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However, persistent or excessive autophagy is also shown to promote cell death following treatments with specific chemotherapeutic agents or radiotherapy, either by enhancing the induction of apoptosis or mediating 'autophagic cell death'.
However, persistent or excessive autophagy is also shown to promote cell death following treatment with specific chemotherapeutic agents, either by enhancing the induction of apoptosis or mediating 'autophagic cell death'.
These data suggest that MHV68 latency by-passes the requirement for TNFα and IL-6 during early Listeria infection by enhancing the induction of IFNγ and downstream effector molecules important for controlling Listeria infection.
Despite its a clear prosurvival role, autophagy has also been viewed as having a prodeath role under certain circumstances and following treatment with a specific set of chemotherapeutic agents, either by enhancing the induction of apoptosis or mediating 'autophagic cell death'.
In contrast, qNLB1.02 B73 appears to condition resistance not to infection, but rather by enhancing the induction of defense reactions surrounding infection sites, as well as by inhibiting hyphal growth into the vascular bundle, and the subsequent necrotrophic colonization in the leaves.
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Alternatively, HSP70-induced regulatory T cells might induce a tolerogenic micro-milieu, by their cytokine production, enhancing the induction of regulatory T cells via infectious tolerance.
Despite enhancing the induction of apoptosis by etoposide (Supplementary Figure S3B), the drug inhibited lipid droplet formation (Supplementary Figure S3C), decreased the incorporation of C-acetate into TAG and increased C incorporation into FFA (Supplementary Figures S3D and S3E).
They inhibit virus replication in lung epithelial cells by enhancing the virus-dependent induction of the type I IFN system.
They inhibit viral replication in lung epithelial cells by enhancing the virus-dependent induction of the IFNB1 gene and interferon-stimulated genes.
Thus, ethanol induction of CYP2E1 could contribute to hepatocarcinogenesis by enhancing the conversion of VCM into toxic intermediates.
To explore the molecular mechanism by which AFMC enhanced the induction of apoptosis by TRAIL in A549 cells, we first examined the effect of AFMC on the expression of DR4 and DR5 by Western blotting.
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