Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Blood flow to the skeleton was measured by the 18F clearance method of Wooton, Reeve & Veall (1976) in 24 patients with untreated Paget's disease. In every patient but one, resting skeletal blood flow was increased. There was a significant positive correlation between skeletal blood flow and serum alkaline phosphatase and between skeletal blood flow and urinary total hydroxyproline excretion. 2. Fourteen patients were re-studied after they had received short-term (7 days or less) or long-term (7 weeks or more) calcitonin. Skeletal blood flow, alkaline phosphatase and urinary hydroxy-proline excretion fell towards normal in every case. There was some evidence from the short-term studies that calcitonin produced a more rapid fall in skeletal blood flow than in alkaline phosphatase. 3. Glomerular filtration rate appeared to increase transiently in response to calcitonin.
Clin Sci Mol Med 1978 Jan
PMID:Skeletal blood flow in Paget's disease of bone and its response to calcitonin therapy. 62 Apr 95

1. Plasma levels of immunoreactive calcitonin were measured in 22 patients with untreated Paget's disease of bone and in 22 control subjects matched for age and sex. 2. No significant differences in plasma calcitonin were found between patients and control subjects, and hormone levels did not correlate significantly with activity of plasma alkaline phosphatase. 3. These results suggest that Paget's disease of bone is not due to deficient of endogenous calcitonin.
Clin Sci Mol Med 1977 Mar
PMID:Plasma calcitonin in Paget's disease of bone. 84 63

1. Twelve patients with symptomatic Paget's disease were studied before starting treatment with salmon calcitonin (12-5 mug) subcutaneously twice daily. Eleven of them were studied again after 3 months on this therapy. 2. Although pretreatment values for urinary total hydroxyproline excretion and cardiac output were considerably increased in some patients, there was no correlation between these two variables in the group as a whole. 3. Treatment resulted in a striking reduction in disease activity; the mean urinary hydroxyproline decreased 67%. 4. There was, however, no significant fall in cardiac output or change in oxygen transport during treatment. 5. Of the eight patients with bone pain who received treatment, five claimed complete pain relief.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Effect of salmon calcitonin on cardiac output, oxygen transport and bone turnover in patients with Paget's disease. 105 85

1. A new method for measurement of skeletal blood flow is described which depends on the complete extraction of 18F in a single passage through bone. 2. Plasma concentration and urinary excretion are measured over a 2 h period. The technique of impulse analysis is used to determine the initial transfer rate of 18F to bone and extravascular extracellular fluid (ECF). The ECF component is evaluated by using a second tracer (51 Cr-EDTA or 82Br) and the bone transfer rate obtained by difference. The 51Cr-EDTA data also provide an estimate of glomerular filtration rate and enable a correction to be applied for urinary bladder retention when necessary. 3. Duplicate measurements of skeletal blood flow in eight normal male volunteers gave mean flows between 4-4 and 5-9% of blood volume/min, or about 4 ml min-1 100 g-1 of bone. The variation between normal subjects was least when the results were expressed as % of blood volume/min rather than ml/min, ml min-1 kg-1 or ml min-1 1-73 m-2 body surface area. The precision of the technique was estimated to be 16-4%. 4. Addition of 1-5% random noise to the input data resulted in an uncertainty of 8-5% in the measurement of skeletal blood flow, suggesting that improved precision depends on closer control of physiological variables. 5. In six patients with severe untreated Paget's disease of bone, skeletal blood flow was 8-4-15-3% of blood volume/min. The increase was significant in all cases. 6. The absorbed radiation dose is low, so that the measurement can be repeated.
Clin Sci Mol Med 1976 Apr
PMID:The clinical measurement of skeletal blood flow. 126 Dec 7

Paget's disease of bone is a disease of unknown etiology. The demonstration of viral-like particles on ultrastructural examination and the putative detection of viral antibodies and nucleic acids in the tissues suggest a possible viral association. The purpose of this study was to search for nucleic acid sequences homologous to measles virus using the recently described reverse transcriptase (RT) polymerase chain reaction (PCR) in situ hybridization (ISH) technique. After performing RT PCR ISH utilizing primers specific for the nucleocapsid region of the measles virus, an intense signal was evident in most measles-infected HeLa cells compared with a weak signal in few of these cells using standard cDNA-RNA ISH analysis. Amplified measles nucleic acid was detected in tissue from a patient who died of measles infection and was not detected in any of the 11 cases of Paget's disease of bone studied or in a giant cell tumor of bone that had tubuloreticular inclusions on electron microscopy. Therefore, these data suggest that infection by the measles virus is not associated with Paget's disease of bone.
Diagn Mol Pathol 1992 Dec
PMID:In situ analysis of Paget's disease of bone for measles-specific PCR-amplified cDNA. 134 74

