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)

The immunoperoxidase method was used to investigate the presence of intracytoplasmic lysozyme, alpha 1-antichymotrypsin (alpha 1-ACT), alpha 1-antitrypsin (alpha 1-AT), transferrin, and albumin in hyperplastic and inflamed human lymph nodes. Lysozyme was demonstrated in eosinophils, neutrophils, histiocytes, in epithelioid cells, mast cells, and some lining cells of lymph node sinuses. alpha 1-ACT was detectable in many, but not all histiocytes that stained for lysozyme, and in sinus histiocytes, epithelioid cells, and mast cells, but not in neutrophils or eosinophils. alpha 1-AT was demonstrable in mast cells, neutrophils, and some epithelioid cells, but not in histiocytes. Transferrin was found in mast cells, but not in any of the other cell types investigated. Albumin was detectable in a few epithelioid cells and giant cells of the Langhans type. Lysozyme, alpha 1-ACT, alpha 1-AT, transferrin, and albumin were never demonstrable in interdigitating reticulum cells, dendritic reticulum cells, or lymphoid cells.
Virchows Arch B Cell Pathol Incl Mol Pathol 1980
PMID:Demonstration of lysozyme, alpha 1-antichymotrypsin, alpha 1-antitrypsin, albumin, and transferrin with the immunoperoxidase method in lymph node cells. 611 Nov 58

The effect of a monomeric polyclonal polyspecific IgG preparation (mIgG) for i.v. use on the capacity of fresh normal human serum (NHS) to inhibit precipitation of immune complexes of tracer-labeled bovine serum albumin (BSA) and anti-BSA (aBSA) rabbit antibody was investigated. Relative to heat-inactivated serum which showed no capacity to inhibit immune complex precipitation (CIICP), fresh NHS at a final dilution of 1:3 or 1:2 showed a 12 and 46% CIICP, respectively, with a BSA:aBSA ratio at equivalence. Addition of incremental amounts of mIgG dose-dependently enhanced CIICP of NHS to reach 63 and 90%, respectively, at a concn of 13.0 mg/ml mIgG. Human serum albumin instead of mIgG had no influence on CIICP of NHS indicating that the phenomenon was not dependent on non-specific protein-protein interactions. Although minimal amounts of BSA cross-reactivity could be demonstrated in mIgG, the extent of this activity was too small to explain the CIICP-supporting effect of mIgG as determined by comparing the effect of mIgG and aBSA serum on CIICP of fresh serum. Furthermore, absorption of mIgG on BSA-Sepharose did not lead to impairment of its CIICP-supporting effect. A direct binding of tritium-labeled mIgG (3H-mIgG) to either insoluble BSA:aBSA complexes or latex-bound IgG (IgG-latex) was found. Incubation of 2.7 micrograms 3H-mIgG with 90 micrograms IgG-latex resulted in a specific binding of 5.2% of the labeled compound. Such binding could be inhibited by unlabeled mIgG. Binding of mIgG was mediated through the Fab as well as the Fc part of the molecules: the 3H-Fc as well as the 3H-Fab fragment of mIgG bound to IgG-latex. The extent of binding of Fc was more than twice that of Fab and amounted to 70-90% of the binding found with intact mIgG. In an immune adherence hemagglutination system that depends on the interaction of complement-reacted immune complexes with C3b receptor-bearing erythrocytes, evidence was obtained that the mIgG preparation facilitated fixation of C3b to performed BSA:aBSA complexes. Addition of 1.45 mg/ml mIgG reduced the quantity of antigen-complexed C3b-bearing aBSA antibodies required to show a given agglutination by a factor of 3-4. We conclude that the facilitating effect of high doses of mIgG on complement-dependent CIICP of NHS and on immune adherence hemagglutination is the amplifying effect of complement after an initial interaction of antigen-nonspecific polyclonal polyspecific IgG with antigen-reacted antibody.
Mol Immunol 1984 Jun
PMID:Immunoglobulin-mediated shifting of immune complexes to increased complement-dependent solubility and immunoadherence. 643 Dec 66

16 alpha-Hydroxyestrone (16 alpha OHE) has been shown previously to react nonenzymatically with proteins via a Heyns rearrangement of a Schiff base intermediate. Albumin modified by the addition of 16 alpha OHE is immunogenic, despite a relatively low molar substitution. High-titre antisera can be elicited which have a very high affinity toward the estrogen hapten. Cross-reactivity analysis reveals a high specificity for the phenolic A-ring and a lack of specificity to chemical substituents in the D-ring, the site of covalent linkage. The antisera reacts equally well with 16 alpha OHE-peptides as with 16 alpha OHE-lysine, suggesting the utility of this antisera in analyzing either enzymatically or chemically hydrolyzed proteins for the presence of 16 alpha OHE adducts. Immunochemical analysis of proteins modified by 16 alpha OHE may provide insight into the pathogenesis of systemic lupus erythematosus, an autoimmune disease in which elevated levels of 16 alpha OHE are known to occur.
Mol Immunol 1983 Dec
PMID:Characterization of antisera to the addition product formed by the nonenzymatic reaction of 16 alpha-hydroxyestrone with albumin. 665 75

