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)

Correlation between the expression of growth factor/receptor systems or the alterations of tumor suppressor genes and biological malignancy of gastric cancer was described. Overexpression of many growth factors/receptors, such as EGF, TGF alpha, EGF receptor and ERBB2, and reduction of type I receptor for TGF beta may be linked with new prognostic factors of gastric carcinomas. The expression of cripto, a novel gene of EGF family, shows a tendency to correlate with tumor staging of well differentiated gastric adenocarcinomas. p53 gene abnormalities take place in 60% of gastric carcinomas including early stage carcinoma. Loss of heterozygosity on chromosomes 1q, 7p and 7q is frequently observed in advanced gastric carcinomas of well differentiated type. Molecules which regulate tumor invasion and metastasis such as nm23, tissue inhibitor of metalloproteinase (TIMP) and endogenous galactoside-binding lectin may provide for prognostic factors of gastric cancer.
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PMID:[New prognostic factors in human gastric carcinomas]. 134 86

Expression of PDGF B-chain and the PDGF receptor beta-subunit (PDGFR beta) is detected immunocytochemically during the development of glomeruli in human kidneys of 54 to 105 days gestational age. During the early stages (vesicular, comma-shape and S-shape) of glomerulogenesis, PDGF B-chain is localized to differentiating epithelium of the glomerular vesicle, while PDGFR beta is expressed in the undifferentiated metanephric blastema, vascular structures, and interstitial cells. During this stage PDGF may be acting as a paracrine growth factor and as a chemoattractant acting to recruit mesangial progenitor cells into the developing glomerulus. As the glomerular tuft forms, both PDGF B-chain and PDGFR beta can be detected in an arboreal pattern radiating from the hilus of the glomerular tuft. Immunocytochemical studies using markers specific to endothelium (Ulex europaeus I lectin, Factor VIII related antigen), and smooth muscle (alpha-smooth muscle actin), indicate that the PDGF B-chain and PDGFR beta are both expressed primarily by mesangial cells. During this stage, PDGF may be acting primarily to provide an autocrine factor to mediate further mesangial cell proliferation. Glomerular expression of alpha-smooth muscle actin is limited to later stages of glomerulogenesis; at these stages the pattern of expression is similar to that of PDGF-B chain and PDGFR beta. The upregulation of mesangial PDGF, PDGFR beta, and alpha-smooth muscle actin expression that has been identified in some disease states in both humans and experimental animals appears to represent a recapitulation of this normal developmental process.
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PMID:Developmental patterns of PDGF B-chain, PDGF-receptor, and alpha-actin expression in human glomerulogenesis. 140 22

We investigated the glycoconjugates of the human bronchial glands at light and electron microscopic level by means of lectin histochemistry in combination with neuraminidase digestion and beta-elimination reaction. Both direct and indirect techniques using lectin-peroxidase, lectin-gold, and glycoprotein-gold complexes were applied. The binding pattern of the six lectins (ConA, HPA, DSA, WGA, LEA, and PNA) used in the present study suggests that mucous and serous cells of human bronchial glands contain both N- and O-glycosylated proteins in the secretory granules. Asparagine-linked oligosaccharides containing Gal(beta-1,4) GlcNAc and Man residues were abundant in serous cells. The demonstration of both the terminal Neu 5Ac (alpha-2,3, or 6) Gal (beta-1,4) GlcNAc sequence in the N-linked oligosaccharides of mucous cells and the terminal disaccharide Gal (beta-1,4) GlcNAc in the N-linked oligosaccharide chains of serous cells suggests the existence of complex type sugar chains N-glycosidically linked to the peptide region of the glycoproteins. The binding pattern of the DSA and the neuraminidase-DSA sequence provides evidence for the existence of sialyltransferase activity in the forming mucous granules of mucous bronchial cells.
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PMID:Ultrastructural localization of glycoconjugates in human bronchial glands: the subcellular organization of N- and O-linked oligosaccharide chains. 155 69

Cell surface molecules play an important role in cellular communication, migration, and adherence. Here, we show the effect of organ-derived biomatrices on endothelial cell surface glycosylation. Five different lectins (with and without neuraminidase treatment) have been used as probes in an enzyme-linked lectin assay to quantitatively detect glycoconjugates on endothelial cells (BAEC) grown on tissue culture plastic or biomatrices isolated from bovine lung, liver, and kidney. BAEC generally exhibit strong binding of concanavalin A (Con A), Ricinus communis agglutinin I (RCA-I), wheat germ agglutinin (WGA), and soybean agglutinin, and peanut agglutinin after neuraminidase pretreatment of cells (Neu-SBA and Neu-PNA), while SBA and PNA consistently bind weakly to BAEC. BAEC grown on organ-derived biomatrices exhibit significantly altered binding intensities of Con A, RCA-I, WGA, and Neu-PNA: BAEC cultured on lung- or kidney-derived biomatrices express significantly stronger binding affinities for Con A and RCA-I than BAEC grown on liver-derived biomatrix or tissue culture plastic. In contrast, BAEC binding of WGA and PNA (after treatment of cells with neuraminidase) is significantly reduced when BAEC are grown on liver- or kidney-derived biomatrix. Quantitative lectin immunogold electron microscopy reveals consistently stronger lectin binding over nuclear regions compared to junctional regions between neighboring cells. These results indicate that extracellular matrix components regulate endothelial cell surface glycoconjugate expression, which determines cellular functions, e.g., preferential adhesion of lymphocytes or metastatic tumor cells.
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PMID:Modulation of endothelial cell surface glycoconjugate expression by organ-derived biomatrices. 198 84

