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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Previously published data obtained by magnesium infusion in man were found to conform to a Tm/glomerular filtration rate (GFR) model on the assumption of 80% diffusibility of plasma magnesium. The lower limit of Tm,Mg/GFR was 625 mumol/l. 2. Previously published data concerning the effect of cellulose phosphate on magnesium metabolism in normal subjects, patients with latent hypoparathyroidism and patients with primary hyperparathyroidism were found to conform to the same model, with the same limit for Tm,Mg/GFR for all three levels of parathyroid function. 3. The threshold for magnesium excretion is sharper with less 'splay' than for phosphate, but as for phosophate it is close to the normal blood concentration. 4. Because of the geometrical relationship between different methods of presentation of data, at a constant value for Tm,Mg/GFR changes in magnesium load or in GFR automatically produce changes in fractional magnesium clearance. This is the explanation for the increase in fractional magnesium clearance which occurs which with diminishing renal function. 5. Renal conservation of magnesium is a passive consequence of the fall in plasma magnesium. There was no evidence of augmented tubular reabsorption of magnesium in response to magnesium deprivation in any of the three groups of subjects. 6. The tubular reabsorption of magnesium was not altered detectably by a moderate deficiency or excess of parathyroid hormore. Changes in parathyroid hormone secretion are probably not concerned in normal magnesium homeostasis.
Clin Sci Mol Med 1976 Aug
PMID:The effect of cellulose phosphate on plasma and urinary magnesium at different levels of parathyroid function in man. 95 62

1. The effect of purified bovine parathyroid hormone on renal tubular reabsorption of sodium and calcium has been studied by micropuncture in intact and recently thyroparathyroidectomized dogs. 2. Parathyroid hormone increased the rejection of sodium and calcium proportionately at the late proximal tubule in both intact and operated dogs. 3. In both groups of dogs, there was increased delivery of sodium and calcium to the distal tubule after the hormone. However, the Ca/Na ratio decreased, suggesting some selective enhancement of calcium reabsorption before the superficial distal puncture site. 4. In the final urine, the Ca/Na ratio decreased highly significantly in both groups of dogs, indicating a further selective effect of parathyroid hormone on calcium reabsorption in or beyond the distal convoluted tubule.
Clin Sci Mol Med 1976 Oct
PMID:Effects of parathyroid hormone on sodium and calcium transport in the dog nephron. 97 75

1. The existence of tubular secretion of inorganic phosphate (Pi) in the mammalian kidney has been investigated by studying the renal response of rats infused with sodium phosphate by three different techniques. 2. Clearance studies indicate that, in anaesthetized rats, the net tubular reabsorption decreases markedly in response to Pi infusion. In conscious rats, the clearance of Pi slightly exceeded that of inulin at high plasma Pi concentration. 3. Free-flow micropuncture in control rats showed a net tubular reabsorption of Pi along the proximal tubule, and probably between the end of the distal tubule and the ureteral urine. In phosphate-loaded rats, whether receiving parathyroid hormone or not, an apparent net secretion of Pi was observed between the end of the distal tubule and the reteral urine. In the phosphate-loaded group receiving parthyroid hormone, net secretion was also observed very early in the proximal tubule followed by a predominant reabsorption along this segment. Thus the early proximal tubule and probably also the terminal nephron can be the site of either net reabsorption or net secretion. 4. Microperfusions of proximal tubules show a fall in the specific radioactivity of the perfused radioactive Pi solution, indicating entry of Pi into the lumen.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Secretion of inorganic phosphate in the rat nephron. 105 78

1. There was no significant change in plasma renin activity over 6 h in five subjects given calcium gluconate or in four subjects given parathyroid hormone. 2. It is concluded that acute hypercalcaemia does not increase plasma renin activity and is unlikely to play a role in the hypertension found with primary hyperparathyroidism.
Clin Sci Mol Med 1976 Jan
PMID:Absence of an acute effect of calcium or parathyroid hormone administration on plasma renin activity in man. 124 6

We employed a cyclic AMP-resistant subclone of UMR 106-01 osteoblastic osteosarcoma cells (UMR 4-7) with a regulated, dominant-negative mutation of cyclic AMP-dependent protein kinase (PK-A), to examine the mechanism(s) whereby parathyroid hormone (PTH) regulates growth of these cells. Expression of a transiently transfected CAT reporter gene controlled by the cAMP response element of the rat somatostatin gene ('SST-CAT') was used to monitor PK-A activation in intact cells. Agonist-stimulated SST-CAT expression was specific for agents known to activate adenylate cyclase, required an intact cAMP response element and was specifically blocked following induction of the mutant cAMP-resistant phenotype in UMR 4-7 cells. Inhibition of the proliferation of UMR 106-01 cells by PTH, which is mimicked by forskolin and 8-bromo-cAMP, was blocked completely in mutant cyclic AMP-resistant UMR 4-7 cells. We conclude that control of proliferation in UMR 106-01 cells by PTH involves the cAMP messenger system and requires activation of PK-A.
Mol Cell Endocrinol 1992 Sep
PMID:Regulation of gene transcription and proliferation by parathyroid hormone is blocked in mutant osteoblastic cells resistant to cyclic AMP. 135 85

