Almut Schulze

The paper identifies extracellular glutathione catabolism as a driver of metastasis by enabling proliferation and oxidative stress resistance in metabolically challenging microenvironments.

This study identifies FAHD1 as a critical regulator of mitochondrial function and cardiomyocyte maturation, showing its deficiency impairs respiration, disrupts sarcomere organization, and leads to cardiac dysfunction.

This study shows that arginine depletion induces senescence and stress response in pancreatic cancer cells, making them susceptible to senolysis and stress response inhibition.

This study identifies GLYATL1 as a mediator of endocrine resistance in luminal breast cancer by promoting metabolic and epigenetic changes that counteract estrogen deprivation.

This study shows that selective class IIa HDAC inhibition improves diastolic dysfunction in HFpEF without adverse effects.

The paper shows that genomic G quadruplexes regulate mRNA splicing by recruiting RNA-binding proteins, with implications for cardiac function.

The paper identifies CAMK2-NR4A1 signaling as a driver of metabolic substrate switching in heart failure with reduced ejection fraction, linking it to cardiac dysfunction through glucose utilization and lipid depletion.

This study improves Ewing sarcoma cell culture conditions to better reflect physiological states, revealing metabolic gene signatures linked to oncogenic fusion proteins.