The heme and HRI-mediated eIF2aP–ATF4 integrated stress response in erythropoiesis has a major global impact, especially under the stress condition of iron deficiency.

Activation of the integrated stress response by stalled translation elongation complexes attenuates neurodegeneration, and demonstrates a protective link between a decrease in the rate of translation initiation and defects in translation elongation.

Unique integrate stress response sensors differentially trigger pro-survival versus pro-apoptotic responses in cells confronted with Hsp70 inhibitor-associated proteotoxic challenges.

Integrated stress response-induced expression of ATF4 and its transactivation of SOX9 causes aberrant chondrocyte differentiation and skeletal defects which can be alleviated by modulating initiation-factor eIF2α phosphorylation translation control.

C9ORF72 antisense repeat expanded RNAs activate PKR/eIF2α dependent integrated stress response and cause neuronal toxicity independent of DPR proteins.

In response to proteotoxic stress, squamous cell carcinoma cells hijack the integrated stress response to promote recovery by bolstering protection of microtubule dynamics.