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While intact mir-17-92 acts as a potent oncogene in a mouse model of Burkitt’s lymphoma, one of the six mir-17-92 components antagonizes its oncogenic cooperation with c-Myc by promoting c-Myc-induced apoptosis.

Targeting the transcription factor c-Myc via one of its coactivator proteins is a promising strategy for cancer therapy.

The male-specific tumor-suppressive effects of minor p53 isoforms were correlated with higher Ackr4 expression levels, which have implications for sex-specific cancer prognosis in humans.

SIRT1, a cellular metabolic sensor, transcriptionally promotes sphingomyelin degradation in embryonic stem cells, which in turn modulates their membrane fluidity and neural differentiation.

A novel synthetic DNA cassette of CTCF-binding sites combined with the drug-controllable induction system of heterochromatin enabled switchable blocking of chromatin conformation and gene-enhancer interaction.

While the transcription factor c-Myc explores the space in the nucleus in an unrestricted manner, the elongation factor P-TEFb's sampling of the nucleus is constrained to a complex domain with fractal characteristics.

MYCN and TFIIIC exert a censoring function during early transcription, limiting the accumulation of inactive RNAPII at the promoter and facilitating promoter-proximal degradation of nascent RNA.

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

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.