Jiejun Shi

TL;DR: It is shown that BAP1 suppresses SLC7A11 expression and cystine uptake, thereby promoting ferroptosis and inhibiting tumour growth and uncovering a previously unappreciated epigenetic mechanism coupling ferroPTosis to tumour suppression.

TL;DR: High-throughput transcriptomics and metabolomics show that the liver has independent circadian functions specific for metabolic processes such as the NAD+ salvage pathway and glycogen turnover, but although BMAL1 occupies chromatin at most genomic targets in Liver-RE mice, circadian expression is restricted to ∼10% of normally rhythmic transcripts.

TL;DR: The finding that SLC7A11 overexpression enhances cancer cell dependence on glucose and renders cancer cells more sensitive to glucose starvation-induced cell death is reported and supports the notion that both glucose and glutamate have important roles in maintaining cancer cell survival.

TL;DR: It is proposed that an ordered histone code can promote progression through the transcription cycle, providing new mechanistic insight indicating that SEC recruitment to certain acetylated histones on a subset of genes stimulates the subsequent release of paused pol II needed for transcription elongation.

TL;DR: It is shown that cancer cells with high levels of SLC7A11 have increased dependency on the pentose phosphate pathway and consequently accumulate disulfide, and can be therapeutically targeted by limiting glucose supply.