Robert N. Eisenman

MYC targeted de novo binders impair tumor growth

Designed protein binders to conserved MYC regions reach low-nanomolar affinity, reduce MYC-MAX proximity in cells, and are depleted from MYC-dependent cancer cells in culture and mouse pancreatic tumors.

MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic ductal adenocarcinoma

This paper shows MondoA is essential for MYC-driven pancreatic cancer survival by coordinating MYC network activity with the integrated stress response, and small-molecule inhibition of MondoA kills cancer cells.

MAX inactivation deregulates the MYC network and induces neuroendocrine neoplasia in multiple tissues

This study shows that MAX inactivation disrupts the MYC network, leading to neuroendocrine tumors in multiple tissues by altering transcription factor balance.

Ablation of Max expression induces meiotic onset in sexually undifferentiated germ cells

This study shows that Max gene disruption in germ cells leads to meiotic onset but results in apoptosis due to stalled meiotic progression.

MLX balances metabolism and stress to suppress apoptosis and maintain spermatogenesis

This paper shows MLX and MondoA are essential for male fertility and tumor survival, with MLX regulating metabolism, stress, and germ cell development.

Distinct gene-selective roles for a network of core promoter factors in Drosophila neural stem cell identity.

This study identifies NSC-TAFs as critical for Drosophila neural stem cell identity by promoting cell cycle progression, polarity, and restraining premature differentiation.

Condensin-dependent chromatin condensation represses transcription globally during quiescence

This study identifies condensin-mediated chromatin condensation as a mechanism repressing transcription during quiescence in yeast and human cells.