CYCLOSPORINE AND GENE EXPRESSION BY HUMAN THYMOCYTES
(1994)
Abstract :
The objective of this proposal is the elucidation of the mechanism of action of cyclosporine (CsA). Cyclosporine acts by inhibiting the activation of tissue specific genes which can be induced in vitro by activating thymocytes and T-cells with agents which initiate a partially known cascade of transducing signals. The mechanism of action of a drug such as cyclosporine which specifically inhibits the expression of genes which are coordinately expressed during the activation of thymocytes or T- cells can be analysed by using approaches aimed at identifying and characterizing cis-acting DNA sequences (recognition elements) required for eukaryotic gene regulation. The known transcription factors of several inducible tissue-specific genes are preexisting and are modified during activation by a posttranscriptional mechanism which does not require protein synthesis; whereas others require newly synthesized proteins to induce their expression. Positive and negative regulatory elements which function in response to extracellular agents have been identified. It is my working hypothesis, that CsA can inhibit the induction of genes coding for lymphokines either directly, by binding to DNA in concert with a regulatory protein, or indirectly by affecting the modification of one or more putative, regulatory proteins (this modification can be either covalent or allosteric), or by influencing the binding of regulatory proteins to "CsA regulatory sequences" on the gene. My goal is to identify subsets of thymocytes resistant to the effects of CsA since it has been proposed that a specific subset of T-cells is relatively resistant to CsA. The comparison of the effects of CsA on uninduced and induced thymocytes will be useful for the understanding of the molecular events which are elicited during induction and inhibited by CsA. The effect of CsA on the cascade of transducing signals elicited by extracellular inducers and its effect on Ca+2 will also be studied.
| Project Number : | 5R01AI026483-05 |
|---|
| ICD : | NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES |
|---|
| IRG : | SRC |
|---|
| Project Terms : | T lymphocyte, cyclosporine, drug metabolism, drug resistance, gene expression, leukocyte activation /transformation, thymus, transcription factor DNA binding protein, blood /lymphatic pharmacology, calcium metabolism, cell population study, chlorpromazine, drug receptor, genetic transduction, interleukin 2, lymphokine, nucleic acid probe, nucleic acid sequence, nucleoprotein, phosphatidylinositol, phosphoprotein, phosphorylation, posttranscriptional RNA processing, protein kinase C, regulatory gene DNA fingerprinting, fluorescence activated cell sorter, human tissue, immunofluorescence technique, monoclonal antibody, nucleic acid hybridization, radioimmunoassay, tissue /cell culture |
|---|
CYCLOSPORINE AND GENE EXPRESSION BY HUMAN THYMOCYTES
(1993)
Abstract :
The objective of this proposal is the elucidation of the mechanism of action of cyclosporine (CsA). Cyclosporine acts by inhibiting the activation of tissue specific genes which can be induced in vitro by activating thymocytes and T-cells with agents which initiate a partially known cascade of transducing signals. The mechanism of action of a drug such as cyclosporine which specifically inhibits the expression of genes which are coordinately expressed during the activation of thymocytes or T- cells can be analysed by using approaches aimed at identifying and characterizing cis-acting DNA sequences (recognition elements) required for eukaryotic gene regulation. The known transcription factors of several inducible tissue-specific genes are preexisting and are modified during activation by a posttranscriptional mechanism which does not require protein synthesis; whereas others require newly synthesized proteins to induce their expression. Positive and negative regulatory elements which function in response to extracellular agents have been identified. It is my working hypothesis, that CsA can inhibit the induction of genes coding for lymphokines either directly, by binding to DNA in concert with a regulatory protein, or indirectly by affecting the modification of one or more putative, regulatory proteins (this modification can be either covalent or allosteric), or by influencing the binding of regulatory proteins to "CsA regulatory sequences" on the gene. My goal is to identify subsets of thymocytes resistant to the effects of CsA since it has been proposed that a specific subset of T-cells is relatively resistant to CsA. The comparison of the effects of CsA on uninduced and induced thymocytes will be useful for the understanding of the molecular events which are elicited during induction and inhibited by CsA. The effect of CsA on the cascade of transducing signals elicited by extracellular inducers and its effect on Ca+2 will also be studied.
