Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many proteins of eukaryotic cells are anchored to membranes by covalent linkage to glycosyl-phosphatidylinositol (GPI). These proteins lack a transmembrane domain, have no cytoplasmic tail, and are, therefore, located exclusively on the extracellular side of the plasma membrane. GPI-anchored proteins form a diverse family of molecules that includes membrane-associated enzymes, adhesion molecules, activation antigens, differentiation markers, protozoan coat components, and other miscellaneous glycoproteins. In the kidney, several GPI-anchored proteins have been identified, including uromodulin (Tamm-Horsfall glycoprotein), carbonic anhydrase type IV, alkaline phosphatase, Thy-1, BP-3, aminopeptidase P, and dipeptidylpeptidase. GPI-anchored proteins can be released from membranes with specific phospholipases and can be recovered from the detergent-insoluble pellet after Triton X-114 treatment of membranes. All GPI-anchored proteins are initially synthesized with a transmembrane anchor, but after translocation across the membrane of the endoplasmic reticulum, the ecto-domain of the protein is cleaved and covalently linked to a preformed GPI anchor by a specific transamidase enzyme. Although it remains obscure why so many proteins are endowed with a GPI anchor, the presence of a GPI anchor does confer some functional characteristics to proteins: (1) it is a strong apical targeting signal in polarized epithelial cells; (2) GPI-anchored proteins do not cluster into clathrin-coated pits but instead are concentrated into specialized lipid domains in the membrane, including so-called smooth pinocytotic vesicles, or caveoli; (3) GPI-anchored proteins can act as activation antigens in the immune system; (4) when the GPI anchor is cleaved by PI-phospholipase C or PI-phospholipase D, second messengers for signal transduction may be generated; (5) the GPI anchor can modulate antigen presentation by major histocompatibility complex molecules. Finally, at least one human disease, paroxysmal nocturnal hemoglobinuria, is a result of defective GPI anchor addition to plasma membrane proteins.
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PMID:Glycosyl-phosphatidylinositol-anchored membrane proteins. 145 Mar 66

We have used immunocytochemical techniques and enzyme cytochemistry to examine the distribution of plasma membrane proteins during coiling phagocytosis of Legionella pneumophila and conventional phagocytosis of Escherichia coli. Whereas class I and class II major histocompatibility complex (MHC) molecules are relatively excluded from nascent phagosomes during conventional and coiling phagocytosis, the CR3 complement receptor persists in nascent phagosomes. The staining pattern for alkaline phosphatase activity resembles that of MHC molecules, with a marked exclusion of phosphatase activity from L. pneumophila coils and nascent phagosomes. The staining pattern for 5'-nucleotidase activity, on the other hand, resembles that of CR3 with intense staining in the inner layers of L. pneumophila coils. These results demonstrate that the cell has the ability to exclude selectively certain membrane proteins from the nascent phagosome during phagocytosis, thereby producing a phagosomal membrane markedly different from the plasma membrane from which it is derived.
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PMID:Membrane sorting during phagocytosis: selective exclusion of major histocompatibility complex molecules but not complement receptor CR3 during conventional and coiling phagocytosis. 156

Alveolar type II cells were isolated from fetal mouse lung by differential adherence and obtained in monolayer culture. Cultures display a high degree of purity as shown by histochemical and immunocytochemical staining procedures. Seventy-five percent of cells stained positive with specific anti-lavage serum mouse (SALS-M), an antiserum specific for (pre)alveolar type II cells of the mouse, and osmiophilic bodies were present in 82% of cells. These and other characteristics of type II cells in culture correspond to those of alveolar type II cells in fetal mouse lung. The pattern of reactivity of these cells with various anti-cytokeratin antibodies is described, and we show that, in contrast to rat type II cells, they do not exhibit alkaline phosphatase activity. Identity of the type II cell cultures was shown by their specific phospholipid composition and surfactant protein A (SP-A) content. The fetal alveolar type II cells in culture were found to synthesize and express class I but not class II major histocompatibility complex (MHC) antigens. The possibility to culture fetal alveolar type II cells of the mouse and the availability of genetically well-defined inbred and transgenic mouse strains opens ways to study the genetics of type II cell differentiation and function. Also, the in vitro availability of alveolar type II cells, the progenitor cells of mouse lung tumors, will enable us to study in vitro several of the processes involved in lung tumorigenesis in the mouse.
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PMID:Fetal mouse alveolar type II cells in culture express several type II cell characteristics found in vivo, together with major histocompatibility antigens. 169 1

