Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P20226 (
TATA-binding protein
)
1,297
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
CK2
is a highly conserved protein kinase with growth-promoting and oncogenic properties. It is known to activate RNA polymerase III (PolIII) transcription in Saccharomyces cerevisiae and is shown here to also exert a potent effect on PolIII in mammalian cells. Peptide and chemical inhibitors of
CK2
block PolIII transcription in human cell extracts. Furthermore, PolIII transcription in mammalian fibroblasts is decreased significantly when
CK2
activity is compromised by chemical inhibitors, antisense oligonucleotides, or kinase-inactive mutants. Coimmunoprecipitation and cofractionation show that endogenous human
CK2
associates stably and specifically with the
TATA-binding protein
-containing factor TFIIIB, which brings PolIII to the initiation site of all class III genes. Serum stimulates TFIIIB phosphorylation in vivo, an effect that is diminished by inhibitors of
CK2
. Binding to TFIIIC2 recruits TFIIIB to most PolIII promoters; this interaction is compromised specifically by
CK2
inhibitors. The data suggest that
CK2
stimulates PolIII transcription by binding and phosphorylating TFIIIB and facilitating its recruitment by TFIIIC2.
CK2
also activates PolI transcription in mammals and may therefore provide a mechanism to coregulate the output of PolI and PolIII.
CK2
provides a rare example of an endogenous activity that operates on the PolIII system in both mammals and yeasts. Such evolutionary conservation suggests that this control may be of fundamental importance.
...
PMID:CK2 forms a stable complex with TFIIIB and activates RNA polymerase III transcription in human cells. 1199 11