| Project Number : | 1R01AI026483-01 |
|---|
| ICD : | NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES |
|---|
| IRG : | SRC |
|---|
| Project Terms : | ANTIBIOTICS, CYCLOSPORIN A, BLOOD AND RE SYSTEM, THYMUS, BLOOD CELLS, T LYMPHOCYTES, DRUGS RESISTANCE, DRUGS, PHARMACOLOGY, BIOCHEMICAL, GENETICS, GENES, GENE EXPRESSION, GENETICS, GENETIC REGULATION, INDUCTION-REPRESSION-DEREPRESSION, REPRESSORS-ACTIVATORS, IMMUNITY, CELLULAR, LEUKOCYTE ACTIVATION, TRANSFORMATION AND PROLIFERATION BLOOD AND RE SYSTEM PHARMACOLOGY, CALCIUM (MINERAL) BALANCE (METABOLISM), GENETICS, BIOCHEMICAL GENETICS, GENETIC CODING, GENETICS, GENES, GENE EXPRESSION, CIS-TRANS POSITION EFFECTS, GENETICS, GENES, REGULATORY GENES, GENETICS, SOMATIC CELL AND TRANSFORMATION, TRANSDUCTION, IMMUNITY, CYTOKINES, LYMPHOKINES, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, NUCLEIC ACIDS STRUCTURE, NUCLEOSIDES (TIDES) SEQUENCE, NUCLEIC ACIDS, NUCLEIC ACID PROBES, PHENOTHIAZINES, CHLORPROMAZINE, PHOSPHOLIPIDS, PHOSPHOGLYCERIDES, PHOSPHOINOSITIDES, PHOSPHOTRANSFERASES-ATP, PROTEIN KINASES, PROTEIN KINASE C, POPULATION STUDIES CELL, PROTEINS, BINDING PROTEINS, DNA-BINDING PROTEINS, PROTEINS, NUCLEOPROTEINS, PROTEINS, PHOSPHOPROTEINS, RECEPTORS, DRUG RECEPTORS, phosphorylation CELL SORTING, LASER, HUMAN, HUMAN TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PR OJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, IMMUNOFLUORESCENCE, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, RADIOIMMUNOASSAY, NUCLEIC ACIDS SEQUENCING, FOOTPRINTING, TISSUE (CELL) CULTURE, nucleic acid hybridization |
|---|
CYCLOSPORINE AND GENE EXPRESSION BY HUMAN THYMOCYTES
(1993)
Abstract :
The objective of this proposal is the elucidation of the mechanism of action of cyclosporine (CsA). Cyclosporine acts by inhibiting the activation of tissue specific genes which can be induced in vitro by activating thymocytes and T-cells with agents which initiate a partially known cascade of transducing signals. The mechanism of action of a drug such as cyclosporine which specifically inhibits the expression of genes which are coordinately expressed during the activation of thymocytes or T- cells can be analysed by using approaches aimed at identifying and characterizing cis-acting DNA sequences (recognition elements) required for eukaryotic gene regulation. The known transcription factors of several inducible tissue-specific genes are preexisting and are modified during activation by a posttranscriptional mechanism which does not require protein synthesis; whereas others require newly synthesized proteins to induce their expression. Positive and negative regulatory elements which function in response to extracellular agents have been identified. It is my working hypothesis, that CsA can inhibit the induction of genes coding for lymphokines either directly, by binding to DNA in concert with a regulatory protein, or indirectly by affecting the modification of one or more putative, regulatory proteins (this modification can be either covalent or allosteric), or by influencing the binding of regulatory proteins to "CsA regulatory sequences" on the gene. My goal is to identify subsets of thymocytes resistant to the effects of CsA since it has been proposed that a specific subset of T-cells is relatively resistant to CsA. The comparison of the effects of CsA on uninduced and induced thymocytes will be useful for the understanding of the molecular events which are elicited during induction and inhibited by CsA. The effect of CsA on the cascade of transducing signals elicited by extracellular inducers and its effect on Ca+2 will also be studied.
| Project Number : | 5R01AI026483-02 |
|---|
| ICD : | NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES |
|---|
| IRG : | SRC |
|---|
| Project Terms : | ANTIBIOTICS, CYCLOSPORIN A, BLOOD AND RE SYSTEM, THYMUS, BLOOD CELLS, T LYMPHOCYTES, DRUGS RESISTANCE, DRUGS, PHARMACOLOGY, BIOCHEMICAL, GENETICS, GENES, GENE EXPRESSION, GENETICS, GENETIC REGULATION, INDUCTION-REPRESSION-DEREPRESSION, REPRESSORS-ACTIVATORS, IMMUNITY, CELLULAR, LEUKOCYTE ACTIVATION, TRANSFORMATION AND PROLIFERATION BLOOD AND RE SYSTEM PHARMACOLOGY, CALCIUM (MINERAL) BALANCE (METABOLISM), GENETICS, BIOCHEMICAL GENETICS, GENETIC CODING, GENETICS, GENES, GENE EXPRESSION, CIS-TRANS POSITION EFFECTS, GENETICS, GENES, REGULATORY GENES, GENETICS, SOMATIC CELL AND TRANSFORMATION, TRANSDUCTION, IMMUNITY, CYTOKINES, LYMPHOKINES, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, NUCLEIC ACIDS STRUCTURE, NUCLEOSIDES (TIDES) SEQUENCE, NUCLEIC ACIDS, NUCLEIC ACID PROBES, PHENOTHIAZINES, CHLORPROMAZINE, PHOSPHOLIPIDS, PHOSPHOGLYCERIDES, PHOSPHOINOSITIDES, PHOSPHOTRANSFERASES-ATP, PROTEIN KINASES, PROTEIN KINASE C, POPULATION STUDIES CELL, PROTEINS, BINDING PROTEINS, DNA-BINDING PROTEINS, PROTEINS, NUCLEOPROTEINS, PROTEINS, PHOSPHOPROTEINS, RECEPTORS, DRUG RECEPTORS, phosphorylation CELL SORTING, LASER, HUMAN, HUMAN TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PR OJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, IMMUNOFLUORESCENCE, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, RADIOIMMUNOASSAY, NUCLEIC ACIDS SEQUENCING, FOOTPRINTING, TISSUE (CELL) CULTURE, nucleic acid hybridization |
|---|
CYCLOSPORINE AND GENE EXPRESSION BY HUMAN THYMOCYTES
(1993)
Abstract :
The objective of this proposal is the elucidation of the mechanism of action of cyclosporine (CsA). Cyclosporine acts by inhibiting the activation of tissue specific genes which can be induced in vitro by activating thymocytes and T-cells with agents which initiate a partially known cascade of transducing signals. The mechanism of action of a drug such as cyclosporine which specifically inhibits the expression of genes which are coordinately expressed during the activation of thymocytes or T- cells can be analysed by using approaches aimed at identifying and characterizing cis-acting DNA sequences (recognition elements) required for eukaryotic gene regulation. The known transcription factors of several inducible tissue-specific genes are preexisting and are modified during activation by a posttranscriptional mechanism which does not require protein synthesis; whereas others require newly synthesized proteins to induce their expression. Positive and negative regulatory elements which function in response to extracellular agents have been identified. It is my working hypothesis, that CsA can inhibit the induction of genes coding for lymphokines either directly, by binding to DNA in concert with a regulatory protein, or indirectly by affecting the modification of one or more putative, regulatory proteins (this modification can be either covalent or allosteric), or by influencing the binding of regulatory proteins to "CsA regulatory sequences" on the gene. My goal is to identify subsets of thymocytes resistant to the effects of CsA since it has been proposed that a specific subset of T-cells is relatively resistant to CsA. The comparison of the effects of CsA on uninduced and induced thymocytes will be useful for the understanding of the molecular events which are elicited during induction and inhibited by CsA. The effect of CsA on the cascade of transducing signals elicited by extracellular inducers and its effect on Ca+2 will also be studied.