PCDRA was designed to provide the average biologist with a user-friendly molecular display on a low-cost personal computer. The package is menu driven and is built so that a biologist, with little or no computing knowledge, finds it easy to use. The system gives a color representation with depth cueing of a protein whose atomic coordinates are stored as a PDB file. Moreover, the system presents several features similar to HYDRA and therefore is a good introduction to molecular graphics, especially for beginners in protein modeling.
J Mol Graph 1990 Mar
PMID:PCDRA: PC interactive molecular representation and modeling system. 226 26

Paget cells from cases of mammary and extramammary Paget's disease were examined for carcinoembryonic antigen (CEA) and CEA-related antigens by the immunoperoxidase method. Paget cells showed a conspicuous positive reaction with antiserum to CEA, but were negative when nonspecific cross-reacting-antigen (NCA)-absorbed antiserum to CEA, or a monoclonal antibody to CEA was used as the detecting agents. Paget cells may contain large amounts of NCA antigen or CEA-related substances.
Virchows Arch B Cell Pathol Incl Mol Pathol 1985
PMID:False positive reaction for carcinoembryonic antigen in Paget cells. Immunohistochemical observation. 241 8

The synergism between H1- and H2-receptors in the histamine-induced stimulation of cAMP accumulation was studied in slices from guinea pig hippocampus. Since H1-receptors appear to be coupled to the phosphatidylinositol cycle, the participation of the two branches of the cycle in this synergism was assessed by using phorbol esters and/or by removing Ca2+ from the external medium. The protein kinase C activator, 4 beta-phorbol 12,13-dibutyrate (4 beta-PDB), strongly potentiated, with an EC50 of 0.2 microM, the accumulation of cAMP elicited by dimaprit, an H2-receptor agonist used at supramaximal concentration (0.3 mM). The effect of 4 beta-PDB was also observed in the presence of impromidine, an H2-receptor agonist, and histamine. 4 beta-Phorbol 12-myristate, 13-acetate, another protein kinase C activator, also potentiated the effect of dimaprit in a concentration-dependent manner although less potently than 4 beta-PDB. In contrast, 4 alpha-phorbol or the phorbol esters, 4 alpha-phorbol 12,13-didecanoate or 4-O-methylphorbol 12-myristate, 13-acetate, all inactive on protein kinase C, had no potentiating effect. 2-Thiazolylethylamine (2-TEA), a predominantly H1-receptor agonist, increased the stimulation induced by dimaprit (0.3 mM), and this response was further enhanced in the presence of 4 beta-PDB in maximal concentration (1 microM). Mepyramine (0.1 microM) antagonized the H1-receptor-mediated effect in the absence as well as the presence of 4 beta-PDB. The phorbol ester did not significantly alter the EC50 of 2-TEA or the magnitude of its effect. In the absence of phorbol esters, removal of Ca2+ from the incubation medium did not change the response elicited by 0.3 mM dimaprit but reduced by 50% the response to a supramaximal concentration of 2-TEA. This effect was more marked when EGTA was added in the Ca2+-free medium. The EC50 value of 2-TEA was only slightly modified in the absence of Ca2+ (180 +/- 20 microM as compared with 70 +/- 4 microM in the presence of 2.6 mM Ca2+). In the presence of 4 beta-PDB (1 microM), removal of Ca2+, particularly in the presence of EGTA, did not affect or slightly increased the response to dimaprit, but still strongly reduced the response to 2-TEA. The Ca2+ ionophore A 23187 (10 microM) showed a tendency to mimic the potentiating effect of 2-TEA.(ABSTRACT TRUNCATED AT 400 WORDS)
Mol Pharmacol 1988 Jan
PMID:Synergism between histamine H1- and H2-receptors in the cAMP response in guinea pig brain slices: effects of phorbol esters and calcium. 282 97

