Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin (PG) D2 bound specifically to a particulate fraction rich in the synaptic membrane of rat brain. The binding was dependent on time and temperature, equilibrium being reached after 5 min at 37 degrees C. The specific binding constituted about 70% of the total binding at 37 degrees C, and 55% at 0 degrees C. The maximal binding was obtained in the presence of 100 mM sodium ion and at pH 8. The equilibrium dissociation constant and the maximal concentration of binding sites as determined by Scatchard analysis were 28 +/- 7 nM and 0.45 pmol/mg of protein (n = 3), respectively. Hill coefficient was 1.15, indicating a single entity of binding sites and no cooperativity. The binding sites were highly specific for PGD2; the Ki values for PGD1 and PGF2 alpha were 523 and 693 nM, respectively. Other PGs including 13,14-dihydro-15-keto-PGD2, an inactive metabolite of PGD2, had 150- to 1000-fold lower affinities than PGD2. The binding was inhibited by boiling or treatment with proteases, phospholipases, or beta-galactosidase. The specific activity of PGD2 binding was highest in the pituitary gland, followed by the hypothalamus and the olfactory bulb od the rat brain, this pattern being almost parallel to that of the cytosolic NADP-linked PGD2 dehydrogenase activity. The results suggest that PGD2 plays a significant role in these regions of the rat brain.
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PMID:Specific binding of prostaglandin D2 to rat brain synaptic membrane. Occurrence, properties, and distribution. 629 97

We provide genetic evidence that HRS1/PGD1, a yeast gene previously identified as a suppressor of the hyper-recombination phenotype of hpr1, has positive and negative roles in transcriptional regulation. We have analyzed three differently regulated promoters, GAL1, PHO5 and HSP26, by beta-galactosidase assays of lacZ-fused promoters and by Northern analysis of the endogenous genes. Transcription of these promoters was derepressed in hrs1delta mutants under conditions in which it is normally repressed in wild type. Under induced conditions it was either strongly reduced or significantly enhanced depending on the promoter system analyzed. Constitutive transcription was not affected, as determined in ADH1 and TEF2. In addition, Hrs1p was required for mating-factor expression, telomere-linked DNA silencing and DNA supercoiling of plasmids. Furthermore, hrs1delta suppressed Ty-insertion mutations and conferred a Gal- phenotype. Many of these phenotypes also result from mutations in GAL11, SIN4 or RGR1, which encode proteins of the RNA polII mediator. We also show that gal11delta and sin4delta partially suppress the hyper-rec phenotype of hpr1 mutants, although to a lesser extent than hrs1delta. Our results provide new evidence for the connection between hpr1delta-induced deletions and transcription. We discuss the possibility that Hrs1p might be a component of the RNA polII transcription machinery.
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PMID:The yeast HRS1 gene is involved in positive and negative regulation of transcription and shows genetic characteristics similar to SIN4 and GAL11. 940 23