| Project Number : | 5R01AI026483-03 |
|---|
| ICD : | NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES |
|---|
| IRG : | SRC |
|---|
| Project Terms : | ANTIBIOTICS, CYCLOSPORIN A, BLOOD AND RE SYSTEM, THYMUS, BLOOD CELLS, T LYMPHOCYTES, DRUGS RESISTANCE, DRUGS, PHARMACOLOGY, BIOCHEMICAL, GENETICS, GENES, GENE EXPRESSION, GENETICS, GENETIC REGULATION, TRANSCRIPTION FACTORS, REPRESSORS AND ACTIVATORS, IMMUNITY, CELLULAR, LEUKOCYTE ACTIVATION, TRANSFORMATION AND PROLIFERATION BLOOD AND RE SYSTEM PHARMACOLOGY, CALCIUM (MINERAL) BALANCE (METABOLISM), GENETICS, BIOCHEMICAL GENETICS, GENETIC CODING, GENETICS, GENES, REGULATORY GENES, GENETICS, GENETIC REGULATION, TRANSCRIPTION FACTORS, GENETICS, SOMATIC CELL AND TRANSFORMATION, TRANSDUCTION, IMMUNITY, CYTOKINES, LYMPHOKINES, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, NUCLEIC ACIDS STRUCTURE, NUCLEOSIDES (TIDES) SEQUENCE, NUCLEIC ACIDS, NUCLEIC ACID PROBES, PHENOTHIAZINES, CHLORPROMAZINE, PHOSPHOLIPIDS, PHOSPHOGLYCERIDES, PHOSPHOINOSITIDES, PHOSPHOTRANSFERASES-ATP, PROTEIN KINASES, PROTEIN KINASE C, POPULATION STUDIES CELL, PROTEINS, BINDING PROTEINS, DNA-BINDING PROTEINS, PROTEINS, NUCLEOPROTEINS, PROTEINS, PHOSPHOPROTEINS, RECEPTORS, DRUG RECEPTORS, phosphorylation CELL SORTING, LASER, HUMAN, HUMAN TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PR OJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, IMMUNOFLUORESCENCE, IMMUNOLOGICAL TESTS AND IMMUNOASSAY, RADIOIMMUNOASSAY, NUCLEIC ACIDS SEQUENCING, FOOTPRINTING, TISSUE (CELL) CULTURE, nucleic acid hybridization |
|---|
CYCLOSPORINE AND GENE EXPRESSION BY HUMAN THYMOCYTES
(1993)
Abstract :
The objective of this proposal is the elucidation of the mechanism of action of cyclosporine (CsA). Cyclosporine acts by inhibiting the activation of tissue specific genes which can be induced in vitro by activating thymocytes and T-cells with agents which initiate a partially known cascade of transducing signals. The mechanism of action of a drug such as cyclosporine which specifically inhibits the expression of genes which are coordinately expressed during the activation of thymocytes or T- cells can be analysed by using approaches aimed at identifying and characterizing cis-acting DNA sequences (recognition elements) required for eukaryotic gene regulation. The known transcription factors of several inducible tissue-specific genes are preexisting and are modified during activation by a posttranscriptional mechanism which does not require protein synthesis; whereas others require newly synthesized proteins to induce their expression. Positive and negative regulatory elements which function in response to extracellular agents have been identified. It is my working hypothesis, that CsA can inhibit the induction of genes coding for lymphokines either directly, by binding to DNA in concert with a regulatory protein, or indirectly by affecting the modification of one or more putative, regulatory proteins (this modification can be either covalent or allosteric), or by influencing the binding of regulatory proteins to "CsA regulatory sequences" on the gene. My goal is to identify subsets of thymocytes resistant to the effects of CsA since it has been proposed that a specific subset of T-cells is relatively resistant to CsA. The comparison of the effects of CsA on uninduced and induced thymocytes will be useful for the understanding of the molecular events which are elicited during induction and inhibited by CsA. The effect of CsA on the cascade of transducing signals elicited by extracellular inducers and its effect on Ca+2 will also be studied.
