 tissues per mouse model and 15 tissues per human subclass.
Quantitative analysis of apoptotic cell death was determined by calculating the apoptotic index (AI).
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CEO of Professional Science Editing for Scientists @ prosciediting.com