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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)

In tumors and embryoid bodies of mouse teratoma a correlation has been established between specific activity of alkaline phosphatase (EC 3.1.3.1) and content of embryonal carcinoma, the stem cell of the tumor. A histochemical study of embryoid bodies has shown that high levels of the enzyme are confined to embryonal carcinoma. Fifteen tissue culture lines could be classified into three groups: (a) lines identifiable as pluripotential embryonal carcinoma by their morphology, tumorigenicity, and capacity to differentiate in vivo; (b) nullipotential embryonal carcinoma, resembling pluripotential embryonal carcinoma in morphology and malignancy but giving rise to undifferentiated tumors; and (c) lines of apparently nonmalignant somatic cells. Both types of embryonal carcinoma possess levels of alkaline phosphatase 5- to a 100-fold higher than the somatic cell lines. The embryonal carcinoma enzyme resembles the enzymes from kidney and placenta in kinetics of thermal inactivation and sensitivity to the inhibitor L-phenylalanine, but is distinguishable from the alkaline phosphatases of liver and intestine. These findings are discussed in relation to the use of teratoma for the study of cell differentiation.
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PMID:Alkaline phosphatase activity in mouse teratoma. 452 Dec 15

Cell lines corresponding to various cell lineages of the mouse embryo have been isolated from murine teratocarcinomas. Embryonal carcinoma cell lines are developmentally equivalent to the embryonic ectoderm or inner cell mass. Most of these cell lines have a modal chromosome number equal or close to 40, the normal mouse complement. However, cell lines corresponding to more advanced cell lineages (e.g., endoderm) are tetraploid or hypotetraploid and display multiple chromosomal rearrangements. This paper describes the isolation of a near-diploid differentiated cell line (LT-D) from an LT teratocarcinoma. The modal chromosome number of LT-D is 40, and this number is stable during at least 12 mo of continuous culture. LT-D cells are morphologically distinct from embryonal carcinoma cells and no longer express the SSEA-1 cell surface antigen or high alkaline phosphatase activity characteristic of embryonal carcinoma cells. LT-D cells can be induced to fuse into structures resembling myotubes. The formation of these structures is accompanied by expression of the muscle-specific isozyme of creatine phosphokinase and desmin, a muscle-specific component of intermediate filaments. Lastly, LT-D cells do not form tumors in syngenetic mice.
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PMID:Isolation and characterization of a near-diploid differentiated cell line from a murine teratocarcinoma that differentiates into muscle. 614 64

Eight independent cell lines, derived from human testicular germ-cell tumors, were examined for the expression of various markers. These included major histocompatibility and embryonic antigens, chorionic gonadotropin, alpha fetoprotein, alkaline phosphatase, plasminogen activator, and infectivity by SV40. No line consisted primarily of choriocarcinoma or yolk sac cells, but several contained cells resembling murine embryonal carcinoma; some of these lines formed tumors with the distinctive features of embryonal carcinoma when injected into immunosuppressed animals. It is proposed that human embryonal carcinoma cells, unlike those of the mouse, correspond to a preblastocyst stage of development.
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PMID:A comparative study of eight cell lines derived from human testicular teratocarcinoma. 616 54

The response of a human embryonal carcinoma cell line LICR LON HT39/7 to 12-O-tetradecanylphorbol 13-acetate (TPA) has been studied. Cells treated with 5 ng/ml of TPA undergo marked morphological changes, becoming flattened with nuclear enlargement and developing a grainy and often vacuolated cytoplasm. Parallel changes in the cell surface phenotype of the treated cells also occur. These include the appearance of membrane fibronectin, the embryonic antigen SSEA-1, and a glycoprotein antigen recognised by a monoclonal antibody. There is also increased expression of histocompatibility antigens. Other membrane molecules, such as peanut agglutinin receptor(s) and a 200 000 membrane glycoprotein appear to be removed from the membrane following TPA treatment. The high levels of alkaline phosphatase normally present in LICR LON HT39/7 are also reduced by TPA. Changes in the ultrastructure of the cells have also been observed, such as increases in nuclear complexity and in the number of intermediate filaments in the treated cells. This latter observation has been confirmed by immunofluorescent staining of the cells for prekeratins, which show an extensive network following the addition of TPA, but not before. 2-Dimensional gel electrophoresis of the proteins synthesized by LICR LON HT39/7 before and after addition of TPA has shown that there are a number of alterations in the proteins synthesised by the treated cells. Furthermore, immunoprecipitation of the culture supernatants from these cells has shown that TPA induces the synthesis and secretion of fibronectin. The alterations in the phenotype of LICR LON HT39/7 induced by TPA are irreversible and the altered cells, whilst they stop dividing, can be maintained for at least three weeks in culture. The analogue of TPA 12-O-tetradecanylphorbol 13-myristate does not produce the effects described above.
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PMID:Effects of 12-O-tetradecanylphorbol 13-acetate (TPA) on a clonal human teratoma-derived embryonal carcinoma cell line. 618 25

Alkaline phosphatase is a useful and reliable marker of germ cell neoplasia that has been almost completely overlooked in the recent medical literature and in the practice of surgical pathology. Its presence in immature germ cells and in germ cell cancers was noted as early as 1953, but a systematic study of its use in the diagnosis and classification of germ cell tumors has not appeared in the literature. Using a recently developed plastic embedding technique combined with enzyme histochemistry, a large series of germ cell tumors and gonadal specimens were examined for the presence of alkaline phosphatase. The neoplastic germ cells in all cases of seminoma and embryonal carcinoma showed strong plasma membrane positivity for alkaline phosphatase. Choriocarcinomas (gestational and nongestational) and mature teratomas were negative. These findings suggest that the alkaline phosphatase reaction is a useful adjunct in the diagnosis of germ cell cancers.
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PMID:Alkaline phosphatase histochemistry in human germ cell neoplasms. 619 86