| Project Number : | 5R01AI026483-04 |
|---|
| ICD : | NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES |
|---|
| IRG : | SRC |
|---|
| Project Terms : | T lymphocyte, cyclosporine, drug metabolism, drug resistance, gene expression, genetic repressor /activator, leukocyte activation /transformation, thymus DNA binding protein, blood /lymphatic pharmacology, calcium metabolism, cell population study, chlorpromazine, drug receptor, genetic code, interleukin 2, lymphokine, nucleic acid probe, nucleic acid sequence, nucleoprotein, phosphatidylinositol, phosphoprotein, phosphorylation, posttranscriptional RNA processing, protein kinase C, regulatory gene, somatic cell transduction, transcription factor DNA fingerprinting, fluorescence activated cell sorter, human tissue from nonrelated source, immunofluorescence technique, monoclonal antibody, nucleic acid hybridization, radioimmunoassay, tissue /cell culture |
|---|
MECHANISM OF IMMUNE INTERFERON SYNTHESIS IN THYMOCYTES
(1988)
Abstract :
This research has as its goal the study of the mechanism of induction of gamma interferon synthesis by human thymocytes in vitro. It is based on our original observation that human thymocytes can be induced to synthesize interferon by two agents: a lectin and products of B-lymphoblastoid cell lines. This is the first observation of induction of gamma interferon, a lymphokine, by precursors of T lymphocytes. It is our aim to identify the thymocyte subsets that are induced and to correlate the induction of interferon synthesis with the acquisition of other immune functions characteristic of mature T lymphocytes. T lymphocytes play a crucial role in cellular immune defense, and the recruitment of thymocytes in immune defense against pathogens or tumor cells may be of vital importance. In view of the response of thymocytes to stimuli that cause gamma interferon synthesis, we also plan to investigate whether thymocytes acquire other immune functions characteristic of mature T lymphocytes when interferon synthesis is induced. It is our goal to investigate the immunoregulatory functions of gamma interferon, in particular its effect on T-cell-dependent immunoglobulin synthesis by thymocytes. Furthermore, we continue our investigation of the relationship between interleukin-2 and gamma interferon synthesis and the pharmacologic regulation of gamma IFN synthesis. The mechanism of induction of gamma interferon is of crucial importance for the understanding of one of the factors that influence host response to invasion by tumor cells in lines. (IS)
| Project Number : | 5R01CA033653-04 |
|---|
| ICD : | NATIONAL CANCER INSTITUTE |
|---|
| IRG : | EI |
|---|
| Project Terms : | BLOOD CELLS, T LYMPHOCYTES, EXPERIMENTAL IMMUNOLOGY STUDY SECTION, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERFERONS, cell differentiation BLOOD CELLS, B LYMPHOCYTES, GLOBULINS, GAMMA GLOBULINS, IMMUNOGLOBULIN BIOSYNTHESIS, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, IMMUNITY, IMMUNOREGULATION, TISSUE COMPATIBILITY-TRANSPLANT, ISOALLOANTIGENS (HISTOCOMPATIBILITY ANTIGENS) HUMAN, TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PROJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, TISSUE (CELL) CULTURE |
|---|
MECHANISM OF IMMUNE INTERFERON SYNTHESIS IN THYMOCYTES
(1987)
Abstract :
This research has as its goal the study of the mechanism of induction of gamma interferon synthesis by human thymocytes in vitro. It is based on our original observation that human thymocytes can be induced to synthesize interferon by two agents: a lectin and products of B-lymphoblastoid cell lines. This is the first observation of induction of gamma interferon, a lymphokine, by precursors of T-lymphocytes. It is our aim to identify the thymocyte subsets which are induced, and to correlate the induction of interferon synthesis with the acquisition of other immune functions characteristic of mature T-lymphocytes. T-lymphocytes play a crucial role in cellular immune defense, and the recruitment of thymocytes in immune defense against pathogens or tumor cells may be of vital importance. In view of the response of thymocytes to stimuli which cause gamma interferon synthesis, we also plan to investigate whether thymocytes acquire other immune functions characteristic of mature T-lymphocytes when interferon synthesis is induced. It is our goal to investigate the immunoregulatory functions of gamma interferon, in particular its effect on T cell dependent immunoglobulin synthesis by thymocytes. The mechanism of induction of gamma interferon is of importance for the understanding of one of the factors which influence host response to invasion by tumor cells or virus.
| Project Number : | 1R01CA033653-01A1 |
|---|
| ICD : | NATIONAL CANCER INSTITUTE |
|---|
| IRG : | EI |
|---|
| Project Terms : | BLOOD CELLS, T LYMPHOCYTES, EXPERIMENTAL IMMUNOLOGY STUDY SECTION, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERFERON, cell differentiation BLOOD CELLS, B LYMPHOCYTES, GLOBULINS, GAMMA GLOBULINS, IMMUNOGLOBULIN BIOSYNTHESIS, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, IMMUNITY, IMMUNOREGULATION, TISSUE COMPATIBILITY-TRANSPLANT, ISOALLOANTIGENS (HISTOCOMPATIBILITY ANTIGENS) HUMAN, TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PROJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, TISSUE (CELL) CULTURE |
|---|
MECHANISM OF IMMUNE INTERFERON SYNTHESIS IN THYMOCYTES
(1987)
Abstract :
