Marco J. Herold

This paper introduces Partita, a high-density CRISPRa platform for comprehensive gene activation studies, demonstrating its utility in identifying cancer dependencies and resistance pathways in vitro and in vivo.

This study identifies renal mononuclear phagocytes as an intracellular reservoir for UPEC in pyelonephritis, showing that complement receptor-mediated entry promotes bacterial persistence and limits β-lactam efficacy.

The paper develops a CRISPR-based system using Cas9-expressing hepatocytes to study Plasmodium falciparum host interactions, validating its utility for screening host genes involved in infection.

This study replaces MCL-1 with other anti-apoptotic proteins in mice to determine the relative importance of MCL-1's anti-apoptotic versus non-apoptotic functions in development and physiology.

This study shows DNMT3A mutations reduce DNA methylation and disrupt p53 pathway, increasing self-renewal and cancer risk in hematopoietic cells.

This study identifies TXNRD3 as a target to sensitize triple-negative breast cancer cells to EGFR inhibitors by enhancing EGFR activation and surface localization.

The paper introduces an enAsCas12a mouse model and associated libraries for efficient gene editing and screening, identifying drug resistance genes and enabling simultaneous gene knockouts and activations.

This paper introduces a xeno-free single-cell cloning method for CRISPR-edited human iPSCs, achieving high clonal survival and editing efficiency for improved disease modeling.

This study identifies VDAC2 as essential for BAX-mediated apoptosis and tumor suppression, showing BAX and BAK are differentially regulated.