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: EC:3.1.27.1 (
RNase
)
16,360
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Glucocorticoids rapidly inhibit the expression of c-myc mRNA in P1798 lymphoma cells. Statistically significant decreases can be observed within 5-10 min after the addition of glucocorticoids. Although transcription of c-myc decreases within a few hours after dexamethasone is added to P1798 cell cultures, nuclear run-on transcription cannot be used to demonstrate that the very early changes in mRNA abundance reflect corresponding changes in transcriptional activity. An
RNase
protection assay has been used to measure the abundance and rates of turnover of the two major c-myc transcripts arising from the P1 and P2 initiation sites. The relative rates of synthesis of the c-myc mRNAs (i.e. transcription) can be calculated from such data. The abundance of the P2 transcript exceeds that of
P1 mRNA
by 3- to 4-fold in midlog phase cells. The turnover rates of the two c-myc mRNAs are essentially identical (0.02 min-1), indicating that the P2 promoter is 3-4 times stronger than P1. This was confirmed by measuring the relative transcriptional activities of templates containing the individual c-myc promoters in P1798 extracts in vitro. The expression of P1 and P2 mRNAs decreases at different rates in glucocorticoid-treated cells. A 50% decrease in the abundance of
P1 mRNA
occurs within 1 h after the addition of dexamethasone. Expression of
P2 mRNA
is reduced by 50% within 4 h. However, the turnover rates of the major c-myc transcripts do not change in glucocorticoid-treated cells. The t1/2 values of P1 and P2 mRNAs are about 25-30 min and not different from the turnover rates measured in control cells.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Glucocorticoid regulation of c-myc promoter utilization in P1798 T-lymphoma cells. 149 94
Hormonal regulation of fructose 2,6-bisphosphate (Fru-2,6-P2) content was studied in H4IIE cells. These cells were found to be very sensitive to physiological concentrations of insulin. Addition of either insulin or dexamethasone alone increased Fru-2,6-P2 in a time- and dose-dependent manner, and the maximal effect of the hormones was seen at 1 h. Neither hormone had any measurable effect on cAMP levels. The effect of addition of both insulin and dexamethasone on Fru-2,6-P2 was synergistic. Insulin, but not dexamethasone, rapidly increased 6-phosphofructo-2-kinase (6PF-2-K) activity by causing dephosphorylation of the enzyme as judged by a decrease in the Km for fructose-6-phosphate. Addition of both hormones also resulted in a synergistic 10-fold increase in enzyme protein as measured by kinase activity and phosphoenzyme formation. Dexamethasone increased liver 6PF-2-K/Fru-2,6-
P2 mRNA
abundance by 10- to 12-fold as measured by a
ribonuclease
protection assay, and insulin increased it by only 4-fold. Effects were observed as early as 1 h after hormone addition, but addition of both hormones together showed no synergy. We conclude that the synergistic effects of insulin and dexamethasone on Fru-2,6-P2 content are mediated by a combination of stimulation of expression of the bifunctional enzyme gene by both hormones and insulin-induced modulation of the activation state of the bifunctional enzyme, both of which are mediated by cAMP-independent mechanisms.
...
PMID:cAMP-independent synergistic effects of insulin and dexamethasone on fructose 2,6-bisphosphate metabolism in H4IIE cells. 819 65
Pre-translational regulation of subunit c has been suggested to control the biosynthesis of mitochondrial ATP synthase (ATPase) in brown adipose tissue (BAT). Subunit c is encoded by the genes P1 and P2, which encode identical mature proteins. We have determined here the levels of P1 and P2 mRNAs in different tissues, in response to cold acclimation in rats, during ontogenic development of BAT in hamsters, and following thyroid hormone treatment in rat BAT and liver. Quantitative
ribonuclease
protection analysis showed that both the P1 and P2 mRNAs were present in all rat tissues measured. Their total amount in each tissue corresponded well with the ATPase content of that tissue. While the P1/
P2 mRNA
ratio is high in ATPase-rich tissues, the
P2 mRNA
dominates in tissues with less ATPase. Cold acclimation affects P1 but not P2 gene expression in rat BAT. A rapid and transient increase in
P1 mRNA
is followed by sustained depression, which is accompanied by a decrease in ATPase content. Similarly, ontogenic suppression of ATPase content in hamster BAT was accompanied by suppression of the
P1 mRNA
levels, while P2 expression was virtually unchanged. Furthermore, when hypothyroid rats were treated with thyroid hormone, the steady-state level of P1 but not of
P2 mRNA
was significantly increased in liver. BAT was unaffected. We conclude that the P1 and P2 genes for subunit c are differentially regulated in vivo. While the P2 gene is expressed constitutively, the P1 gene responds to different physiological stimuli as a means of modulating the relative content of ATP synthase.
...
PMID:ATP synthase subunit c expression: physiological regulation of the P1 and P2 genes. 916 27