Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 30 pregnant women with EPH-gestosis activity of myeloperoxidase was significantly decreased and activity of acid phosphatase was not much increased. Results of scientific researches can confirm the fact of weakness of anti-infection immunity among women with EPH-gestosis in compare with healthy pregnant women.
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PMID:[Activity of acidic granulocyte phosphatase and myeloperoxidase among women with EPH gestosis]. 133 34

Circadian rhythms in acid phosphatase (ACP), hexosaminidase (HEX) and beta-glucuronidase (RON) activity were studied in the pineal glands of adult male Syrian hamsters exposed to control (20 +/- 2 degrees C and 14:10 LD) conditions or to naturally decreasing autumn photoperiod and temperature conditions (outside) for 8 weeks. Testes and testosterone levels (p less than 0.001 in both instances) were severely depressed in animals exposed to natural environmental conditions illustrating that the treatment period was of sufficient length to produce pineal-mediated gonadal atrophy. Significant rhythms were found in all enzymes in the pineal glands of control and outside animals with the exception of HEX activity in the control animals. Significant acrophase differences in outside vs. control animals were noted in ACP (7.9 hr earlier, p less than 0.001) and RON (9.8 hr later, p less than 0.001). A significant drop in RON and HEX activity (p less than 0.01 in both instances) was noted in association with the acute lights exposure in the morning to which control animals were exposed. The around-the-clock mean value of each enzyme was significantly lower in outside vs. control hamsters. These results demonstrate that environmental changes which provoke the pineal-mediated depression in gonadal activity also alter the activity of and shift the circadian rhythmicity of lysosomal enzymes in the pineal itself.
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PMID:Pineal lysosomal enzyme circadian rhythms in male hamsters exposed to natural decreasing photoperiod and temperature conditions. 214 37

The following 10 enzymes were assayed in 187 amniotic fluid and maternal serum samples at 15-42 weeks of gestation: alkaline phosphatase, heat-stable alkaline phosphatase (only in amniotic fluid), acid phosphatase, alanine aminotransferase, aspartate aminotransferase, alpha-amylase, gamma-glutamyltransferase, creatine kinase, lactate dehydrogenase, and lysozyme. The normal reference ranges are reported for amniotic fluid and maternal serum enzymes, together with the abnormal values accompanying neural tube defects and EPH-gestosis. The determination of gamma-glutamyltransferase, heat-stable alkaline phosphatase and creatine kinase was found to be of appreciable diagnostic significance in clinical practice.
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PMID:Variation in some enzymes in amniotic fluid and maternal serum during pregnancy. 256 24

Neuraminidase-1 (NEU-1) is one of two neuraminidase isozymes which can be detected electrophoretically in mouse liver extracts. The inheritance of variation in NEU-1 and the linkage relationships of the gene controlling this variation were studied through a backcross analysis involving the SM/J and MA/MyJ inbred strains, and by examination of NEU-1 phenotypes in three congenic strains: B10.SM, B10.SM(22R) and B10.RVB. The data indicate that NEU-1 is controlled by Neu-1, a gene previously identified by its effect on total liver neuraminidase activity in whole tissue homogenates. Analysis of the congenic strains revealed identical low activity (SM/J-type: Neu-1a/Neu-1a) NEU-1 phenotypes in all three strains. This indicates that Neu-1 lies in the segment of the SM/J-derived H-2 region that is common to all three strains: H-2E alpha to H-2D. In addition, we examined the relationship between NEU-1 and phenotypic variation in liver acid phosphatase (AP; for which a new typing method is described) and linkage order among several other enzyme-coding genes linked to H-2. In all animals that could be scored confidently for AP, the NEU-1 and AP phenotypes were concordant, adding support to the hypothesis that both phenotypes are controlled by Neu-1. Recombination rates among six H-2-linked marker loci were unexpectedly low, but were sufficient to verify the position of Upg-1 as the telomeric flanking marker relative to Glo-1, H-2 (C4), Neu-1 (Apl), Ce-2 and Pgk-2.
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PMID:Electrophoretic analysis of liver neuraminidase-1 variation in mice and additional evidence concerning the location of NEU-1. 374 25

Much of the total genomic variation in eukaryotic organisms may be due to genes other than those coding the primary translation product. Allelic variation, especially as detectable by electrophoresis, in the post-translational processing of enzymes has been briefly reviewed with considerable attention given to a mouse gene (Neu-1) and its pleiotropic effects on several lysosomal hydrolases. Liver acid phosphatase, alpha-mannosidase, arylsulfatase B, and alpha-glucosidase are differentially sialylated as the result of allelic variation for a gene controlling liver neuraminidase activity. Strain SM/J has only 15-20% of the total neuraminidase activity of control strains and is almost totally deficient in the more heat labile of two components of liver activity. The locus controlling this variation (Neu-1) maps very near the D end of H-2 on chromosome 17, apparently within the S region of H-2. A homologous gene has been mapped near the MHC of the rat. The exact nature of the mouse mutant and its relationship to several human diseases characterized by neuraminidase deficiency has not been determined.
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PMID:Post-translational modification of enzymes: processing genes. 635 Feb 18

Injectable progestogen, norethisterone enanthate (NET-EN, 200 mg/ml at 60 day intervals), was administered to 150 women for 2 years as their method of contraception. Blood levels of acid phosphatase, alkaline phosphatase, glutamate pyruvate transaminase, glutamate oxaloacetate transaminase, acetylcholinesterase (AChe), sialic acid were determined in all subjects to ascertain whether NET-EN therapy causes any adverse metabolic effect or damage to the functional status of the liver. NET-EN contraception did not alter the liver function enzymes but there is a significant increase (P0.001) in AChE activity after 2 years. Serum sialic acid level showed a transient increase up to 1 year, which however returned to control level later. The mechanism responsible for these changes and whether the rise in sialic acid and AChE activity are related to any pathological condition remain unclear at this stage.
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PMID:Studies on some enzymes and sialic acid during progestational contraceptive therapy. 646 44