The synthesis of 1,25(OH)2D3 is a critical control point in the regulation of calcium metabolism, and possibly in the growth and differentiation of a number of cell types. This paper reviews our current understanding of the regulation of this process at the cellular and molecular levels, with the emphasis on the mechanisms of feedback control 1,25(OH)2D3 itself, control of parathyroid hormone, the roles of cyclic AMP dependent protein kinase and protein kinase C, and the interaction between the various intracellular regulators of 1,25(OH)2D3 production.
J Steroid Biochem Mol Biol 1992 Mar
PMID:The cellular and molecular regulation of 1,25(OH)2D3 production. 156 13

Activin, a disulfide-linked polypeptide dimer first isolated from gonadal tissue extracts, has amino acid sequence and structural homology with transforming growth factor beta (TGF beta). Along with other activities, TGF beta regulates replication and differentiation and interacts with a defined set of binding sites on isolated bone cells. To determine if activin shares these properties, recombinant human activin-A (A-chain homodimer) was examined in osteoblast-enriched cultures obtained from fetal-rat parietal bone. After 23 h of treatment, 60 to 6,000 pM activin-A increased the rate of [3H]thymidine incorporation into DNA 1.5- to 4.0-fold, and at 600 to 6,000 pM, it enhanced the rate of [3H]proline incorporation into collagen and noncollagen protein by up to 1.7-fold. Like earlier studies with TGF beta in primary osteoblast-enriched cultures, the stimulatory effects of activin-A on DNA and protein synthesis were opposed by parathyroid hormone, and the influence of activin-A on collagen synthesis was independent of cell replication. Binding studies with 125I-activin-A indicated approximately 8,000 high-affinity (Kd = 0.4 nM) and 300,000 low-affinity (Kd = 40 to 50 nM) binding sites per cell. Polyacrylamide gel analysis revealed 125I-activin-A-binding complexes of Mr greater than 200,000 and 73,000 which did not appear to correspond to primary TGF beta-binding sites. These results indicate that activin-A produces TGF beta-like effects in bone and that some of these effects may be mediated, at least in part, by distinct activin receptors on bone cells.
Mol Cell Biol 1991 Jan
PMID:Activin-A binding and biochemical effects in osteoblast-enriched cultures from fetal-rat parietal bone. 184 21

The ontogeny of parathyroid hormone (PTH) and PTH-related protein (PTHrP) gene expression was studied by hybridization histochemistry in the rat at various stages between implantation and full term. PTHrP mRNA was demonstrable in the early postimplantation trophoblastic giant cells but disappeared from this site before 13.5 days. Localized gene expression, detectable by the in-situ technique, began between 12.5 and 15.5 days in embryonic tissues. The distribution of gene expression suggests that PTHrP may be concerned with the process of implantation. Its widespread, yet clearly localized, distribution in embryonic and fetal tissues is consistent with a paracrine or autocrine function which may relate to the transforming growth factor-beta family of growth factors. PTH expression occurred solely in the parathyroid and was detectable in the fetal parathyroid at 13.5 days of gestation.
J Mol Endocrinol 1991 Jun
PMID:Expression of parathyroid hormone-related protein mRNA in the rat before birth: demonstration by hybridization histochemistry. 188 89

This article critically reviews the current state of knowledge regarding the recently identified and cloned novel hormone parathyroid hormone-related protein (PTHrP). PTHrP is produced by tumors associated with the syndrome of humoral hypercalcemia of malignancy giving rise to the parathyroid hormone (PTH)-like symptoms characteristic of the syndrome. Areas that will be reviewed include identification, purification and cloning, localization, actions, and significance of PTHrP in cancers and normal physiology. The structure and regulation of the PTHrP gene that may be ancestrally related to the PTH gene will also be discussed. Studies in vivo and in vitro with synthetic and recombinant PTHrP sequences and antibodies developed against them have established that the PTH-like actions of PTHrP are mediated via the N-terminal sequences, which show some limited sequence homology with PTH. Evidence for PTH and non-PTH-like actions of PTHrP in normal physiology, which implicate a role for PTHrP in fetal and neonatal development, is also presented.
Crit Rev Biochem Mol Biol 1991
PMID:Parathyroid hormone-related protein: biochemistry and molecular biology. 193 71

Using a polyclonal antiserum raised against the first 34 amino acids of human parathyroid hormone-related peptide (PTHrP), we have localized PTHrP throughout the uro-genital tract of the human fetus aged between 8 and 40 weeks. Staining was present in the developing mesonephros, metanephros, gonads and in both the adrenal cortex and medulla. In particular, the developing mesonephric and metanephric renal tubules were intensely positive. Using Northern hybridization analysis we have detected a complex pattern of PTHrP mRNA transcripts ranging in size from 1.4 to 4.5 kb in early second trimester human fetal kidney. The presence of PTHrP in the mesonephros and metanephros provides evidence for a role for PTHrP in the regulation of fetal calcium metabolism. However, its presence in the gonad and adrenal gland invites the possibility of a wider role for PTHrP.
Mol Cell Endocrinol 1990 Mar 05
PMID:Parathyroid hormone-related peptide in the human fetal uro-genital tract. 218 58


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