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)
As a step toward delineating mechanisms that regulate its activity, we have characterized the mouse
epidermal growth factor
(
EGF
) promoter. Primer extension and S1 nuclease analyses identified prominent (+1/+2) and minor (+28) transcription start sites, with the dominant +1/+2 site located 33 bases downstream from a TTTAAA sequence. A restriction fragment that spanned these start sites and contained 390 base pairs of 5'-flanking sequence directed transcription from the +1/+2 site in vitro in the presence of HeLa cell nuclear extracts. Additionally, it promoted expression of a coupled luciferase reporter gene in transfected cell lines. The inclusion of additional 5'-flanking sequence either stimulated or inhibited luciferase expression depending on the cell line. Approximately 2 kilobases of
EGF
5'-flanking sequence was determined and found to contain several motifs with partial homology to steroid hormone response elements. Despite this fact and evidence that
EGF
expression might be regulated by androgens in vivo,
EGF
promoter-luciferase constructs were not steroid-responsive in cells cotransfected with steroid receptor expression vectors. An oligonucleotide containing the aforementioned TTTAAA sequence specifically bound
TATA-binding protein
and TFIIA in gel shift assays, and an
EGF
promoter-luciferase construct in which the core TA dinucleotide was mutated to CG was not active in transfected cells. These data suggest that the TTTAAA sequence functions as an atypical TATA box.
...
PMID:Characterization of the mouse epidermal growth factor promoter and 5'-flanking region. Role for an atypical TATA sequence. 894 71
Emerging evidence supports the idea that the c-Jun N-terminal kinases (JNKs) possess overlapping but distinct functions. The potential roles of the ubiquitously expressed JNK1 and JNK2 in regulating expression of the central transcription initiation factor,
TATA-binding protein
(
TBP
), were examined. Relative to wild-type fibroblasts,
TBP
was decreased in Jnk1(-/-) cells and increased in Jnk2(-/-) cells. Similarly, reduction of JNK1 in human hepatoma cells decreased
TBP
expression, whereas reduction of JNK2 enhanced it. JNK-mediated regulation of
TBP
expression occurs at the transcriptional level through their ability to target Elk-1, which directly regulates the
TBP
promoter in response to
epidermal growth factor
stimulation. JNK1 increases, whereas JNK2 decreases, the phosphorylation state of Elk-1, which differentially affects Elk-1 occupancy at a defined site within the
TBP
promoter. These JNK-mediated alterations in
TBP
expression, alone, serve to regulate c-Jun expression and fibroblast proliferation rates. These studies uncovered several new molecular events that distinguish the functions of JNK1 and JNK2 that are critical for their regulation of cellular proliferation.
...
PMID:TBP is differentially regulated by c-Jun N-terminal kinase 1 (JNK1) and JNK2 through Elk-1, controlling c-Jun expression and cell proliferation. 1707 9