Single molecule mRNA imaging uncovers post-transcriptional regulation of myc mRNA, via a cell-intrinsic mechanism allowing individualised control of neural stem cell proliferation during Drosophila brain development.
Interaction of oncoprotein transcription factor MYC with chromatin-associated protein host cell factor–1 controls expression of genes important for ribosome biogenesis and mitochondrial vigor, loss of which promotes tumor regression.
Myc-dependent induction of amino acid transporter expression in response to T cell receptor activation is essential to enable T cell proteome remodelling upon immune activation.
A new potent and selective CDK9 inhibitor induces the expression of the proto-oncogene MYC via a mechanism that depends on the bromodomain protein BRD4.
MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.
Epstein-Barr virus controls B-cell growth and survival through large-scale reorganization of the enhancers of the MYC and BCL2L11 genes, and may promote MYC translocations as a result.
We reveal TAPBPR is a peptide exchange catalyst which restricts the peptide repertoire presented by MHC I on cells, a finding which has important implications for all aspects of immune recognition.
An insulin-Myc feed-forward loop triggered by transient JNK boosts transcription of genes essential for mitochondrial respiration and biogenesis during early oogenesis to support massive mtDNA replication and inheritance in Drosophila.
The recently discovered peptide editor TAPBPR binds to UDP-glucose:glycoprotein glucosyltransferase 1 to provide quality control in the antigen presentation pathway by facilitating the reglucosylation of the glycan on MHC class I molecules.