1. In the present paper two questions are discussed: (A) Does protein kinase C (PKC) participate in the modulation of evoked noradrenaline release in brain tissue? and (B) Is there any link between presynaptic alpha 2-adrenoceptors and regulatory G proteins? 2. Slices of the middle part of the rabbit hippocampus, labeled with 3H-noradrenaline, were superfused with medium containing the reuptake inhibitor cocaine. During superfusion the tissue was stimulated twice electrically for 2 min each. 3. The PKC activators 4 beta-phorbol 12,13-dibutyrate (4 beta-PDB) and 12-O-tetradecanoyl phorbol 13-acetate (TPA) increased the stimulation-evoked transmitter release in a concentration-dependent manner. 4 alpha-PDB and 4-O-methyl-TPA, which do not activate PKC, were without effect on transmitter release. Polymyxin B, an inhibitor of PKC, diminished the stimulus-evoked overflow and counteracted the effects of the phorbol esters. The increases in release caused by phorbol esters and the alpha 2-adrenoceptor antagonist yohimbine were additive. 4. Treatment of hippocampal tissue with islet-activating protein (IAP) or N-ethylmaleimide (NEM), both known to inactivate the regulatory G proteins Gi and Go by chemical modification, led to a marked increase in evoked noradrenaline release. In addition, the effects of both the alpha 2-adrenoceptor agonist clonidine and the alpha 2-adrenoceptor antagonist yohimbine were inhibited. 5. The facilitatory effects of IAP and NEM on transmitter release were not additive. In synaptosomes prepared from rabbit hippocampus two polypeptides with molecular weights corresponding to those of alpha i and alpha o were 32P-ADP-ribosylated with IAP. Pretreatment of synaptosomes with NEM reduced the subsequent ADP ribosylation by IAP concentration dependently. 6. The above results suggest that PKC is involved in the modulation of noradrenaline release in the rabbit hippocampus. The presynaptic alpha 2-autoreceptors modulate transmitter release by a mechanism which is not directly affected by PKC. The alpha 2-autoreceptor-mediated signals seem to be transduced across the plasma membrane via regulatory G proteins.
Cell Mol Neurobiol 1988 Mar
PMID:Participation of protein kinase C and regulatory G proteins in modulation of the evoked noradrenaline release in brain. 284 Oct 25

We have evaluated the catalytic and receptor-binding properties of protein kinase C in swine luteal cytosol using two complementary approaches: assay of catalytic activity assessed as the enzymatic transfer of radiolabeled phosphate to histone III-s acceptor protein in the presence of specific phospholipid, diacylglycerol, or phorbol ester and ionic calcium; and, the high-affinity binding of [3H]phorbol-12,13-dibutyrate ([3H]PDB) to the protein kinase C receptor. Catalytic properties of pig luteal protein kinase C included: absolute dependence on calcium ions for maximal activation (approximate ka = 0.5 microM); synergistic activation by 1,2-sn-diolein, phospholipid and calcium ions; and rank order of specific phospholipid activational potency: phosphatidylserine greater than phosphatidic acid greater than phosphatidylinositol greater than phosphatidylethanolamine greater than phosphatidylcholine. The enzyme was also activated by specific phorbol esters at the following half-maximally effective (ED50) concentrations: 12-O-tetradecanoylphorbol-13-acetate (TPA) 11 nM; phorbol-12,13-dibenzoate (PDBe) 26 nM; phorbol-12,13-dibutyrate (PDBu) 33 nM; mezerein 65 nM; and phorbol-12,13-diacetate (PDA) 130 nM. Phorbol-ester receptor properties of protein kinase C included specific, high-affinity (kd congruent to 19 nM), saturable, low-capacity (congruent to 44 pmol/mg protein) [3H]PDB binding sites. Moreover, the rank order of the equilibrium binding ID50s for various phorbol compounds was similar to that of catalytic ED50s: viz. 3 nM TPA; 8 nM PDBe; 16 nM PDBu; 19 nM mezerein; and 590 nM PDA. Thus, swine luteal cytosol contains catalytically active protein kinase C with specific phospholipid sensitivity, synergistic activation by diacylglycerol, phospholipid and calcium, and a strict dependence on ionic calcium concentrations that is influenced markedly by the presence of diacylglycerol.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Endocrinol 1987 Mar
PMID:Catalytic and receptor-binding properties of the calcium-sensitive phospholipid-dependent protein kinase (protein kinase C) in swine luteal cytosol. 347 79


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