This research has as its goal the study of the mechanism of induction of gamma interferon synthesis by human thymocytes in vitro. It is based on our original observation that human thymocytes can be induced to synthesize interferon by two agents: a lectin and products of B-lymphoblastoid cell lines. This is the first observation of induction of gamma interferon, a lymphokine, by precursors of T-lymphocytes. It is our aim to identify the thymocyte subsets that are induced and to correlate the induction of interferon synthesis with the acquisition of other immune functions characteristic of mature T-lymphocytes. T-lymphocytes play a crucial role in cellular immune defense, and the recruitment of thymocytes in immune defense against pathogens or tumor cells may be of vital importance. In view of the response of thymocytes to stimuli that cause gamma interferon synthesis, we also plan to investigate whether thymocytes acquire other immune functions characteristic of mature T-lymphocytes when interferon synthesis is induced. It is our goal to investigate the immunoregulatory functions of gamma interferon, in particular its effect on T-cell-dependent immunoglobulin synthesis by thymocytes. Furthermore, we continue our investigation of the relationship between interleukin 2 and gamma interferon synthesis and the pharmacologic regulation of gamma IFN synthesis. The mechanism of induction of gamma interferon is of crucial importance for the understanding of one of the factors that influence host response to invasion by tumor cells in lines. (IS)
| Project Number : | 5R01CA033653-02 |
|---|
| ICD : | NATIONAL CANCER INSTITUTE |
|---|
| IRG : | EI |
|---|
| Project Terms : | BLOOD CELLS, T LYMPHOCYTES, EXPERIMENTAL IMMUNOLOGY STUDY SECTION, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERFERON, cell differentiation BLOOD CELLS, B LYMPHOCYTES, GLOBULINS, GAMMA GLOBULINS, IMMUNOGLOBULIN BIOSYNTHESIS, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, IMMUNITY, IMMUNOREGULATION, TISSUE COMPATIBILITY-TRANSPLANT, ISOALLOANTIGENS (HISTOCOMPATIBILITY ANTIGENS) HUMAN, TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PROJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, TISSUE (CELL) CULTURE |
|---|
MECHANISM OF IMMUNE INTERFERON SYNTHESIS IN THYMOCYTES
(1987)
Abstract :
This research has as its goal the study of the mechanism of induction of gamma interferon synthesis by human thymocytes in vitro. It is based on our original observation that human thymocytes can be induced to synthesize interferon by two agents: a lectin and products of B-lymphoblastoid cell lines. This is the first observation of induction of gamma interferon, a lymphokine, by precursors of T lymphocytes. It is our aim to identify the thymocyte subsets that are induced and to correlate the induction of interferon synthesis with the acquisition of other immune functions characteristic of mature T lymphocytes. T lymphocytes play a crucial role in cellular immune defense, and the recruitment of thymocytes in immune defense against pathogens or tumor cells may be of vital importance. In view of the response of thymocytes to stimuli that cause gamma interferon synthesis, we also plan to investigate whether thymocytes acquire other immune functions characteristic of mature T lymphocytes when interferon synthesis is induced. It is our goal to investigate the immunoregulatory functions of gamma interferon, in particular its effect on T-cell-dependent immunoglobulin synthesis by thymocytes. Furthermore, we continue our investigation of the relationship between interleukin-2 and gamma interferon synthesis and the pharmacologic regulation of gamma IFN synthesis. The mechanism of induction of gamma interferon is of crucial importance for the understanding of one of the factors that influence host response to invasion by tumor cells in lines. (IS)
| Project Number : | 5R01CA033653-03 |
|---|
| ICD : | NATIONAL CANCER INSTITUTE |
|---|
| IRG : | EI |
|---|
| Project Terms : | BLOOD CELLS, T LYMPHOCYTES, EXPERIMENTAL IMMUNOLOGY STUDY SECTION, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERFERON, cell differentiation BLOOD CELLS, B LYMPHOCYTES, GLOBULINS, GAMMA GLOBULINS, IMMUNOGLOBULIN BIOSYNTHESIS, IMMUNITY, CYTOKINES, LYMPHOKINES, INTERLEUKIN 2, IMMUNITY, IMMUNOREGULATION, TISSUE COMPATIBILITY-TRANSPLANT, ISOALLOANTIGENS (HISTOCOMPATIBILITY ANTIGENS) HUMAN, TISSUES, FLUIDS ETC. FROM NON-RELATED SOURCES OUTSIDE IMMEDIATE PROJECT, IMMUNOLOGICAL PREPARATIONS, MONOCLONAL ANTIBODIES, TISSUE (CELL) CULTURE |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1979)
Abstract :
The objective of this project is the investigation of purine metabolism in gout and in neoplastic disease; the elucidation of the causes for purine overproduction, and the examination of the pharmacologic regulation of purine biosynthesis in man. Purine synthesis de novo and by the "salvage" pathway will be studied in peripheral leukocytes in vitro of leukemic and gouty patients, and in cultured lymphocytes of these patients. The characteristics of the enzyme activities which catalyze the synthesis of the first intermediate of the purine biosynthetic pathway will be studied in enzyme preparations from peripheral leukocytes of leukemia patients and in cultured lymphocytes of selected gouty subjects. The correlation between the pharmacologic regulation of purine metabolism in intact cells and in cell free enzyme preparations will yield pertinent information on the understanding and treatment of gout and myeloproliferative diseases. The role of ammonia in purine biosynthesis de novo will also be defined in these studies. The activity of the purine biosynthetic enzymes is stimulated in hematopoietic tissues in experimental leukemia, and in peripheral leukocytes in the acute phase of chronic myelocytic leukemia in man, and therefore may reflect changes in gene expression in malignant desease. Factors which control cellular differentiation will be studied in cells maintained in tissue culture; the source of material for these studies will include human lymphocyte cell lines of patients with genetic diseases of purine metabolism and leukemia; a cell line cloned from spleens of mice infected with Friend leukemia virus, and a neuroblastoma cell line with a genetic abnormality in purine metabolism.
