scispace - formally typeset
A

Ana C. D’Alessio

Researcher at Massachusetts Institute of Technology

Publications -  16
Citations -  7081

Ana C. D’Alessio is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Bivalent chromatin & Embryonic stem cell. The author has an hindex of 14, co-authored 16 publications receiving 6384 citations. Previous affiliations of Ana C. D’Alessio include University of North Carolina at Chapel Hill & University of California, Los Angeles.

Papers
More filters
Journal ArticleDOI

Role of Tet proteins in 5mC to 5hmC conversion, ES-cell self-renewal and inner cell mass specification

TL;DR: It is demonstrated that all three mouse Tet proteins (Tet1, Tet2 and Tet3) can also catalyse a similar reaction, uncover the enzymatic activity of the Tet proteins, and demonstrate a role for Tet1 in ES cell maintenance and inner cell mass cell specification.
Journal ArticleDOI

Poised Chromatin at the ZEB1 Promoter Enables Breast Cancer Cell Plasticity and Enhances Tumorigenicity

TL;DR: It is demonstrated that non-CSCs of human basal breast cancers are plastic cell populations that readily switch from a non- CSC to CSC state, and this findings support a dynamic model in which interconversions between low and high tumorigenic states occur frequently, thereby increasing tumorigenics and malignant potential.
Journal ArticleDOI

Dual functions of Tet1 in transcriptional regulation in mouse embryonic stem cells

TL;DR: This study shows in mouse ES cells that Tet1 is preferentially bound to CpG-rich sequences at promoters of both transcriptionally active and Polycomb-repressed genes, and reveals a dual function of Tet1 in promoting transcription of pluripotency factors as well as participating in the repression ofPolycomb-targeted developmental regulators.

Poised Chromatin at the ZEB1 Promoter Enables Breast Cancer Cell Plasticity and Enhances Tumorigenicity

TL;DR: In this paper, the authors demonstrate that non-CSCs of human basal breast cancers are plastic cell populations that readily switch from a nonCSC to a CSC state, and that the observed cell plasticity is dependent on ZEB1, a key regulator of the epithelial-mesenchymal transition.