Evidence for a role of RUNX1 as recombinase cofactor for TCRβ rearrangements and pathological deletions in ETV6-RUNX1 ALL.

T-cell receptor gene beta (TCRβ) gene rearrangement represents a complex, tightly regulated molecular mechanism involving excision, deletion and recombination of DNA during T-cell development. RUNX1, a well-known transcription factor for T-cell differentiation, has recently been described to act in addition as a recombinase cofactor for TCRδ gene rearrangements. In this work we employed a RUNX1 knock-out mouse model and demonstrate by deep TCRβ sequencing, immunostaining and chromatin immunoprecipitation that RUNX1 binds to the initiation site of TCRβ rearrangement and its homozygous inactivation induces severe structural changes of the rearranged TCRβ gene, whereas heterozygous inactivation has almost no impact.

Synthesis and reactivity of [Au(NHC)(Bpin)] complexes.

A new class of [Au(NHC)(Bpin)] complexes has been synthesized and their unusual reactivity was investigated using computational and experimental methods. The gold-boryl complexes exhibit unexpected high stability and reactivity.

A simple synthetic entryway into palladium cross-coupling catalysis.

The simple synthesis of a family of palladates containing an imidazolium counterion is presented. These "ate" complexes can be easily converted into well-defined palladium-N-heterocyclic carbene (NHC) complexes. The synthetic protocols leading to the "ate" and to the Pd-NHC neutral complexes have been exemplified with various NHC ligands.

Oestrogen receptor β regulates epigenetic patterns at specific genomic loci through interaction with thymine DNA glycosylase.

Background: DNA methylation is one way to encode epigenetic information and plays a crucial role in regulating gene expression during embryonic development. DNA methylation marks are established by the DNA methyltransferases and, recently, a mechanism for active DNA demethylation has emerged involving the ten-eleven translocator proteins and thymine DNA glycosylase (TDG). However, so far it is not clear how these enzymes are recruited to, and regulate DNA methylation at, specific genomic loci.