Building on previous work (Ly et al., 2014), we show that elutriated cells and arrested cells have similar patterns of DNA content and cyclin expression: however, a large fraction of the proteome changes detected in arrested cells are found to reflect arrest-specific responses rather than physiological cell cycle regulation.

Molecular pathways controlling autophagic cell death are regulated at the level of the lysosome through the activity of the pro-death Bcl-2 family member Bax/Bak.

Under normal nutritional conditions, G-protein coupled receptors can control autophagy by regulating the degradation of key autophagic regulator Atg14L through ZBTB16-mediated ubiquitination and proteasome degradation.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

Quantitative super resolution imaging, in live mammalian cells, reveals a direct relationship between protein clustering dynamics and the number of mRNA transcribed at an endogenous gene locus.

The anaphase promoting complex (APC) has an essential role in ubiquitin-mediated proteolysis in the disassembly of cilia.

Acetate concentration, which is significantly increased in association with energy stresses such as those that occur with diabetes or starvation, is emerging as a novel 'ketone body' with potential as a parameter for evaluating the progression of energy stress.

A novel genome-wide transcriptional activation screening in Drosophila cells revealed the activation of InR-Akt-mTOR pathway by cholesterol in plasma membrane to confer resistance to Rapamycin.

The lack of haem biosynthetic and degradative pathways in ticks offers new strategies to combat these parasites.

Activation by amino acids causes mTORC1 to translocate transiently to the lysosomal surface.