N. Locker

Turnover of PPP1R15A mRNA encoding GADD34 controls the molecular memory of the cellular integrated stress response

The paper identifies a mechanism by which PPP1R15A mRNA stability regulates GADD34 expression, controlling the cellular integrated stress response's memory and adaptation to stress.

Activation of the mitochondrial unfolded protein response regulates the formation of stress granules

The paper shows that the mitochondrial unfolded protein response (UPRmt) interacts with stress granules (SGs) to regulate cellular stress responses and mitochondrial homeostasis.

Paracrine granules are cytoplasmic RNP granules distinct from stress granules assembling in response to viral infection.

The paper identifies paracrine granules as distinct from stress granules, induced by viral infection and linked to antiviral activity.

Murine Norovirus infection results in anti-inflammatory response downstream of amino acids depletion in macrophages

This study shows that murine norovirus induces metabolic stress in macrophages, leading to anti-inflammatory responses through amino acid depletion and GCN2/ATF2 signaling, rather than a typical innate immune response.

Electrochemical measurements reveal reactive oxygen species in stress granules.

The paper uses electrochemical measurements to show that reactive oxygen species, particularly H2O2, are present in stress granules and may play a role in cellular stress communication and regulation.

Infectious bronchitis virus regulates cellular stress granule signaling

This study investigates how infectious bronchitis virus modulates cellular stress granule signaling and translational repression during infection.

Noroviruses subvert the core stress granule component G3BP1 to promote viral VPg-dependent translation.

This study identifies G3BP1 as a host factor essential for norovirus infection and reveals its role in VPg-dependent translation initiation.

Norovirus infection results in assembly of virus-specific G3BP1 granules and evasion of eIF2α signaling.

This study shows that norovirus infection leads to the formation of virus-specific granules and disrupts eIF2α signaling to evade host stress responses.