| Project Number : | 5R01AM015262-08 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | ENZYME MECHANISMS, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), IMMUNOPATHOLOGY, AUTOIMMUNE DISORDERS, METABOLISM STUDY SECTION, NEOPLASMS OF BLOOD AND RE SYSTEM, LEUKEMIA, PHOSPHOTRANSFERASES, RIBOSEPHOSPHATE PYROPHOSPHOKINASE, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS BLOOD CELLS, ERYTHROCYTES, ENZYME INDUCTION-REPRESSION-DEREPRESSION, GENETICS, GENETIC REGULATION, GENETIC INDUCTION-REPRESSION-DEREPRESSION, GENETICS, MUTATION, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, IMMUNITY, CELLULAR, LYMPHOCYTE ACTIVATION, TRANSFORMATION AND PROLIFERATION, METABOLIC DISORDERS INBORN DIAGNOSIS, NEOPLASMS CHARACTERISTICS, MOLECULAR LEVEL STUDIES (GENERAL), NEOPLASMS GENETICS, NEOPLASTIC TRANSFORMATION, CARCINOGENESIS, LEUKEMOGENESIS, VIRAL, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME, cell differentiation CHEMISTRY, CLINICAL, BLOOD, CHILDREN, GENETICS, MICROBIAL, TRANSFORMATION MICROBIAL, HUMAN, CLINICAL, PHYSICAL SEPARATION, CHROMATOGRAPHY, AFFINITY, TISSUE (CELL) CULTURE |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1979)
Abstract :
The objective of this project is the investigation of purine metabolism in gout and in neoplastic disease; the elucidation of the causes for purine overproduction; and the examination of the pharmacologic regulation of purine biosynthesis in man. Purine synthesis de novo and by the "salvage" pathway will be studied in peripheral leukocytes in vitro of leukemic and gouty patients, and in cultured lymphocytes of these patients. The characteristics of the enzyme activities which catalyze the synthesis of the first intermediate of the purine biosynthetic pathway will be studied in enzyme preparations from peripheral leukocytes of leukemia patients and in cultures lymphocytes of selected gouty subjects. The correlation between the pharmacologic regulation of purine metabolism in intact cells and in cell free enzyme preparations will yield pertinent information on the understanding and treatment of gout and myeloproliferative diseases. The role of ammonia in purine biosynthesis de novo will also be defined in these studies. The activity of the purine biosynthetic enzymes is stimulated in hematopoietic tissues in experimental leukemia, and in peripheral leukocytes in the acute phase of chronic myelocytic leukemia in man, and therefore may reflect changes in gene expression in malignant disease. Factors which control cellular differentiation will be studied in cells maintained in tissue culture; the source of material for these studies will include human lymphcoyte cell lines of patients with genetic diseases of purine metabolism and leukemia; a cell line cloned from spleens of mice infected with Friend leukemia virus, and a neuroblastoma cell line with a genetic abnormality in purine metabolism. Modulation of gene expression and the factors which control gene functions will be studied in these model systems. Changes in specialized cell functions will be correlated with changes in the activity of the enzymes of purine metabolism.
| Project Number : | 2R01AM015262-04 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | BLOOD AND RE DISORDERS, BONE MARROW, MYELOPROLIFERATIVE, BLOOD AND RE NEOPLASMS, LEUKEMIA, ENZYME MECHANISMS, METABOLISM STUDY SECTION, NEOPLASTIC TRANSFORMATION, PENTOSES, PHOSPHORIBOSYLAMINES, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS, GOUT BLOOD CELLS, LEUKOCYTES, BLOOD CELLS, LYMPHOCYTES, CARBOHYDRATES METABOLISM, GLUCOSE METABOLISM, CHEMISTRY, CLINICAL, BLOOD, DICARBOXYLIC AMINO ACIDS, GLUTAMINE, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), GENETICS, GENES, GENE EXPRESSION, GENETICS, GENETIC REGULATION, GENETIC INDUCTION-REPRESSION-DEREPRESSION, GENETICS, MUTATION, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, METABOLIC DISORDERS DIAGNOSIS*, NEOPLASMS GENETICS, NERVOUS NEOPLASMS, NEUROBLASTOMA, PHOSPHOTRANSFERASES, RIBOSEPHOSPHATE PYROPHOSPHOKINASE, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME, ammonia, cell differentiation BLOOD AND RE NEOPLASMS, LEUKEMIA MOUSE (GENERAL), HUMAN, CLINICAL*, MAMMALS, MICE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, DEAE CELLULOSE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, GEL FILTRATION (PERMEATION)*, PHYSICAL SEPARATION, ELECTROPHORESIS*, PHYSICAL SEPARATION, ULTRACENTRIFUGATION, DENSITY GRADIENT*, TISSUE (CELL) CULTURE*, VIRUSES, ONCORNA, LEUKEMIA MOUSE FRIEND |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1979)
Abstract :
The objective of our research is the study of purine metabolism in gout and in neoplastic disease; the elucidation of causes for purine overproduction and the examination of the pharmacologic regulation of purine biosynthesis in man. The properties of the enzymes which are involved in the synthesis of phosphoribosyl-l-amine (PRA), the first intermediate in purine biosynthesis, are being investigated in cultured lymphocytes of normal subjects and of patients with abnormalities in purine metabolism. Repression and derepression of these enzyme activities are being studied in virus-induced erythroleukemic cell lines. A correlation is being sought between the regulation of isolated enzyme activities and the rate of purine biosynthesis in intact cells.
