Maria Hatzoglou

The paper investigates the cellular response to puromycin-induced translation stress and identifies ribosome dimerization mediated by rRNA expansion segments as a conserved stress response mechanism.

This paper shows eIF2B activates mutant KRAS by forming a complex with SOS at the plasma membrane and regulating glycosphingolipid biosynthesis.

The paper identifies DDX3X as a dual switch regulator of mRNA translation, promoting or suppressing translation in non-stressed cells and switching roles in acute ER stress.

This study shows that activation of the integrated stress response (ISR) drives tumor evolution and therapy resistance by promoting dedifferentiation and stemness in lung adenocarcinoma.

This study shows that VAPB P56S mutation causes mitochondrial dysfunction and enhances the integrated stress response, leading to motor neuron disease in ALS.

The paper identifies a stem-loop and modified adenines in the uORF2/ATF4 overlap that regulate ATF4 translation under stress, revealing a more complex mechanism than previously thought.

This study identifies a human homologue of a mitochondrial noncoding RNA that translocates to the nucleus and enhances mitochondrial bioenergetics in response to cigarette smoke, but its levels decline in chronic obstructive pulmonary disease.

The paper investigates how newly synthesized mRNA, specifically XBP1 mRNA, escapes translational repression during the acute phase of the UPR by accumulating long poly(A) tails, enhancing cell survival.

This study shows chronic ER stress induces β-cell plasticity, but excessive stress leads to identity loss and is linked to T1D progression.

The paper shows that cells use an adaptive pausing response to survive severe stress by pausing translation and limiting ATP use, followed by recovery through ISR signaling.

The paper identifies start-stop elements in 5' UTRs that repress translation by halting ribosomes, showing their prevalence in human genes and impact on cellular processes.

The paper identifies a Redox Thiol Switch (RTSGS) that regulates cellular energy metabolism by switching between S-glutathionylation and S-sulfhydration, with PCK2 as a novel target.

This study identifies Dazl's role in germ cell survival by mapping its RNA interactions and showing its regulation of genes critical for proliferation and survival.