Joseph T. Opferman

This study identifies OPA1's role in fatty acid release from lipid droplets and links its function to human metabolism.

This study identifies co-targeting of MCL-1 and ETC complex I as a synergistic therapy for high-risk AML, showing improved viability reduction and survival in preclinical models.

The paper identifies that the helical bundle domain of human MIC60 is dispensable for its core functions, revealing unexpected modularity in MICOS organization.

This study identifies IRF2BP2 cytoplasmic sequestration by MCL1 as a mechanism driving venetoclax and azacitidine resistance in AML through ACSL1 derepression.

This study shows that deleting Immt, which encodes MIC60, in mice causes lethal disruption of the MICOS complex, leading to intestinal defects and bone marrow issues.

This study shows that MCL-1 is essential for the survival of early erythroid progenitors, while BCL-xL takes over in later stages of erythropoiesis.