From a series of hybridomas that produced monoclonal antibodies reactive with the surface of human embryonal carcinoma cells, two that specifically recognized determinants of the liver/bone/kidney isozyme of alkaline phosphatase were isolated. They did not cross-react with the intestinal or placental isozymes. Phylogenetic studies revealed that both antibodies cross-reacted strongly with liver alkaline phosphatase from higher primates, but exhibited marked differences in their respective cross-reactions with liver alkaline phosphatase from other mammalian species.
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PMID:Two monoclonal antibodies recognizing determinants on human embryonal carcinoma cells react specifically with the liver isozyme of human alkaline phosphatase. 620 84

A micromethod for the determination of alkaline phosphatase activity in a few cells from two cell lines, undifferentiated embryonal carcinoma F 9 cells and differentiated embryonal mouse fibroblast STO cells, is presented. In F 9 cells a 4- to 5-fold higher activity of alkaline phosphatase than in STO cells extrapolated from 10 cells was evaluated and compared with the results of the specific activity from cell extracts of these two cell lines. The significance of the results and the application of the method is discussed.
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PMID:A micromethod for the determination of alkaline phosphatase in mammalian cells. 667 Sep 98

We report the isolation of six cell lines (designated EB cell lines) from cultures of the hypoxanthine guanine phosphoribosyl transferase-deficient (HGPRT-) feeder-dependent embryonal carcinoma cell line PSA4TG12 which have undergone in vitro differentiation, and of clonal derivatives of these lines. Whereas some lines possess quasi-diploid karyotypes similar to that of PSA4TG12, others are markedly aneuploid. Cell line EB26/1 and its clonal derivatives undergo adipogenesis in cultures maintained at confluence; in tumours formed by injection into syngeneic mice they produce muscle-like cells, cartilage and bone in addition to adipose cells. We therefore propose that EB26/1 and its clones are aneuploid derivatives of an uncommitted mesodermal cell. Cell line EB28/5 forms tumours with a histological appearance resembling that of yolk sac carcinoma but does not express biochemical markers characteristic of visceral or parietal endoderm. Cell line EB28/10n has a myoblast-like culture morphology and in tumours is capable of producing muscle-like cells, cartilage and bone. A high specific activity of alkaline phosphatase is present is two of five EB cell lines assayed, and plasminogen activator activity is present in all five. Since the EB cell lines represent populations of cells each expressing a particular subset of the genetic information present in a common ancestral genome, they will be invaluable for studying the developmental regulation of gene expression.
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PMID:Isolation of cell lines from differentiating embryonal carcinoma cultures. 668 50

The mouse embryonal carcinoma (EC) line, PCC4, was used to construct a series of somatic cell hybrids which contain a single or a few human chromosomes. The hybrids all retained the EC phenotype as determined by morphology, expression of SSEA-1, lack of cell surface H-2 antigen and cytokeratin filaments, high alkaline phosphatase levels, the ability to form EC tumors ectopically in nude mice, and the ability to differentiate in response to retinoic acid. Constitutively differentiated cloned lines were derived from retinoic acid-treated hybrid cultures. Several derived lines had a phenotype indistinguishable from that of parietal endoderm cells, which includes synthesis of large amounts of laminin, type IV procollagen, and plasminogen activator. One differentiated line showed a fibroblast-like morphology. The differentiated lines derived from two of the hybrids, MCP6 and GEOC4, stably maintained the sole human chromosomal component present in the EC progenitors. These EC hybrids therefore provide a system to study developmental regulation of the introduced and stably maintained human genetic material derived from a variety of cell types.
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PMID:Differentiation in vitro of human-mouse teratocarcinoma hybrids. 668 81

The appearance of differentiated cells in embryonal carcinoma (EC) cultures can be inhibited by culturing the cells on fibroblast feeder layers. To determine whether or not feeder layers act by increasing the probability of stem cell renewal, growth and differentiation were monitored in cultures of F9 (subclone OTF9 -63) EC cells exposed to retinoic acid (RA) in either the presence or absence of feeder layers. By measuring the fraction of laminin-positive TROMA 1-positive or alkaline phosphatase-negative cells, it was determined that the frequency of differentiated cells in RA-treated F9 cultures was reduced by 70-80% when cells were cultured on fibroblast feeder layers instead of gelatin-coated dishes. Experiments in which EC cells were cultured in close proximity to a feeder layer demonstrated that cell-cell contact was required for maximal inhibition of differentiation. The probability of stem cell renewal was determined by measuring the number of colony-forming cells in RA-treated cultures as a function of time. Analysis of the data demonstrated that the probabilities of stem cell renewal were 0.5 and 0.25 during the first and second 48 h periods, respectively, following addition of RA for cells cultured without feeder layers. Cultures maintained on feeder layers exhibited a stem cell renewal probability of 0.72. Thus, feeder layers reduce the frequency of differentiated cells in RA-treated cultures by increasing the probability of stem cell renewal. Determining the mechanism by which feeder layers counteract the effect of a chemically defined differentiation inducer should help to uncover the processes that regulate the probability of stem cell renewal.
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PMID:Fibroblast feeder layers inhibit differentiation of retinoic acid-treated embryonal carcinoma cells by increasing the probability of stem cell renewal. 672 94


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