Albumin complementary DNA (cDNA) was transcribed from purified albumin mRNA from the liver of Xenopus laevis. The resultant cDNA was an almost full length copy as defined by denaturing gel electrophoresis; was hybridized specifically to albumin mRNA with pseudo-first-order reaction kinetics and the mRNA . cDNA hybrid exhibited a sharp melting profile with a Tm of 83 degrees C. The identity of the cDNA was confirmed by gel electrophoresis following hybridization-arrested translation.
Mol Cell Biochem 1983
PMID:Synthesis and characterization of a DNA complementary to Xenopus laevis albumin mRNA. 668 90

Effects of free fatty acids (palmitate and linoleate) on myocardial contractility and slow action potentials (APs) were examined in Langendorff-perfused chick hearts. To study the slow APs exclusively, the fast Na+ channels were voltage-inactivated in elevated K+ (25 mM), and the concentration of Ca2+ ion was increased to 5.4 mM in order to induce slow APs. Palmitate (0.18, 0.54 or 0.72 mM) along with albumin (0.12 mM) was added to the perfusate. Albumin by itself did not affect contractility or the slow APs during normoxia and hypoxia. Under well oxygenated conditions, palmitate had no effect on contractility or the slow APs. However, palmitate accelerated the decline of contractility during hypoxia in a dose-dependent fashion. Hypoxia suppressed the slow APs, and palmitate and linoleate further exacerbated the suppression of slow APs produced by hypoxia. Nevertheless, palmitate and linoleate did not enhance the hypoxic reduction of the tissue high energy phosphate level. The present results suggest that free fatty acids elicit cardio-depressant effects on hearts through their direct action on the myocardial cell membrane (slow channels) rather than through any metabolic effects.
J Mol Cell Cardiol 1984 Mar
PMID:Enhanced suppression of myocardial slow action potentials during hypoxia by free fatty acids. 671 92

Albumin-like glycoprotein (Gp66) with a molecular mass of 66 kDa has been isolated from human fetal tissue by size-exclusion, ion-exchange chromatography and reverse-phase HPLC. Reactivity of Gp66 with antiserum raised against the major protein components fraction of human fetal serum was observed. The N-terminal 35 amino acid residues of Gp66 were identical to human serum albumin. Meanwhile Gp66 differed from albumin by a/ the presence of 3-5 Trp residues instead of 1 according to fluorescence and UV-spectra, b/ the glycosylation pattern: bi-, tri-, and tetraantennary sialooligosaccharides of a complex type were present. Isoelectric focusing revealed 4 isoforms (pI ranging within 4.8 to 5.1) of Gp66. Gp66 (but not asialo-Gp66) was able to inhibit the cytotoxic effect of TNF against the tumor cell line L929. Inhibition of WEHI-3 and L929 tumor cells proliferation by Gp66 was similar to that of albumin.
Biochem Mol Biol Int 1994 May
PMID:Albumin-like glycoprotein from human fetal tissue. 752 4

We prepared a series of modified proteins and peptides by derivatizing the positively charged epsilon-amino groups of the lysine amino acids through reaction with anhydrides of succinic acid (Suc) and aconitic acid (Aco). Human serum albumin (HSA) was modified by introduction of a single carboxylic group (Suc-HSA) or two carboxylic groups (Aco-HSA) per amine function, yielding strongly negatively charged compounds. The in vitro anti-human immunodeficiency virus (HIV)-1 IC50 of Suc-HSA was about 1 microgram/ml, and the most polyanionic modified albumin of the series (Aco-HSA) exhibited an IC50 as low as 0.02 microgram/ml. Similar derivatization of the plasma protein orosomucoid or the synthetic polypeptide polylysine did not produce compounds with significant anti-HIV-1 activity, indicating an HSA-specific effect. The mechanism of action of Suc-HSA was reported to be the inhibition of a post-binding virus-cell fusion event, probably due to interference with the gp41-mediated fusion process. In the present study we demonstrate that the more potent Aco-HSA also interferes with this fusion process but, additionally, this compound inhibits (i) the binding of soluble CD4 to HIV-infected cells, (ii) the binding of HIV particles to MT-4 cells, and (iii) the binding of anti-gp120 monoclonal antibody to the gp120 molecule. This indicates that Aco-HSA, apart from post-binding fusion, also inhibits virus-cell binding by shielding viral gp120. The simultaneous inhibition of binding and fusion may lead to a synergistic effect, explaining the extreme potency of Aco-HSA. The polyanionic HSAs are significantly less active against HIV-2 and do not interfere with the replication of feline immunodeficiency virus or 12 other DNA or RNA viruses, indicating a HIV-1-specific effect. In contrast, another polyanionic compound, the sulfated polysaccharide dextran sulfate, inhibits the replication of various viruses in a more nonspecific way, as a general polyanion. Dextran sulfate also exhibits strong anticoagulant activity, whereas Suc-HSA and Aco-HSA do not show this unwanted side effect.
Mol Pharmacol 1993 Nov
PMID:Novel, negatively charged, human serum albumins display potent and selective in vitro anti-human immunodeficiency virus type 1 activity. 790 28

