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:Q9UIJ5 (
Rec
)
58,342
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Over the past two decades, a great deal of evidence has accumulated in favor of the hypothesis that steroid hormones act at the level of nuclear DNA to regulate gene expression (
Jensen
EV, Suzuki T, Kawashima T, Stumpf WE, Jungblut PW, DeSombre ER, Proc Natl Acad Sci USA 1968; 59:632-638; Gorski J, Toft D, Shyamala G, Smith D, Notides A,
Rec
Prog Horm Res 1968; 24:45-80; O'Malley BW, Means AR, Science 1974; 183:610-620; O'Malley BW, Roop DR, Lai EC, Nordstrom JL, Catterall JF, Swaneck GE, Colbert DA, Tsai M-J, Dugaiczyk A, Woo SLC,
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Prog Horm Res 1979; 35:1-46). The earliest studies were qualitative and involved experiments showing that steroid hormones (1) cause accumulation of new species of hybridizable RNAs that did not exist prior to stimulation; (2) cause stimulation of synthesis of new specific proteins; (3) cause a corresponding increase in the cellular levels of specific mRNAs; and (4) stimulate the rate of transcription of certain nuclear genes (O'Malley BW, McGuire WL, Kohler PO, Korenman SG,
Rec
Prog Horm Res 1969; 25:105-000). At that time, the early 1970s, the primary pathway for steroid hormone action was defined as follows: steroid----(steroid-receptor)----(steroid-receptor-DNA)----mRNA----fu nct ional response (O'Malley BW, Roop DR, Lai EC, Nordstrom JL, Catterall JF, Swaneck GE, Colbert DA, Tsai M-J, Dugaiczyk A, Woo SLC,
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Prog Horm Res 1979; 35:1-46. Steroid enters cells by passive diffusion and allosterically activates receptors in either the cytoplasm or nucleus. The activated receptor binds usually at the 5'-flanking region of target genes and stimulates transcription and protein synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular pathways of steroid receptor action. 153 90
Two isozymes of 3-deoxy-d-arabino-heptulosonate 7-phosphate synthase are partitioned into plastid (DS-Mn) and cytosolic (DS-Co) compartments of at least several higher plants (RA
Jensen
1986
Rec
Adv Phytochem 20: 257-258). Differential variation of isozyme levels and in the timing of their expression was observed during growth of Nicotiana silvestris in suspension culture. The ratio of DS-Co to DS-Mn varied about fivefold in comparison of the different physiological stages of growth. Cultures maintained in exponential phase for >10 generations (EE cells) possessed balanced-growth properties and did not exhibit the considerable variation of isozyme levels found during the initial 2 to 3 generations of exponential growth (E cells) that followed subculture of stationary-phase cultures. The plastid isozyme level declined substantially in stationary phase, responded immediately to subculture, and reached a peak in early exponential growth similar to the steady-state level of DS-Mn in EE cells. In contrast, the cytosolic isozyme level peaked in late exponential growth. A recent history of stationary-phase physiology appeared to foster elevated synthesis of DS-Co since the steady-state level of DS-Co in EE cells was much lower than in E cells.
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PMID:Response of Cytosolic-Isozyme and Plastid-Isozyme Levels of 3-Deoxy-d-arabino-Heptulosonate 7-Phosphate Synthase to Physiological State of Nicotiana silvestris in Suspension Culture. 1666 75