A subset of EC/VCs have CD4+T cells with resistance specific to R5-tropic HIV infection associated with transcriptional down-regulation of ccr5, a phenotype that appears to be heritable, across multiple generations.
The discontinuous speed of transcription enables riboswitch molecules to adopt meta-stable structures in response to the presence of their cognate ligand, thereby gene-regulation by means of structure induced transcription termination can occur.
The ion channel accessory subunit KChIP2 has a transcriptional role that provides regulation over miRNA targets, driving the adverse remodeling of key ion channels during cardiac stress and leading to the development of arrhythmia.
Biochemical analyses of transcription complexes, including kinetic studies and probes of translocational and conformational states, establish the elemental mechanism of pausing, which underlies regulation of gene expression in all organisms.
A structural analysis of the transcription regulator Mot1 in complex with promoter DNA and the proteins TBP and NC2 provides a first structural framework for how a Swi2/Snf2 type remodeler interacts with a histone fold protein:DNA complex.
OCT4 and SOX2 display partially independent activity to regulate chromatin accessibility, and highly dynamic activity of OCT4 is required throughout the cell cycle to maintain pluripotency enhancer accessibility.