Lista de obras -

A natural regulatory mutation in the proximal promoter elevates fetal globin expression by creating a de novo GATA1 site

artículo científico publicado en 2019

An erythroid-specific ATP2B4 enhancer mediates red blood cell hydration and malaria susceptibility.

artículo científico publicado en 2017

BCL11A enhancer dissection by Cas9-mediated in situ saturating mutagenesis

artículo científico publicado en 2015

CRISPR-Cas9 interrogation of a putative fetal globin repressor in human erythroid cells

artículo científico publicado en 2019

Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch.

artículo científico publicado en 2018

Dual base editor catalyzes both cytosine and adenine base conversions in human cells

artículo científico publicado en 2020

Genome-wide association study of red blood cell traits in Hispanics/Latinos: The Hispanic Community Health Study/Study of Latinos.

artículo científico publicado en 2017

Induction of fetal hemoglobin synthesis by CRISPR/Cas9-mediated editing of the human β-globin locus.

artículo científico publicado en 2018

KLF1 directly activates expression of the novel fetal globin repressor ZBTB7A/LRF in erythroid cells

artículo científico publicado en 2017

KLF1 drives the expression of fetal hemoglobin in British HPFH.

artículo científico publicado en 2017

Natural regulatory mutations elevate the fetal globin gene via disruption of BCL11A or ZBTB7A binding.

artículo científico publicado en 2018

PLGA-Nanoparticles for Intracellular Delivery of the CRISPR-Complex to Elevate Fetal Globin Expression in Erythroid Cells

artículo científico publicado en 2020

Rational targeting of a NuRD subcomplex guided by comprehensive in situ mutagenesis

scientific article published on 28 June 2019

Reactivation of γ-globin expression through Cas9 or base editor to treat β-hemoglobinopathies

artículo científico publicado en 2020

Robust CRISPR/Cas9 Genome Editing of the HUDEP-2 Erythroid Precursor Line Using Plasmids and Single-Stranded Oligonucleotide Donors

scientific article published on 30 July 2018

Transcription factors LRF and BCL11A independently repress expression of fetal hemoglobin

artículo científico publicado en 2016

Variant-aware saturating mutagenesis using multiple Cas9 nucleases identifies regulatory elements at trait-associated loci.

artículo científico publicado en 2017

Lista de obras de

A natural regulatory mutation in the proximal promoter elevates fetal globin expression by creating a de novo GATA1 site

An erythroid-specific ATP2B4 enhancer mediates red blood cell hydration and malaria susceptibility.

BCL11A enhancer dissection by Cas9-mediated in situ saturating mutagenesis

CRISPR-Cas9 interrogation of a putative fetal globin repressor in human erythroid cells

Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch.

Dual base editor catalyzes both cytosine and adenine base conversions in human cells

Genome-wide association study of red blood cell traits in Hispanics/Latinos: The Hispanic Community Health Study/Study of Latinos.

Induction of fetal hemoglobin synthesis by CRISPR/Cas9-mediated editing of the human β-globin locus.

KLF1 directly activates expression of the novel fetal globin repressor ZBTB7A/LRF in erythroid cells

KLF1 drives the expression of fetal hemoglobin in British HPFH.

Natural regulatory mutations elevate the fetal globin gene via disruption of BCL11A or ZBTB7A binding.

PLGA-Nanoparticles for Intracellular Delivery of the CRISPR-Complex to Elevate Fetal Globin Expression in Erythroid Cells

Rational targeting of a NuRD subcomplex guided by comprehensive in situ mutagenesis

Reactivation of γ-globin expression through Cas9 or base editor to treat β-hemoglobinopathies

Robust CRISPR/Cas9 Genome Editing of the HUDEP-2 Erythroid Precursor Line Using Plasmids and Single-Stranded Oligonucleotide Donors

Transcription factors LRF and BCL11A independently repress expression of fetal hemoglobin

Variant-aware saturating mutagenesis using multiple Cas9 nucleases identifies regulatory elements at trait-associated loci.