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Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electron microscopic, immunologic, and biochemical methods have been used in an attempt to detect and characterize oncornaviruses in human prostatic carcinoma (PCa) and benign prostatic hyperplasia (BPH), and in prostates of mice of high and low mammary cancer or leukemia strains. Ultrastructural examination of 37 PCa and nine BPH specimens has revealed the presence of particles resembling type C virus in five cases of PCa and one of BPH, and also two different types of intracisternal virus-like particles in seven other cases of PCa. Type B virus particles have been observed in prostate of old mice of high mammary cancer strains, while type C virus particles have been found in the prostates of most mice of all the ten strains examined. Immunofluorescence tests with sera from patients with PCa and BPH and with cells derived in vitro from PCa have shown that sera of patients with PCa contained antibodies directed mainly against Forssman-like and tumor-related antigens. In immunofluorescence tests of antisera to major proteins of oncornaviruses with cells of PCa and BPH tissues grown in vitro, positive reactions have been obtained with antisera to p30 protein of murine, feline, and simian type C viruses. Fixed immunofluorescence (FIF) tests of sera of PCa (38%) and BPH (25%) and of some normal donors (27%) gave positive cytoplasmic reaction with mouse prostate cells infected with Soehner-Dmochowski murine sarcoma virus (SD-MSV). Immunoferritin tests of 11 sera positive by FIF gave ferritin labeling of type C virus particles in the SD-MSV-infected mouse prostate cells...
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PMID:Search for oncogenic viruses in human prostate cancer. 6 17

A technique of in situ embedding of cells grown in BEEM capsules has been devised for immunoelectron microscopic studies of oncornaviruses. As compared to other immunoelectron microscopic procedures, this technique is less time and reagent-consuming. The quality and specificity of this method were tested on well-characterized mouse mammary tumor virus (type B virus) and murine sarcoma virus (type C virus particles). This method gave good results in labeling of the virus particles with ferritin or peroxidase in the cells of mouse tissue cultures. In an application of this method, peroxidase labeling of type B virus particles was obtained in frozen sections of normal prostatic tissues of C3H/Dm and A/Dm strain mice treated with rabbit antiserum to mouse mammary tumor virus from A/Dm strain mouse milk. These results indicate that this method is useful and reliable for immunoelectron microscopy studies of oncornaviruses in tissue culture cells and also in frozen sections of tissues.
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PMID:In situ embedding method of cells grown in beem capsules for immunoelectron microscopic studies of oncornaviruses. 20 26

Statistical procedures were utilized to evaluate the concentration dependence of labeling by ferritin-conjugated lectins on four different rat cells: hepatocytes, normal thymocytes, Friend virus-induced rat tumor cells and feline sarcoma virus-induced rat sarcoma cells. Labeling by ferritin conjugates of concanavalin A, wheat germ agglutinin and Ricinus communis agglutinins I and II was quantitated by counting the number of ferritin granules on 600 Angstrom membrane segments. Relationships between the arithmetic means and variances for sample populations from each cell and ferritin-lectin combination were used to define four types of topographical distributions: uniform/ordered, uniform/random, random and clustered. It was found that the distribution and/or density of surface-bound lectin was concentration-dependent for all four ferritin-lectins. The nature of this dependency was complex and varied with both lectin and cell type.
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PMID:A statistical evaluation of the binding of ferritin-conjugated lectins to the surface of rat cells. Topographical variations as a function of lectin concentration and cell type. 31 39

Serum of 70 patients with malignant lymphoma was tested for concentration of ferritin by immunoradiometric assay. Serum of patients with Hodgkin's disease showed an apparently increased ferritin concentration only in the stage III and IV. Concentration of serum ferritin was found normal in patients with chronic lymphocytic leukemia and non-Hodgkin's lymphoma of low malignancy. Among patients with non-Hodgkin's lymphome of high malignancy only one who suffered from advanced immunoblastic sarcoma showed increased concentration of serum ferritin. Patients with elevated concentration of serum ferritin had a decreased level of serum iron and showed also anemia. Their bone marrow reticulum was rich in dyeing iron. These results suggest that hyperferritinemia in patients with advanced Hodgkin's disease is related to a lack of release of iron from reticuloendothelial system.
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PMID:[Serumferritin in patients with malignant lymphomas (author's transl)]. 59 80

Cellular uptake of ferritin amounting to 0-5 mug/mg cell protein or more can be measured colorimetrically on the basis of ferritin-iron content. 131I-serum albumin, soluble ferritin and aggregated ferritin used in equimolar concentrations are taken up differently by Sarcoma SI80 cells in culture. The net uptakes in 2 h at 37 degrees C are 0-065, 4-3 and 24-7 mug/mg cell protein or 0-93, 8-0 and 45-7 mumol, respectively. Albumin uptake is not inhibited by a 26-fold molar ferritin excess but is significantly inhibited by a 43-fold excess. The transport mechanism of the ferritins differs from that of albumin in that it is significantly inhibitable by 2 times 10(-4) M monoiodoacetate. Soluble ferritin contains small aggregates which are removed by filtration through Millipore membranes of 0-05, 0-1 and 0-22 mum. When the 0-1-mum filtrate is re-examined, uptake is no longer inhibited by iodoacetate. Since it can be inferred from other work that albumin is taken up by pinocytosis and ferritin aggregates by phagocytosis, the difference in susceptibility to inhibition is proposed as a way to distinguish pinocytosis from phagocytosis. Ferritin may form larger visible aggregates in culture medium. The transport mechanism of this aggregated ferritin differs from that of soluble unfiltered ferritin in that it causes concomitant enhancement of albumin uptake. Albumin transported by virtue of this effect becomes partially susceptible to iodoacetate. Thus, in addition to a distinction between pinocytosis and phagocytosis, our data single out 2 forms of albumin transport and 3 forms of ferritin transport.
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PMID:Cellular uptake of soluble and aggregated ferritin: distinction between pinocytosis and phagocytosis. 117 45

