Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P51532 (transcriptional activator)
 6,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mouse beta-casein gene promoter contains a region termed block C which is crucial for its gene transcription induced by lactogenic hormones. Nuclear extracts from mouse mammary glands contain at least two binding complexes (DS1 and DS2) which specifically bind to double-stranded block C region DNA. The binding sequence of these complexes was identified to be 5'-AAATTAGCATGT-3' which contains a sequence element related to the consensus octamer motif's complement ATTTGCAT. In the present study, we demonstrate that this sequence element indeed is the binding site for octamer-binding transcription factors (Octs) and Octs represent the double-stranded DNA binding proteins specifically binding to the block C region. Formation of the specific double-stranded binding complexes can be completely blocked by Oct binding motif oligonucleotides and anti-rOct-1 antiserum. We also show that Oct-1B represents at least partial, if not all, double-stranded binding protein, DS1, in mammary nuclear extract. Oct-1B may function as a transcriptional activator on casein gene promoter. The Oct binding activity to beta-casein gene promoter in the mammary gland is affected under influence of hormones both in vitro and in vivo. The DS1 binding activity can be induced by the combination of lactogenic hormones insulin, hydrocortisone and prolactin in organ culture of virgin mouse mammary gland. The binding activity in vivo can be induced by injection of progesterone or its combination with estradiol in virgin mice.
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PMID:Involvement of Oct-1 in transcriptional regulation of beta-casein gene expression in mouse mammary gland. 1215 Oct 92

Pseudomonas putida DS1 is able to utilize dimethyl sulfone as a sulfur source. Expression of the sfnFG operon responsible for dimethyl sulfone oxygenation is directly regulated by a sigma(54)-dependent transcriptional activator, SfnR, which is encoded within the sfnECR operon. We investigated the transcription mechanism for the sulfate starvation-induced expression of these sfn operons. Using an in vivo transcription assay and in vitro DNA-binding experiments, we revealed that SfnR negatively regulates the expression of sfnECR by binding to the downstream region of the transcription start point. Additionally, we demonstrated that a LysR-type transcriptional regulator, CysB, directly activates the expression of sfnECR by binding to its upstream region. CysB is a master regulator that controls the sulfate starvation response of the sfn operons, as is the case for the sulfonate utilization genes of Escherichia coli, although CysB(DS1) appeared to differ from that of E. coli CysB in terms of the effect of O-acetylserine on DNA-binding ability. Furthermore, we investigated what effector molecules repress the expression of sfnFG and sfnECR in vivo by using the disruptants of the sulfate assimilatory genes cysNC and cysI. The measurements of mRNA levels of the sfn operons in these gene disruptants suggested that the expression of sfnFG is repressed by sulfate itself while the expression of sfnECR is repressed by the downstream metabolites in the sulfate assimilatory pathway, such as sulfide and cysteine. These results indicate that SfnR plays a role independent of CysB in the sulfate starvation-induced expression of the sfn operons.
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PMID:Transcription factors CysB and SfnR constitute the hierarchical regulatory system for the sulfate starvation response in Pseudomonas putida. 1845 3