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The BCL-2 protein family: Opposing activities that mediate cell death.
Bu siniftaki inhibitorler icin kullanilan Bcl-2 inhibitor terimi, hucre yasamini tesvik eden protein ailesi uyelerini baglayan ilaclari kapsamaktadir.
Conclusion: Ferulic acid could significantly descend osteosarcoma cell viability through the promoting apoptosis pathway in which FA activates both caspase-3 and Bax and inactivates Bcl-2.
20] P53 is a protein which has a role in the repairment of DNA, apoptosis, and cycle cell, [26] whereas Bcl-2 is a protein of anti-apoptotic activity.
The aim of current study was to observe the intensity of caspase-3, lipid peroxidation Bcl-2 mRNA, and Glutathione, in MDCK cell lysates after the treatment through AFB1 and the protection exerted through beta-carotene.
To this end, Jurkat cells stably transfected with Bcl-2 or the empty control vector were irradiated with 0, 5, or 10 Gy by 6 MV photons.
Bcl-2 presence has been reported in areas of cholangiolar proliferation and focally, in hepatocytes in patients with cirrhosis caused by HCV.
BAX was the first identified P53-regulated, proapoptotic Bcl-2 family member.
Results showed that telomerase and Bcl-2 expression was significantly lower in group C compared with group B (0.
Dentre alguns fenomenos que geralmente regulam esses processos, podemos citar genes pro e antiapoptoticos da familia BCL-2, mecanismos de detoxificacao intracelular e super-expressao de moleculas que transportam as drogas para fora da celula ou para outros compartimentos celulares, como a glicoproteina-p (produto do gene MDR-1); alem de sistemas de reparo do DNA associados com a familia do TP53.
The study findings potentially could refine this approach so that chemotherapy can be timed more effectively, killing off cancer cells and preventing a relapse when the BCL-2 gene is sufficiently weak.
1) In this regard, B Cell CLL/lymphoma-2 protein (bcl-2), which is an anti-apoptotic member of the bcl-2 protein family, has been implicated as a key player in the neuroprotective actions of lithium (2) and the pathophysiology of BD.