| Project Number : | 5R01AM015262-05 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | ENZYME MECHANISMS, METABOLISM STUDY SECTION, NEOPLASMS OF BLOOD AND RE SYSTEM, LEUKEMIA, PENTOSES, PHOSPHORIBOSYLAMINES, PHOSPHOTRANSFERASES, RIBOSEPHOSPHATE PYROPHOSPHOKINASE, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS, GOUT, neoplastic transformation BLOOD CELLS, LEUKOCYTES, BLOOD CELLS, LYMPHOCYTES, ENZYME INDUCTION-REPRESSION-DEREPRESSION, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), GENETICS, GENES, GENE EXPRESSION, GENETICS, GENETIC REGULATION, GENETIC INDUCTION-REPRESSION-DEREPRESSION, GENETICS, MUTATION, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, METABOLIC DISORDERS INBORN DIAGNOSIS*, NEOPLASMS CHARACTERISTICS, MOLECULAR LEVEL STUDIES (GENERAL), NEOPLASMS GENETICS, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME, cell differentiation CHEMISTRY, CLINICAL, BLOOD, GENETICS, MICROBIAL, TRANSFORMATION MICROBIAL, HUMAN, CLINICAL, MAMMALS, MICE*, NEOPLASMS OF BLOOD AND RE SYSTEM, LEUKEMIA MOUSE (GENERAL), NEOPLASMS RELATED CONTROL TAG, PHYSICAL SEPARATION, CHROMATOGRAPHY, DEAE CELLULOSE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, GEL FILTRATION (PERMEATION)*, PHYSICAL SEPARATION, ELECTROPHORESIS*, PHYSICAL SEPARATION, ULTRACENTRIFUGATION, DENSITY GRADIENT*, TISSUE (CELL) CULTURE*, VIRUSES, ONCORNA, LEUKEMIA MOUSE FRIEND |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1979)
Abstract :
The objective of this project is the investigation of purine metabolism in gout and in neoplastic disease; the elucidation of the causes for purine overproduction; and the examination of the pharmacological regulation of purine biosynthesis in man. Purine synthesis de novo and by the "salvage" pathway will be studied in peripheral leukocytes in vitro of leukemic and gouty patients, and in cultured lymphocytes of these patients. The characteristics of the enzyme activities which catalyze the synthesis of the first intermediate of the purine biosynthesis pathway will be studied in enzyme preparations from peripheral leukocytes of leukemia patients and in cultured lymphocytes of selected gouty subjects. The correlation between the pharmacologic regulation of purine metabolism in intact cells and in cell free enzyme preparations will yield pertinent information on the understanding and treatment of gout and myeloproliferative diseases. The role of ammonia in purine biosynthesis de novo will also be defined in these studies. The activity of the purine biosynthetic enzymes is stimulated in hematopoietic tissues in experimental leukemia, and in peripheral leukocytes in the acute phase of chronic myelocytic leukemia in man, and therefore may reflect changes in gene expression in malignant disease. Factors which control cellular differentiation will be studied in cells maintained in tissue culture; the source of material for these studies will include human lymphocyte cell lines of patients with genetic diseases of purine metabolism and leukemia; and cell lines cloned from spleens of mice infected with Friend leukemia virus. BIBLIOGRAPHIC REFERENCES: Reem, G.H. Phosphoribosylpyrophosphate Overproduction, a New Genetic and Metabolic Abnormality in the Lesch Nyhan Syndrome and in Hypoxanthine Guanine Phosphoribosyltransferase Deficiency. Science 190: 1098-1099 (1975). Reem, G.H. and Friend, C. Purine Metabolism in Murine Virus-Induced Erythroleukemic Cells During Differentiation in Vitro. Proc. Nat. Acad. Sci. 72 (4): 1630-1634 (1975).
| Project Number : | 5R01AM015262-06 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | ENZYME MECHANISMS, METABOLISM STUDY SECTION, NEOPLASMS OF BLOOD AND RE SYSTEM, LEUKEMIA, PHOSPHOTRANSFERASES, RIBOSEPHOSPHATE PYROPHOSPHOKINASE, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS, GOUT BLOOD CELLS, LEUKOCYTES, ENZYME INDUCTION-REPRESSION-DEREPRESSION, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), GENETICS, GENES, GENE EXPRESSION, GENETICS, GENETIC REGULATION, GENETIC INDUCTION-REPRESSION-DEREPRESSION, GENETICS, MUTATION, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, METABOLIC DISORDERS INBORN DIAGNOSIS*, NEOPLASMS CHARACTERISTICS, MOLECULAR LEVEL STUDIES (GENERAL), NEOPLASMS GENETICS, NEOPLASMS OF BLOOD AND RE SYSTEM, LEUKEMIA MOUSE (GENERAL), NEOPLASTIC TRANSFORMATION, CARCINOGENESIS, LEUKEMOGENESIS, VIRAL, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME, ammonia, cell growth regulation CHEMISTRY, CLINICAL, BLOOD, GENETICS, MICROBIAL, TRANSFORMATION MICROBIAL, HUMAN, CLINICAL, MAMMALS, RODENTS, MYOMORPHA, MICE (LABORATORY)*, NEOPLASMS, VIRUS INDUCED, PHYSICAL SEPARATION, CHROMATOGRAPHY, DEAE CELLULOSE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, GEL FILTRATION (PERMEATION)*, PHYSICAL SEPARATION, ELECTROPHORESIS*, PHYSICAL SEPARATION, ULTRACENTRIFUGATION, DENSITY GRADIENT*, TISSUE (CELL) CULTURE*, VIRUSES, ONCORNA, LEUKEMIA MOUSE FRIEND, cell differentiation |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1979)
Abstract :
The objective of this project is the investigation of purine metabolism in gout and in neoplastic disease; the elucidation of the causes for purine overproduction, and the examination of the pharmacologic regulation of purine biosynthesis in man. Purine synthesis de novo and by the "salvage" pathway will be studied in peripheral leukocytes in vitro of leukemic and gouty patients, and in cultured lymphocytes of these patients. The characteristics of the enzyme activities which catalyze the synthesis of the first intermediate of the purine biosynthetic pathway will be studied in enzyme preparations from peripheral leukocytes of leukemia patients and in cultured lymphocytes of selected gouty subjects. The correlation between the pharmacologic regulation of purine metabolism in intact cells and in cell free enzyme preparations will yield pertinent information on the understanding and treatment of gout and myeloproliferative diseases. The role of ammonia in purine biosynthesis de novo will also be defined in these studies. The activity of the purine biosynthetic enzymes is stimulated in hematopoietic tissues in experimental leukemia, and in peripheral leukocytes in the acute phase of chronic myelocytic leukemia in man, and therefore may reflect changes in gene expression in malignant disease. Factors which control cellular differentiation will be studied in cells maintained in tissue culture; the source of material for these studies will include: human lymphocyte cell lines of patients with genetic diseases of purine metabolism and leukemia; a cell line cloned from spleens of mice infected with Friend leukemia virus, and a neuroblastoma cell line with a genetic abnormality in purine metabolism. Modulation of gene expression and the factors which control gene functions will be studied in these model systems. Changes in specialized cell functions will be correlated with changes in the activity of the enzymes of purine metabolism. BIBLIOGRAPHIC REFERENCES: Reem, G.H. Adenosine metabolism in permanent lymphocyte lines and in erythrocytes of patients with the Lesch-Nyhan syndrome in Advances in Experimental Medicine and Biology Volume 76A, 384-390, 1976. Reem, G.H. and Friend, C. Stability of the azaguanine resistant phenotype in vivo. Advances in Experimental Medicine and Biology Volume 76A, 181-185, 1976.
