Differences in promoter affinity and MYC levels explain distinct expression profiles induced by physiological and oncogenic MYC.

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.

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.

The number of different peptides presented by major histocompatibility complex class I molecules to the immune system's T lymphocytes is inversely correlated with cell surface expression and is strongly associated with the response to infectious disease.

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.

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.

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.

The endoplasmic reticulum (ER) folding sensor UGGT1 essentially cooperates with the peptide editor TAPBPR to provide quality control of MHC I molecules in the antigen presentation pathway.

Genome sequencing analysis dissects the origins and evolution of cancer transmission between clam species in the Seas of Southern Europe.

Oligodendroglia express major histocompatibility complex (MHC) pathways in response to inflammation and MHC reporter mice allow for the investigation of MHC molecule expressing cells in vivo.