Quantification of all the major on- and off-pathway kinetic parameters in the transcription elongation cycle reveals that RNA polymerase II translocates slowly in a linear, non-branched Brownian ratchet mechanism.
The elongation rate of RNA polymerase II broadly affects the profile of poly(A) sites, and hence 3' mRNA isoforms, and it can mediate alternative polyadenylation in response to environmental conditions.
NusG enhances transcription elongation by stabilizing DNA base pairs immediately upstream of the RNA-DNA hybrid but does not measurably affect the nucleotide incorporation and the forward translocation by RNA polymerase.
Eukaryotic translation elongation factor 1A1 controls the process of heat shock response, from transcriptional activation of the HSP70 gene, to HSP70 mRNA stabilization, nuclear export, and translation.
Transcription elongation by the elongation factor P-TEFb promotes the epithelial–mesenchymal transition and metastasis of breast cancer cells, implicating inhibition of this factor as a potential treatment for the late stages of this cancer.
The elongation rate of RNA Polymerase II varies greatly between and along genes, as this enzyme accelerates from stable pausing to rapid elongation within genes, and is influenced by CG-content, exons and chromatin.
Structure-function analysis of the super elongation complex formed when HIV replicates inside cells reveals that the HIV-1 Tat protein binds to a cleft between P-TEFb, an enzyme that is involved in normal transcription, and AFF4, a protein that is used to build the super elongation complex