Mark Stoneley

TL;DR: The cellular situations when IRESs are required, the trans-acting factors that are necessary for IRES function and deregulation of IRES-mediated translation in tumorigenesis are discussed.

TL;DR: Data is shown which demonstrates that the 5′ UTR of the proto-oncogene c-myc contains an IRES, the first example of a proto- oncogene regulated in this manner and suggests that aberrant translational regulation of c- myc is likely to play a role in tumorigenesis.

TL;DR: There is now an overwhelming body of evidence to suggest that internal ribosome entry is required to maintain the expression of specific proteins during patho‐physiological situations when cap‐dependent translation is compromised, for example, following heat shock or during mitosis, hypoxia, differentiation and apoptosis.

TL;DR: The data suggest that the initiation of translation via the c-myc IRES during apoptosis is mediated by the p38 MAPK pathway, and cotransfection with plasmids which harbor either wild-type or constitutively active MKK6, a specific immediate upstream activator of p38 mitogen-activated protein kinase (MAPK), increases IRES-mediated translation.

TL;DR: It is demonstrated that the promoter used to transcribe the mRNA influences the type of miRNA-mediated translational repression, establishing a link between the nuclear history of an mRNA and the mechanism of miRNAs- mediated translational regulation in the cytoplasm.