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Federica Santoro

Researcher at Karolinska Institutet

Publications -  13
Citations -  606

Federica Santoro is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: DNA methylation & Genomic imprinting. The author has an hindex of 9, co-authored 13 publications receiving 511 citations. Previous affiliations of Federica Santoro include Austrian Academy of Sciences.

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Megabase-scale deletion using CRISPR/Cas9 to generate a fully haploid human cell line

TL;DR: In this paper, the authors employed a CRISPR/Cas9-based genome engineering strategy to excise this sizeable chromosomal fragment and to efficiently and reproducibly derive clones that retain their haploid state.
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Programming and reprogramming a human heart cell

TL;DR: The fundamental principles that govern the “programming” and “reprogramming" of a human heart cell are considered and updated therapeutic strategies to regenerate a damaged heart are discussed.
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Imprinted Igf2r silencing depends on continuous Airn lncRNA expression and is not restricted to a developmental window

TL;DR: It is shown that Airn expression is both necessary and sufficient to silence Igf2r throughout ESC differentiation and that the somatic methylation imprint, although not required to initiate or maintain silencing, adds a secondary layer of repressive epigenetic information.
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Population and Single-Cell Analysis of Human Cardiogenesis Reveals Unique LGR5 Ventricular Progenitors in Embryonic Outflow Tract.

TL;DR: Comprehensive gene expression profiles of human cardiac derivatives from multipotent CPCs to intermediates and mature cardiac cells by population and single-cell RNA-seq using human embryonic stem cell-derived and embryonic/fetal heart-derived cardiac cells micro-dissected from specific heart compartments are reported.
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Silencing and transcriptional properties of the imprinted Airn ncRNA are independent of the endogenous promoter

TL;DR: It is shown by deletion of the Airn ncRNA promoter and replacement with a constitutive strong or weak promoter that splicing suppression and termination, as well as silencing activity, are maintained by strong Airn expression from an exogenous promoter.