As part of an on-going clinical trial of immunotherapy for recurrent malignant gliomas, using alkaline phosphatase-anti-alkaline phosphatase method with monoclonal antibodies, we investigated the correlation between expression of the major histocompatibility complex (MHC) and the subpopulation of tumor-infiltrating lymphocytes (TILs) in 38 glioma specimens (20 grade IV, 11 grade III, and 7 grade II) from 33 patients. Thirty specimens (78.9%) were positive to class I MHC antigen and 20 (52.6%) were positive to class II MHC antigen. The correlations between class I MHC antigen expression and the number of infiltrating T8 (p less than 0.01), and also between class II MHC antigen expression and the number of infiltrating T4 (p less than 0.05) were significant. We conclude that TILs are the result of immunoreaction (host-defense mechanism). 31.6% of specimens had perivascular infiltration of T cells. The main infiltrating lymphocyte subset in moderate to marked perivascular cuffing was T4. Our results may indicate that lack of MHC antigen on the glioma cell surface has a share in the poor immunogenicity in glioma-bearing patients. In addition, considering the effector/target ratio, the number of infiltrating lymphocytes against glioma cells was too small, so the immunological intervention seems to be essential in glioma therapy. Previous radiation therapy and chemotherapy, including steroid therapy, did not influence lymphocyte and macrophage infiltration.
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PMID:Immunohistochemical detection and correlation between MHC antigen and cell-mediated immune system in recurrent glioma by APAAP method. 170 54

Chronic graft-versus-host reaction (GVHR) due to male specific (H-Y) antigen was induced by the injection of syngeneic (DA x Lewis) F1 female cells into (DA x Lewis)F1 male rats. Chronic host-versus-graft reaction (HVGR) based on major histocompatibility complex (MHC) (RT1a) occurred when host Lewis (RT1(1)) rats were transplanted (DA x Lewis)F1 donor cells (RT1a & RT1I). Chronic GVHR and HVGR were activated at fixed periods. The first attacks of the GVHR and HVGR were recognized 50-80 days after cell transplantation, but the most intensive attacks of both responses were observed 120-175 days after cell transplantation. During the most intensive attacks, two rats died from either GVHR or HVGR. Rat immunoglobulin assays measured by radial immunodiffusion (RID) showed that serum IgG2b rose to 10.600-11.500 mg/ml in the rats that had the advanced GVHR or HVGR. The tissue mast cells derived from the loose lymphoid tissues of the medullary and subcapsular sinuses have proliferated in the mesenteric lymph nodes of the rats. IgM and IgG1 binding Fc receptors expressed on the mast cells were demonstrated indirectly using alkaline phosphatase conjugated ant-rat IgM and anti-rat IgG1.
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PMID:Increased serum IgG2b and IgM & IgG1 Fc receptors expressed on tissue mast cells in experimental GVHR and HVGR rat models. 179 38

Using monoclonal antibodies (MAB) in combination with the alkaline phosphatase anti-alkaline phosphatase technique, 20 meningiomas were examined for the expression of major histocompatibility complex (MHC) antigens. Most of the tumor cells were labeled with the MAB for class I MHC antigens. In addition, class I reactivity was seen in the tumor blood vessels, presumably reflecting labeling of the endothelial cells. Tumor cells and endothelium were not labeled with the MAB for class II MHC antigen HLA-DR. Occasionally a staining of periendothelial cells was detected. The presence of MHC antigens supports the assumption that endothelial cells play a role in antigen presentation, perhaps relevant to the initiation of an immune response, and that meningioma cells can be a target of T cell-mediated immune reactions.
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PMID:Monoclonal antibody analysis of major histocompatibility complex expression in human meningiomas. 258 94

Among the major histocompatibility complex (MHC)-linked complement genes, the loci for C4A and C4B exhibit the most extensive structural polymorphisms. Therefore the differentiation of variant and complex C4 phenotypes often proves difficult in conventional immunofixation electrophoresis. To improve the available technique of C4 typing a closed horizontal electrophoresis system was combined with poly- and monoclonal alkaline phosphatase immunoprobing on contact diffusion blots. The high resolution and sensitivity of this method not only facilitated C4 allotyping but also revealed additional polymorphic variation. Relative electrophoretic mobilities specific for each C4 allotype were established by computerized remission densitometry and provided the basis for a quantitative denomination of C4 variants. Typing by high resolution electrophoresis and the proposed relational C4 nomenclature could be valuable for further immunogenetical studies of the C4 protein polymorphism.
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PMID:High resolution electrophoresis for the allotyping of human C4. Proposal of a relational nomenclature. 349 59

