DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cells

Article Abstract:

Cell proliferation is deregulated by expression of adenovirus to facilitate DNA replication by quick initiation of apoptosis signaled through proapoptotic BAK in productively infected cells. BAK is complexed with the anti-apoptotic BCL-2 family member Myeloid Cell Leukemia 1 (MCL-1) in uninfected cells.

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NBK/BIK antagonizes MCL-1 and BCL-[X.sub.L] and activates BAK-mediated apoptosis in response to protein synthesis inhibition

Article Abstract:

The apoptotic activity of a MazF, a toxin from the bacteria Escherichia coli, in mammal cells is studied. It is demonstrated that MazF breaks down the cellular mRNA by displacing anti-apoptotic proteins MCL-1 and BCL-[X.sub.L], mediated by proapoptotic BAK and its regulatorBH3-only protein NBK/BIK.

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BH3-only proteins in control: Specificity regulates MCL-1 and BAK-mediated apoptosis

Article Abstract:

BH3, a member of BCL-2 family of proteins, which are the most apical regulators of death-signaling cascade like cancer, is studied. The goal of activating apoptosis in tumor cells with acquired resistance could be understood by interpreting the mode of interaction and regulation of these proteins.

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