Genetic and biochemical evidence shows that the basal transcription machinery of muscle cells invariably relies on TBP/TFIID because TBP2 is not expressed in muscle cells, and thus resolves a longstanding issue raised by previous conflicting data.
Integrative structural biology reveals a novel complex comprising the TATA-box-binding protein, TBP, and two subunits, TAF11 and TAF13, of General Transcription Factor TFIID, suggesting a new regulatory state in TFIID function in RNA polymerase II transcription initiation.
The transcription coactivators SAGA and TFIID have redundant function at a subset of yeast genes while SAGA also contributes to transcription of all genes through regulation of chromatin modifications.
Analyses with genetically engineered mouse models in combination with biochemical approaches reveal a crucial role of the receptor tyrosine kinase Tie2 mediated signals in venogenesis via an Akt mediated regulation of COUP-TFII protein stabilization.
An inorganic tin oxochloride cluster specifically binds to an intrinsically disordered, histidine-rich, low complexity protein region and arrests de novo transcription initiation without affecting reinitiation.
The requirements for preinitiation complex formation/stability and transcription by RNA polymerase II in yeast cells are different from those in vitro, thereby altering the current view of basal transcription.
Cooperativity between two transcription regulators occurs through protein-protein interactions with a general transcription factor complex and potentiates the parallel evolution of their DNA binding sites.