A procedure is described using antigen-coated beads of calf serum as immunadsorbent for the purification of antibodies against ferritin and against leukemia-sarcoma virus-induced antigens.
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PMID:The use of antigen-coated protein beads as immunoadsorbent for the purification of antibodies. 118 28

We investigated plasma levels of plasminogen activator inhibitor 2 (PAI-2) in 40 patients with hematological malignancies including acute leukemia, chronic leukemia, hemophagocytic histiocytosis (HH) and histiocytic sarcoma (HS). The plasma PAI-2 levels in the patients with mononuclear phagocyte system (MPS) proliferative disorders (M4, M5, and CMMoL on FAB classification, HH and HS) were all above the cut-off value in healthy subjects. In a patient of reactive HH, there was a close correlation between Plasma PAI-2 and serum ferritin levels during the clinical course. These results indicate that the increase of plasma PAI-2 would be a diagnostic indicator of MPS proliferative disorders.
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PMID:[Plasma concentrations of plasminogen activator inhibitor 2 in patients with hematological malignancies and their clinical significance]. 202 44

We have recently shown that urokinase-type plasminogen activator (u-PA) and plasminogen activator inhibitor type 1 are both found extracellularly beneath cultured human skin fibroblasts and HT-1080 sarcoma cells, but in distinct localizations. Here, the ultrastructural distribution of u-PA was studied using immunoferritin electron microscopy. In HT-1080 cells, u-PA on the extracellular aspect of the plasma membrane was detected at sites of direct contact of the cell with the growth substratum beneath all parts of the ventral cell surface. The ferritin-labeled adhesion plaques, which were enriched in submembraneous microfilaments, were frequently seen at the leading lamellae of the cells as well as in lamellipodia and microspikes. Besides the cell-substratum adhesion plaques, ferritin label was detected at cell-cell contact sites. Double-label immunofluorescence showed a striking colocalization of u-PA and vinculin in both HT-1080 cells and WI-38 lung fibroblasts, which is consistent with u-PA being a focal contact component. The u-PA-containing focal contacts of WI-38 cells had no direct codistribution with fibronectin fibrils. In WI-38 cells made stationary by cultivation in a medium containing 0.5% FCS, vinculin plaques became highly elongated and more centrally located, whereas u-PA immunolabel disappeared from such focal adhesions. These findings show that plasma membrane-associated u-PA is an intrinsic component of focal contacts, where, we propose, it enables directional proteolysis for cell migration and invasion.
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PMID:Ultrastructural localization of plasma membrane-associated urokinase-type plasminogen activator at focal contacts. 312 96

The distribution of cell surface negatively-charged macromolecules was determined electron microscopically on untreated and on retinoic acid (RA)-treated cultured human osteosarcoma Hs791 and chondrosarcoma Hs705 cells using cationized ferritin (CF), an electron-dense marker of anionic sites. Labeling on the surface of prefixed cells was continuous and uniform whether they were grown in the absence or presence of RA. In contrast, CF distribution on unfixed cells was markedly affected by RA; CF labeling of untreated cells occurred in patches and clusters whereas the label on RA-treated cells was continuous, as on prefixed cells. CF labeling of unfixed cells decreased considerably after incubation of the cells either with hyaluronidase or neuraminidase. There was also a reduction in patching and clustering. Changes induced by RA in the apparent membrane microviscosity, in neuraminidase-releasable sialic acid, or in transglutaminase activity could not be related to the effect of RA on CF-induced anionic site redistribution since these characteristics were modulated differently in the two cell lines. In contrast, RA increased the sialylation of specific cell surface membrane glycoproteins on both cell types. These results suggest that RA prevents redistribution of cell surface sialoglycoconjugates and glycosaminoglycans by CF. This effect may be the result of increased sialylation of specific surface components and may be related causally to the suppression of the transformed phenotype in the sarcoma cells.
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PMID:Prevention by retinoic acid of anionic site redistribution on the surface of cultured human sarcoma cells. 615 8

Endothelial histogenesis of sarcoma Kaposi was referred to in a case of 36-year old man studied by electron microscopy. Characteristic features corresponding to the literature were found: Weibel-Palade bodies, a ferritin-like material, phagocytosed erythrocytes, nuclear bodies, microfilaments and microtubules. Myelinated and unmyelinated axons were considered as remnants of original nervous tissue destroyed by the tumour or as nerve fibres accompanying proliferated vascular structures.
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PMID:[Kaposi's sarcoma (an electron microscope case study)]. 674 48


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