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.
A multi-transcriptional CDKs inhibitor suppresses MYC and induces regression of ovarian tumors, indicating that targeting CDK7, 12, 13 with THZ1 may be an effective approach for treating MYC-dependent malignancies.
A c-Myc-transcribed long noncoding RNA namely LAST (LncRNA-assisted stabilization of transcripts) collaborates with a cellular factor CNBP to promote the stability of CCND1/cyclin D1 mRNA post-transcriptionally, ensuring the proper G1/Sphase transition of the cell cycle.
In addition to its cytoplasmic role for translation, the seryl-tRNA synthetase also antagonizes the c-Myc transcription factor in the nucleus to transcriptionally repress the growth factor VEGFA and ensure proper development of the vasculature in vertebrates.
Immunopeptidomics in combination with novel cell-based assays that assess peptide exchange reveal a critical role for the K22-D35 loop of TAPBPR in mediating peptide dissociation and peptide selection on MHC I.