Ester M. Hammond

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: These studies directly implicate XBP1 as an essential survival factor for hypoxic stress and tumor growth.

TL;DR: It is reported that hypoxia induces p53 protein accumulation, but in contrast to DNA damage,Hypoxia fails to induce endogenous downstream p53 effector mRNAs and proteins, leading to a model in which different cellular pools of p53 can modulate transcriptional activity through interactions with transcriptional coactivators or corepressors.

TL;DR: It is demonstrated that severe hypoxia leads to ER stress and induces ATF4-dependent autophagy through LC3 as a survival mechanism, and small interfering RNA and microarray analysis is used to provide the first whole-genome analysis of genes regulated by ATF4 in cancer cells in response to severe and prolonged hypoxic stress.

TL;DR: It is shown that, under severe hypoxic conditions, p53 protein accumulates only in S phase and this accumulation correlates with replication arrest, andHypoxia-induced cell growth arrest is tightly linked to an ATR-signaling pathway that is required for p53 modification and accumulation.