MR1T cells are human polyclonal T cells endowed with diverse effector functions in response to endogenous antigens presented by MHC-class 1-related molecule, MR1.

Natural Tr1-like cells do not form a functionally stable memory response to allergens, and this instability may limit efforts to re-establish tolerance by expanding Tr1.

Telomeric TRF1 controls the transcriptional programmes of pluripotent stem cells by recruiting PRC2 to pluripotency and differentiation genes by controlling the expression of those gene sites and the binding of TERRA RNAs to them.

An atomic model of the 3744-residue Tra1 protein reveals multiple transcription activator binding sites, its integration within the SAGA chromatin coactivator complex, and a striking similarity to DNA-repair factor DNA-PKcs.

Joint sequence, structure, and phylogenetic analyses identify highly conserved features in transmembrane domains of transient receptor potential (TRP) ion channel proteins that offer a novel explanation for how TRPs could integrate stimuli into cellular signals.

Structure-based alignment of TRP channels enables comparison of structural changes, ion permeation pathways and ligand-binding sites and reveals over-representation of structures that represent non-conducting states.

XIAP/TRIP-Br1-mediated degradation of multiple adenylyl cyclase isoforms is a previously unrecognised general mechanism for controlling adenylyl cyclase expression and the homeostasis of cAMP signalling.

Genetic analyses reveal that the TIR1/AFB auxin receptors have broadly overlapping functions throughout plant development, but that the AFB1 receptor has a specialized role in a rapid auxin response.

T-regulatory type 1 cells inherit a broad repertoire of epigenetic marks from T-follicular helper T-cells, offering new insights into the developmental biology of this subset.

Folding and unfolding pathways are described for a ribosome-binding 3' cap-independent translation enhancer at the center of a conformational rearrangement that is implicated in the transition from translation to replication of an RNA virus.