Cell surface glycoconjugate expression of endothelial cells in canine cutaneous hemangiomas and hemangiosarcomas was compared to normal cutaneous endothelial cells using eight different lectins (with and without neuraminidase pretreatment) in an indirect immunoperoxidase technique. Direct comparison of lectin binding pattern of neoplastic endothelial cells with adjacent normal endothelial cells revealed minor changes in the binding intensity of several lectins (enhanced: Wheat germ agglutinin [WGA]; reduced: Griffonia simplicifolia-I [GS-I], Ricinus communis agglutinin-I [RCA-I], Soybean agglutinin after neuraminidase pretreatment [Neu-SBA], and Wheat germ agglutinin after neuraminidase treatment [Neu-WGA]). Neoplastic endothelial cells in some tumors exhibited varying binding of Ulex europaeus agglutinin-I (UEA-I; not binding to normal canine endothelial cells) and no Soybean agglutinin (SBA) binding (variably binding to normal endothelial cells in small cutaneous vessels). Lectin binding of neoplastic cells was rather heterogenous within one tumor compared to the uniform binding pattern of normal endothelial cells. These lectin binding studies demonstrate the phenotypic heterogeneity of neoplastic endothelial cells, indicating changes of cell surface glycosylation during neoplastic transformation.
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PMID:Phenotypic characterization of normal and neoplastic canine endothelial cells by lectin histochemistry. 218 54

The present study describes biochemical and morphological differences of pseudophakic bullous keratopathy (PBK) corneas as compared with normal corneas. At the ultrastructural level, all PBK corneas studied had abnormal fibrillar material posterior to the Descemet's membrane. In addition, two of the six PBK buttons had subepithelial fibrocellular materials disrupting the epithelial basement membrane and Bowman's layer. Aggregates of collagen fibrils with 110 nm periodicity were occasionally seen within the stroma of the PBK corneas. Isolation and purification of the collagen from the Descemet's membrane/posterior collagenous layer (DM/PCL) showed an increased amount of material with molecular weight in the range of 50-60K daltons (presumably type VIII collagen) and decreased amounts of higher molecular weight, disulfide-bonded collagenous materials (presumably type IV collagen) as compared with normals. Sugar-specific lectin studies showed an increased deposition of peanut agglutinin (PNA) and Ricinus communis agglutinin I (RCA120) in the DM/PCL of the PBK corneas. Our data suggest that the DM/PCL of PBK corneas have an increased accumulation of terminal B-galactose and B-D-galactose (1-3)-D-N-acetylgalactosamine residues and altered ratios of low and high molecular weight collagenous proteins.
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PMID:Abnormal extracellular matrix in corneas with pseudophakic bullous keratopathy. 232 80

Human thymocytes were fractionated to a low or high specific gravity fraction (LF or HF) by the BSA incontinuous density gradient method, and stimulated by lectin, lymphokine and mixed lymphocyte culture (MLC) in order to induce natural killer (NK)-like nonspecific killer (activated lymphocyte killer, ALK) cell activity. The results are summarized below. Thymocytes of LF induced a higher amount of interleukin 2 (IL2) by PHA stimulation than those of HF. Although PHA induced ALK activity from thymocytes of LF but not from thymocytes of HF, crude IL2 induced ALK activity from both fractions. The ALK activity induced by PHA or IL2 was abrogated by treatment of OKT3 and complement but not by OKT4 or OKT8 and complement. ALK activity and allospecific cytotoxic killer cell (allo-CTL) activity were induced from thymocytes of LF by MLC and from both fractions by MLC with IL2, but there were some differences between these two activities. Hydrocortisone suppressed the induction of ALK activity but not of allo-CTL activity. Interferon-gamma enhanced the induction of ALK activity but not of allo-CTL activity. Treatment of OKT8 and complement abrogated the ALK activity but not the allo-CTL activity. There were negligible thymocytes with NK cell markers (OKMI, Leu7, Leu11) and there was no increase of these markers or large granular lymphocytes after the induction of ALK activity. These results suggest that IL2 might be essential to induce ALK activity from human thymocytes and that this killer cell might be different from NK cells and allo-CTL.
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PMID:[Induction of nonspecific killer cell activity from human thymocyte]. 294 60

