Anna Bigas

This study shows SMARCA4 mutations in T-ALL lead to chemotherapy resistance by altering chromatin remodeling at AP-1 regulatory regions, reducing stress response genes.

This study identifies a developmental program for hematopoietic stem cell (HSC) dormancy established during embryogenesis through evasion of Notch signaling, revealing a mechanism for long-term regenerative potential.

This paper introduces a 3D hemogenic gastruloid model to study infant acute myeloid leukemia origins, showing MNX1-driven transformation of erythroid-myeloid progenitors.

The paper analyzes patient-derived SS cells to identify transcriptomic, mutational patterns, and functional pathway alterations, finding limited pathway changes but potential for MALT1 inhibition in therapy.

This study identifies the IFNγ pathway's role in accelerating iPSC reprogramming and X-chromosome reactivation through STAT3 signaling and TET-mediated demethylation.

The paper identifies NOTCH1-JAG1 cis interactions regulated by RADICAL FRINGE that maintain hematopoietic stem cell fate during development.

The paper shows that phosphorylated IκB binds chromatin via acetylated H4 and that proteolytic cleavage of H4 inhibits this binding, affecting intestinal cell differentiation.

This study identifies a role for C. elegans I{kappa}B homologs in chromatin regulation, showing they bind histones, Polycomb proteins, and alter chromatin marks, suggesting ancestral I{kappa}B functions in development.

The paper shows that Dll4 inhibits cell recruitment into aortic clusters, reducing hematopoietic stem cell formation.