Congenic lines B10.KPA42, B10.KPA132, B10.SNA57, B10.DRB62, and B10.WOA105 carry H-2 haplotypes of wild mice on the genetic background of the strain C57BL/10Sn. Two of the lines (B10.DRB62 and B10.WOA105) have H-2 haplotypes indistinguishable from H-2v of B10.SM. The H-2 haplotype of one line (B10.SNA57) seems to have arisen from H-2v by recombination between the D and Qa-2 loci. The H-2 haplotypes of the remaining two lines probably arose from H-2v by recombination between the C4 and D loci. Since all six and no other lines carry the rare Neu-1a allele, the neuraminidase-1 locus is probably located proximal to the H-2D locus. Typing of H-2s recombinants for the enzyme acid phosphatase liver, the processing of which is controlled by the Neu-1 locus, suggests that the locus resides between the E alpha and D loci, that is in the S region.
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PMID:Evidence for placing the Neu-1 locus within the mouse H-2 complex. 711 40

The low activity of liver neuraminidase that is characteristic of mouse strain SM/J is inherited as a single gene on chromosome 17, near the major histocompatibility complex. This gene, neuraminidase-1 (Neu-1), is represented by the low activity allele Neu-1s in SM/J and the high activity allele Neu-1b in C57BL/6J and most other strains. Previously described variations in the posttranslational processing of acid phosphatase, alpha-mannosidase, arylsulfatase-B, and alpha-glucosidase are attributed to pleiotropic effects of this gene.
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PMID:Gene for neuraminidase activity on mouse chromosome 17 near h-2: pleiotropic effects on multiple hydrolases. 720 20

beta-arrestin is a cytosolic protein thought to be responsible for uncoupling agonist-activated beta 2-adrenergic receptors from their guanine-nucleotide-binding proteins (G-protein) subsequent to receptor phosphorylation by the beta-adrenergic receptor kinase (beta ARK). In order to investigate this interaction, we generated a recombinant baculovirus for the expression of beta-arrestin in Sf9 insect cells. Apparently homogeneous beta-arrestin preparations were obtained in a one-step purification on heparin-Sepharose. Purified beta-arrestin bound to rhodopsin in a phosphorylation-dependent plus light-dependent manner. Binding to beta 2-adrenergic receptors was investigated using purified receptors reconstituted into lipid vesicles. The accessibility of the reconstituted receptors was determined using the agonist isoproterenol for the ligand-binding site and an antibody binding to an attached myc tag for the C-terminus, the site of receptor phosphorylation. On the basis of these data, the binding of purified beta-arrestin to beta ARK-phosphorylated beta 2-adrenergic receptors was found to occur with a KD of 1.8 nM and with a maximum of 1 beta-arrestin/receptor. beta-arrestin also bound to receptors which had been completely dephosphorylated with acid phosphatase, but the affinity was approximately 30-fold lower. In contrast to regulation by phosphorylation, binding of agonists or antagonists to the receptors had negligible effects on beta-arrestin binding. Finally, beta-arrestin and beta ARK were shown to be capable of producing synergistic inhibition of beta 2-adrenergic-receptor-stimulated adenylyl cyclase activity of cell membranes. These data show that high-affinity stoichiometric binding of beta-arrestin to beta 2-adrenergic receptors occurs in a beta ARK-dependent manner and is sufficient to impair adenylyl cyclase stimulation by the receptors.
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PMID:Binding of purified recombinant beta-arrestin to guanine-nucleotide-binding-protein-coupled receptors. 755 95

Increasing evidence suggests that transforming growth factor-beta (TGF-beta) is involved in bone formation during remodeling. Using a recently cloned human leukemic cell line (FLG 29.1 cells) we demonstrate that these cells synthesize and secrete TGF-beta 1 and that exogenous or autocrine TGF-beta 1 can induce the same features of osteoclastic-like cells, exerting its effects through the binding to TGF-beta specific receptors. Scatchard analysis of 125I-labeled TGF-beta 1 to FLG 29.1 cells revealed the presence of a single high affinity binding site with a Kd value of approximately 25 pM and a binding capacity of approximately 900 sites/cell. Affinity labeling experiments showed that FLG 29.1 cells express type I and type II TGF-beta receptors. Stimulation of FLG 29.1 cells with low TGF-beta 1 doses reduced cell proliferation and increased cell adhesion and tartrate resistant acid phosphatase (TRAcP) activity. Pretreatment of FLG 29.1 cells with TGF-beta 1 caused a significant and dose-dependent response to calcitonin. Northern blot of total mRNA and analysis of the conditioned media (CM) showed that TGF-beta 1 was synthesized by FLG 29.1 cells. TPA treatment, which induces partial differentiation of these cells, markedly increased TGF-beta 1 mRNA expression and growth factor release. The majority of TGF-beta 1 secreted by TPA-treated cells was in its latent form. However, anti-TGF-beta antibodies inhibited TGF-beta 1 and TPA-induced growth inhibition, calcitonin responsiveness, and TRAcP activity, suggesting that the TPA effect is mediated in part by autocrine TGF-beta 1 and indicating that the cells can activate and respond to the TGF-beta that they secrete. These findings support a potential autocrine role for TGF-beta 1 in osteoclast differentiation.
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PMID:Role for autocrine TGF-beta 1 in regulating differentiation of a human leukemic cell line toward osteoclast-like cells. 807 86


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