The relationship of lectin-dependent cell-mediated cytotoxicity (LDCC) to interleukin-2 (IL-2) production was studied in healthy subjects and in patients with systemic lupus erythematosus (SLE). Profoundly depressed levels of LDCC were elicited by peripheral blood mononuclear cells (PBMC) from nine patients with active SLE in comparison to LDCC from seven controls, and eleven inactive SLE donors, using 3H-TdR-prelabelled adherent HEP-2 cells as targets in a 24 h assay with 25 micrograms/ml Con A. In parallel experiments, no individual correlation was found between LDCC activity and IL-2 production for healthy or SLE subjects. Further, no major differences were detected in IL-2 release when the three groups of donors were compared, a tendency observed at the Con A doses (5 and 25 micrograms/ml) and incubation times (24, 48, and 72 h) used to induce IL-2 production. In additional studies, impaired Con A-induced blastogenesis was noted for PBMC from active SLE patients in comparison to the PBMC from the controls or patients with inactive SLE. While strong individual correlation was obtained between blastogenesis and IL-2 secretion in controls and patients with inactive SLE, no such relationship was found in patients with active SLE. While addition of exogenous IL-2 to the cytotoxicity assay considerably enhanced LDCC by healthy donors it failed to improve LDCC by patients with active SLE. These data suggest that depressed LDCC and Con A-induced blastogenesis of patients with active SLE may not be related to impaired IL-2 production but rather to an inherent dysfunction of the effector lymphocytes, including their unresponsiveness to IL-2.
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PMID:Independence of depressed lectin-dependent cell-mediated cytotoxicity from interleukin 2 production in patients with systemic lupus erythematosus. 349 6

Lectin and rhodopsin antibody binding sites were studied in developing and adult rat photoreceptors in order to compare changes in the total carbohydrate pool with the movement of a known glycoprotein rhodopsin. Electron microscope immunocytochemical techniques utilizing modified colloidal gold methods were used. At birth, all three lectins - Concanavalin A (ConA), Ricinus communis agglutinin II (RCA II) and wheat germ agglutinin (WGA) - showed heavy labelling of the photoreceptor surface scleral to the outer limiting membrane. At the same age, a monoclonal antibody against rhodopsin, RET-P1, revealed sparse labelling of only occasional immature photoreceptor surfaces. At postnatal day 4(P4), all three lectins showed variable binding to the inner segment and along the length of the newly forming connecting cilium. There was generally a region of more intense label at the base of the cilium. RET-P1 binding to P4 retina showed a discontinuous distribution, with heavily labelled inner segments being adjacent to unlabelled inner segments. This pattern indicates that the initial expression of rhodopsin is not a coordinate event but occurs in discrete cells, possibly related to the end of mitosis. RET-P1 binding at this age was reduced or absent from the proximal connecting cilium. AT P7, when the outer segments are beginning to develop, all the lectins and RET-P1 showed reduced binding to the inner segment plasma membrane and heavy labelling of the outer segment surface. In favourable sections, heavy labelling of the photoreceptor cell body plasma membrane by ConA and RCA II was also observed, terminating abruptly at the outer limiting membrane. The variation in ligand binding between different cellular compartments which are all formed from a continuous plasma membrane may indicate the presence of special barriers to diffusion of membrane components. This labelling pattern persisted into maturity. RET-P1 and lectin binding did not always correspond in developing retina, indicating that at least part of the observed lectin label must be due to other glycoproteins or glycolipids. Post-embedding thin section labelling of adult rat retina revealed a uniform binding pattern across the outer segment for ConA, WGA and RET-P1. However, RCA II exhibited labelling only along the basal edge of outer segments. Labelling of isolated, opened discs from bovine rod outer segments revealed binding to a single surface for ConA, WGA and RET-P1, but RCA II only labelled a small amount of membrane. Hence RCA II seems to recognize a determinant present only on the outer segment plasma membrane.
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PMID:Lectin and antibody labelling of developing rat photoreceptor cells: an electron microscope immunocytochemical study. 375 63

The red cell membrane appears to possess receptors for malarial parasites which are species specific. Plasmodium falciparum invades red cells that have the surface sialoglycoproteins, glycophorins A, B and C. Several regions of these molecules are critical to parasite binding. Invasion of red cells by merozoites can be blocked by both antibodies directed to specific sites on glycophorin and tryptic fragments of these molecules. The parasites appear to bind to the red cells in a lectin-like fashion, since three monosaccharides, namely N-acetyl-glucosamine (Glu NAc), N-acetyl-galactosamine (Gal NAc) and N-acetyl-neuraminic acid (Neu NAc), can specifically block parasite invasion in vitro. Neoglycoproteins made by coupling these sugars to BSA are particularly effective. Possible mechanisms of parasite attachment to and invasion of red cells are discussed.
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PMID:Studies on the biochemical basis of the interaction of the merozoites of Plasmodium falciparum and the human red cell. 391 66


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