The structure of the chromatin remodeller CHD4 bound to a nucleosome reveals differences to the known Chd1-nucleosome complex and maps cancer mutations.

In fusion-positive rhabdomyosarcoma, CHD4 positively regulates super-enhancer-mediated gene expression by allowing a chromatin architecture at these cis-regulatory regions, which is permissive to the binding of the transcription factor PAX3-FOXO1.

Neural crest cells differentiated from patient-derived cells with mutations in the chromatin remodeler CHD7 show defective delamination, migration and motility in vitro, and defective migration in chick embryos.

Sepsis leads to lasting changes in the composition of the pre-existing memory CD8 T cell compartment leading to altered localization, changes in their transcriptional landscape and chromatin accessibility, differential function, and reduced capacity to control infection.

The interplay between the cytokine TGFβ and the PD-1/PD-L1 pathway promotes CD8+ T cell anergy and tolerance towards transplanted tissues.

Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.

The unwrapping two turns of DNA on Chd1-bound nucleosomes cause the histone H3 tail and ubiquitin to be re-positioned.

HLA-B*35:01 molecules that are peptide-deficient are thermostable, bind CD8 with higher affinity than their peptide-filled versions, accumulate at immunological synapses and enhance antigen-specific CD8+ T cell immune responses.

Immunological analysis of wild-type and Crlf2^-/- mice reveals a role for the cytokine thymic stromal lymphopoietin on memory CD8⁺ T-cell responses to viral infection, findings with potential translational implications.

The ATP-dependent chromatin remodeler Chd1 controls nucleosome turnover to allow RNA Polymerase to transcribe in vivo.