The binding of retinoic acid to serum albumin induces quenching of the protein fluorescence when it is excited at 280 nm, on the other hand the bound ligand acquires intrinsic fluorescence. Albumin has two kinds of binding sites for retinoic acid with an affinity constant of 10(5) M-1 and 10(4) M-1 respectively. The binding is entropically driven and produces a conformational change at the environment of the albumin tryptophan residues. This change was described by an equilibrium constant assuming two conformational states of the albumin tryptophan residues. Retinoic acid binds to the albumin fatty acid binding sites, producing a perturbation in the warfarin and benzodiazepine binding sites of this protein.
Biochem Mol Biol Int 1994 Mar
PMID:Use of retinoic acid as a fluorescent probe to study conformational change of the albumin molecule. 803 27

The effects of the recombinant interleukin-1 receptor antagonist (rIL-1ra) on the systemic vascular and lung injury following intraperitoneal Salmonella enteritidis lipopolysaccharide (LPS) were determined in male Sprague-Dawley rats. Initial experiments identified that maximal mortality occurred with an intraperitoneal LPS dose of 20 mg/kg, and this dose was used in subsequent experiments. Albumin permeability, measured in an ex vivo perfused heart-lung preparation from the rats 2 h after injection of LPS, was increased with endotoxin as was the wet:dry weight ratio. Pretreatment of the rats with intravenous rIL-1ra, 1 to 10 mg/kg, followed by a continuous intravenous infusion at 30 to 50 micrograms/kg/min resulted in restoration of blood pressure at 100 min following endotoxin administration. Moreover, coadministration of rIL-1ra with endotoxin totally prevented the rise in albumin permeability of the pulmonary vasculature and the increase in wet:dry lung weight ratios observed in rats treated with LPS alone. LPS injected intraperitoneally caused a marked decrease in circulating leukocyte count, an effect not reversed by rIL-1ra. RNA extraction of whole-lung homogenates revealed that mRNA for IL-1 beta was constitutively expressed in the absence of endotoxin, but transcripts increased progressively from 0.5 to 2 h after endotoxin administration. Increases in mRNAs for tumor necrosis factor-alpha (TNF-alpha) and for macrophage inflammatory protein-2 (MIP-2), a potent neutrophil chemoattractant, were also observed from 0.5 until 2 h after endotoxin administration.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Respir Cell Mol Biol 1994 Feb
PMID:Role of interleukin-1 in endotoxin-induced lung injury in the rat. 811 Apr 77

A sensitive RNAse protection method was used to show that serine protease inhibitor-1 (Spi-1) is expressed in rat liver and heart, but not in kidney or brain. Bovine somatotropin (bGH) and placental lactogen (bPL) induced rat hepatocyte cultures to express both Spi-1 and IGF-1 mRNA, with bPL approximately 100-fold more potent than bGH. Bovine prolactin (bPrL) did not induce hepatocyte Spi-1 mRNA, demonstrating lack of involvement of lactogenic receptors. Albumin mRNA levels were stable during hepatocyte culturing and were unaffected by growth hormone (GH) treatment, showing that neither culture conditions nor GH treatment affected cellular differentiation. Eliminating serum-free medium hormone supplements one at a time, estradiol, testosterone and T3 were shown to be unnecessary for GH induction of Spi-1, while dexamethasone removal decreased Spi-1 mRNA levels to 10% of GH-stimulated controls. bGH induction of Spi-1 mRNA in the presence of only dexamethasone and glucagon was 75% higher (p < 0.01) than levels seen with insulin also present.
Mol Cell Endocrinol 1993 Dec
PMID:Spi-1: an hepatic serine protease inhibitor regulated by GH and other hormones. 814 11


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