Lewis rat thymocytes were incubated with different ligands: specific rat alloantisera, rabbit xenoantisera against whole-rat thymocytes or against thymocyte plasma-membrane vesicles and the two mitogens: concanavalin A and the Ca++ ionophore A 23187. After treatment, a crude plasma-membrane fraction was repaired, and the activities of two plasma-membrane marker enzymes, alkaline phosphatase and gamma-glutamyl transferase, and a general membrane marker enzyme, lysolecithin acyltransferase, were determined. An increase of all marker enzyme activities was observed only when thymocytes had been incubated with alloantiserum directed against the gene products of their major histocompatibility complex (MHC) or with rabbit antiserum against syngeneic thymocytes. Anti-MHC alloantiserum against a nonrelevant haplotype increased moderately the gamma-glutamyltransferase activity. Alloantiserum directed against the weak histocompatibility antigens had no significant effect as had rabbit antiserum raised against thymocyte plasma-membrane vesicles. The mitogens concanavalin A and A 23187 both increased the activity of the alkaline phosphatase and lysolecithin acyltransferase. Scanning electron microscopy showed that treatment with alloantisera did not alter the cell shape drastically. In contrast, incubation with rabbit xenoantiserum against thymocytes resulted in cell rounding and deformation. Rabbit xenoantiserum against the plasma-membrane vesicles of thymocytes resulted in markedly disturbed or damaged plasma membranes.
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PMID:Modulation of morphology and plasma-membrane enzyme activities of rat thymocytes induced by specific antisera. 612 54

During a systematic cell surface antigen expression profile analysis of 76 primary childhood brain tumors (34 medulloblastomas/primitive neuroectodermal tumors and 42 astrocytomas), we employed the following library of monoclonal antibodies (MoABs): anti-Leu-2/a; anti-Leu-3/a; anti-Leu-M5; anti-Leu-11b; anti-HLA-A, -B, -C; anti-HLA-DR; anti-HLe-1 (leukocyte common antigen); and UJ 308. The MoABs identified the expression of various leukocyte-associated, lymphocyte cell line differentiated, cell surface antigens in childhood brain tumors. The antigens were detected with an indirect, biotin-streptavidin-conjugated alkaline phosphatase (AP) immunocytochemical technique. Leu-2/a+ cells comprise the significant CD8+ cytotoxic T-lymphocyte (CTL) population of the tumor-infiltrating lymphocytes. CTLs are major histocompatibility complex (MHC) class I restricted, tumor-associated antigen-specific, cytotoxic cells and were identified in 58 of 76 (76.32%) brain tumors. CTLs usually represented 1-10% of all cells, but in some cases 30-44% of the cells were CD8+. CD4+, MHC class II restricted helper lymphocytes, detected with MoAB anti-Leu-3/a, were present in 65 of 76 (85.53%) brain tumors. Usually 1-10% of the observed cells reacted with MoAB anti-Leu 3/a. Macrophages (Leu-M5 antigen-positive cells) were expressed in 74 of 76 (97.37%) brain tumors. Their number also represented 1-10% of all observed cells in the frozen brain tumor sections. All 76 (100%) brain tumors contained cells that reacted positively with MoABs anti-HLA-A, -B, -C and anti-HLA-DR, demonstrating a strong MHC class I restriction of the tumor cell population and an overall leukocyte antigen expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunophenotypic characterization of infiltrating polynuclear and mononuclear cells in childhood brain tumors. 761 61

An immunohistochemical analysis of skin biopsies was performed in 18 patients with cutaneous lupus erythematosus (LE), using the alkaline phosphatase and monoclonal anti-alkaline phosphatase method (APAAP). The study group was subdivided on the basis of clinical criteria into 10 patients with chronic discoid LE (CDLE) and eight patients with subacute cutaneous LE (SCLE). Using a panel of monoclonal antibodies the following results were obtained: (i) ICAM-1 was expressed on epidermal keratinocytes, dermal inflammatory cells, and endothelial cells in most biopsies, whereas LFA-1 was confined to the dermis. Attachments between keratinocytes or endothelial cells and activated T lymphocytes via ICAM-1/LFA-1 may be a possible mechanism of target/effector recognition in cutaneous LE. (ii) HLA-DR was expressed on epidermal keratinocytes and cells of the dermal infiltrate, but not on endothelial cells. HLA-DR+ cells probably function as antigen-presenting cells, leading to major histocompatibility complex-restricted cellular cytotoxicity in cutaneous LE. (iii) Interleukin 2 receptor expression on dermal inflammatory cells was weak, indicating non-specific activation of T lymphocytes. (iv) The dermal inflammatory cells were T lymphocytes, mainly of the helper/inducer subtype. B lymphocytes were rarely found in the dermis. In general, no significant immunohistochemical differences were found between CDLE and SCLE, suggesting that these variants represent clinical subtypes rather than different pathogenetic entities.
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PMID:Immunohistochemical analysis of chronic discoid and subacute cutaneous lupus erythematosus--relation to immunopathological mechanisms. 775 49


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