Jon Kerry

Oxford, ENG, United Kingdom

Last Updated: 09/26/2026

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Found 11 publications

High-resolution targeted 3C interrogation of cis-regulatory element organization at genome-wide scale.

High-resolution targeted 3C interrogation of cis-regulatory element organization at genome-wide scale.

Journal: Nature communications
Published: April 06, 2020

Dynamics of the 4D genome during in vivo lineage specification and differentiation.

Dynamics of the 4D genome during in vivo lineage specification and differentiation.

Journal: Nature communications
Published: February 06, 2020

BET inhibition disrupts transcription but retains enhancer-promoter contact.

BET inhibition disrupts transcription but retains enhancer-promoter contact.

Journal: Nature communications
Published: December 14, 2019

Editing an α-globin enhancer in primary human hematopoietic stem cells as a treatment for β-thalassemia.

Editing an α-globin enhancer in primary human hematopoietic stem cells as a treatment for β-thalassemia.

Journal: Nature communications
Published: April 05, 2017

The basic helix-loop-helix transcription factor SHARP1 is an oncogenic driver in MLL-AF6 acute myelogenous leukemia.

The basic helix-loop-helix transcription factor SHARP1 is an oncogenic driver in MLL-AF6 acute myelogenous leukemia.

Journal: Nature communications
Published: March 22, 2017

MLL-AF4 binds directly to a BCL-2 specific enhancer and modulates H3K27 acetylation.

MLL-AF4 binds directly to a BCL-2 specific enhancer and modulates H3K27 acetylation.

Journal: Experimental hematology
Published: July 27, 2016

The chromatin remodelling factor ATRX suppresses R-loops in transcribed telomeric repeats.

The chromatin remodelling factor ATRX suppresses R-loops in transcribed telomeric repeats.

Journal: EMBO reports
Published: July 20, 2016

MLL-AF4 Spreading Identifies Binding Sites that Are Distinct from Super-Enhancers and that Govern Sensitivity to DOT1L Inhibition in Leukemia.

MLL-AF4 Spreading Identifies Binding Sites that Are Distinct from Super-Enhancers and that Govern Sensitivity to DOT1L Inhibition in Leukemia.

Journal: Cell reports
Published: June 22, 2016

Instructive Role of MLL-Fusion Proteins Revealed by a Model of t(4;11) Pro-B Acute Lymphoblastic Leukemia.

Instructive Role of MLL-Fusion Proteins Revealed by a Model of t(4;11) Pro-B Acute Lymphoblastic Leukemia.

Journal: Cancer cell
Published: January 14, 2016

MLL-Rearranged Acute Lymphoblastic Leukemias Activate BCL-2 through H3K79 Methylation and Are Sensitive to the BCL-2-Specific Antagonist ABT-199.

MLL-Rearranged Acute Lymphoblastic Leukemias Activate BCL-2 through H3K79 Methylation and Are Sensitive to the BCL-2-Specific Antagonist ABT-199.

Journal: Cell reports
Published: May 07, 2015

RUNX1 is a key target in t(4;11) leukemias that contributes to gene activation through an AF4-MLL complex interaction.

RUNX1 is a key target in t(4;11) leukemias that contributes to gene activation through an AF4-MLL complex interaction.

Journal: Cell reports
Published: June 18, 2012
Showing 1-11 of 11

Last Updated: 09/26/2026