| Project Number : | 5R01AM015262-07 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | ENZYME MECHANISMS, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), IMMUNOPATHOLOGY, AUTOIMMUNE DISORDERS, METABOLISM STUDY SECTION, NEOPLASMS OF BLOOD AND RE SYSTEM, LEUKEMIA, PHOSPHOTRANSFERASES, RIBOSEPHOSPHATE PYROPHOSPHOKINASE, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS BLOOD CELLS, ERYTHROCYTES, ENZYME INDUCTION-REPRESSION-DEREPRESSION, GENETICS, GENETIC REGULATION, GENETIC INDUCTION-REPRESSION-DEREPRESSION, GENETICS, MUTATION, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, IMMUNITY, CELLULAR, LYMPHOCYTE ACTIVATION, TRANSFORMATION AND PROLIFERATION, METABOLIC DISORDERS INBORN DIAGNOSIS*, NEOPLASMS CHARACTERISTICS, MOLECULAR LEVEL STUDIES (GENERAL), NEOPLASMS GENETICS, NEOPLASTIC TRANSFORMATION, CARCINOGENESIS, LEUKEMOGENESIS, VIRAL, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME, cell differentiation CHEMISTRY, CLINICAL, BLOOD, CHILDREN, GENETICS, MICROBIAL, TRANSFORMATION MICROBIAL, HUMAN, CLINICAL, PHYSICAL SEPARATION, CHROMATOGRAPHY, AFFINITY, TISSUE (CELL) CULTURE* |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1974)
| Project Number : | 5R01AM015262-02 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | BLOOD AND RE NEOPLASMS, LEUKEMIA, BLOOD AND RE NEOPLASMS, LYMPHOMA, GENETICS, GENETIC INDUCTION-REPRESSION, GENETICS, TRANSFORMATION MICROBIAL, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, NEOPLASTIC TRANSFORMATION, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS, GOUT, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME BLOOD AND RE NEOPLASMS, HODGKIN'S DISEASE, BLOOD AND RE NEOPLASMS, LYMPHOMA, BURKITT'S, DRUGS RESISTANCE, DRUGS SCREENING, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), GENETICS, GENE EXPRESSION, GENETICS, MUTATION, METABOLISM STUDY SECTION, NEOPLASTIC THERAPY, ANTINEOPLASTIC AGENTS, VIRUSES, ONCORNA, LEUKEMIA MOUSE FRIEND MAMMALS, MICE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, DEAE CELLULOSE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, GEL FILTRATION (PERMEATION)*, PHYSICAL SEPARATION, ELECTROPHORESIS*, PHYSICAL SEPARATION, ULTRACENTRIFUGATION, DENSITY GRADIENT*, TISSUE (CELL) CULTURE* |
|---|
PURINE METABOLISM IN GENETIC DISEASE AND LEUKEMIA
(1974)
| Project Number : | 5R01AM015262-03 |
|---|
| ICD : | NAT INST OF ARTHRITIS, DIABETES, DIGESTIVE & KIDNEY DISEASES |
|---|
| IRG : | MET |
|---|
| Project Terms : | BLOOD AND RE NEOPLASMS, LEUKEMIA, GLYCOSYLTRANSFERASES, RIBOSYLAMINE-5-PHOSPHATE:PYROPHOSPHATE PHOSPHORIBOSYLTRANSFERASE, NEOPLASTIC TRANSFORMATION, PURINES, PURINES-PYRIMIDINES METABOLISM ERRORS, GOUT, PURINES-PYRIMIDINES METABOLISM ERRORS, LESCH-NYHAN SYNDROME DRUGS RESISTANCE, DRUGS SCREENING, GENETIC DISORDERS (SEE ALSO APPROPRIATE CONGENITAL ABNORMALITIES), GENETICS, MUTATION, METABOLISM STUDY SECTION, NEOPLASTIC THERAPY, ANTINEOPLASTIC AGENTS, PURINE NUCLEOTIDES, HYPOXANTHINE NUCLEOTIDES, INOSINE MONOPHOSPHATE, THIOPURINES, 6-MERCAPTOPURINE, VIRUSES, ONCORNA, LEUKEMIA MOUSE FRIEND HUMAN, NONCLINICAL*, MAMMALS, MICE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, DEAE CELLULOSE*, PHYSICAL SEPARATION, CHROMATOGRAPHY, GEL FILTRATION (PERMEATION)*, PHYSICAL SEPARATION, ELECTROPHORESIS*, PHYSICAL SEPARATION, ULTRACENTRIFUGATION, DENSITY GRADIENT*, TISSUE (CELL) CULTURE* |
|---|