Sie suchten nach: Uracil

Artikel-Nr: (BOSSBS-13521R-FITC)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-13521R-FITC

Beschreibung: G protein-coupled receptor 17, GPR17, also known as uracil nucleotide/cysteinyl leukotriene receptor or P2Y-like receptor (P2YL), is a 367 amino acid member of the G-protein coupled receptor 1 family of proteins. While GPR17 is expressed in kidney, heart and umbilical vein endothelial cells, it is expressed in the highest levels in the brain. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl leukotrienes (CysLTs), two families of endogenous signaling molecules, increase significantly at the site of damage. In some neurons, GPR17, a membrane receptor for uracil nucleotide and CysLTs, is upregulated as well, infiltrating the lesioned area. GPR17 is thought to play a role in mediating neuronal death, remodeling brain circuitries by microglia and initiating remyelination in damaged neurons. Two named isoforms of GPR17 exist as a result of alternative splicing events.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-13521R-A750)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-13521R-A750

Beschreibung: G protein-coupled receptor 17, GPR17, also known as uracil nucleotide/cysteinyl leukotriene receptor or P2Y-like receptor (P2YL), is a 367 amino acid member of the G-protein coupled receptor 1 family of proteins. While GPR17 is expressed in kidney, heart and umbilical vein endothelial cells, it is expressed in the highest levels in the brain. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl leukotrienes (CysLTs), two families of endogenous signaling molecules, increase significantly at the site of damage. In some neurons, GPR17, a membrane receptor for uracil nucleotide and CysLTs, is upregulated as well, infiltrating the lesioned area. GPR17 is thought to play a role in mediating neuronal death, remodeling brain circuitries by microglia and initiating remyelination in damaged neurons. Two named isoforms of GPR17 exist as a result of alternative splicing events.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-8288R-CY7)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-CY7

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-8288R-CY3)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-CY3

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-8288R-CY5)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-CY5

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-8288R-A350)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-A350

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-8288R)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

Sale

Artikel-Nr: (BOSSBS-8288R-A647)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-A647

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

Sale

Artikel-Nr: (BOSSBS-8288R-A750)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-A750

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterised by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-12022R)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-12022R

Beschreibung: G protein-coupled receptor 17, GPR17, also known as uracil nucleotide/cysteinyl leukotriene receptor or P2Y-like receptor (P2YL), is a 367 amino acid member of the G-protein coupled receptor 1 family of proteins. While GPR17 is expressed in kidney, heart and umbilical vein endothelial cells, it is expressed in the highest levels in the brain. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl leukotrienes (CysLTs), two families of endogenous signaling molecules, increase significantly at the site of damage. In some neurons, GPR17, a membrane receptor for uracil nucleotide and CysLTs, is upregulated as well, infiltrating the lesioned area. GPR17 is thought to play a role in mediating neuronal death, remodeling brain circuitries by microglia and initiating remyelination in damaged neurons. Two named isoforms of GPR17 exist as a result of alternative splicing events.

UOM: 1 * 100 µl

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Artikel-Nr: (BOSSBS-13521R-A680)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-13521R-A680

Beschreibung: G protein-coupled receptor 17, GPR17, also known as uracil nucleotide/cysteinyl leukotriene receptor or P2Y-like receptor (P2YL), is a 367 amino acid member of the G-protein coupled receptor 1 family of proteins. While GPR17 is expressed in kidney, heart and umbilical vein endothelial cells, it is expressed in the highest levels in the brain. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl leukotrienes (CysLTs), two families of endogenous signaling molecules, increase significantly at the site of damage. In some neurons, GPR17, a membrane receptor for uracil nucleotide and CysLTs, is upregulated as well, infiltrating the lesioned area. GPR17 is thought to play a role in mediating neuronal death, remodeling brain circuitries by microglia and initiating remyelination in damaged neurons. Two named isoforms of GPR17 exist as a result of alternative splicing events.

UOM: 1 * 100 µl

Sale

Artikel-Nr: (BOSSBS-13521R-A647)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-13521R-A647

Beschreibung: G protein-coupled receptor 17, GPR17, also known as uracil nucleotide/cysteinyl leukotriene receptor or P2Y-like receptor (P2YL), is a 367 amino acid member of the G-protein coupled receptor 1 family of proteins. While GPR17 is expressed in kidney, heart and umbilical vein endothelial cells, it is expressed in the highest levels in the brain. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl leukotrienes (CysLTs), two families of endogenous signaling molecules, increase significantly at the site of damage. In some neurons, GPR17, a membrane receptor for uracil nucleotide and CysLTs, is upregulated as well, infiltrating the lesioned area. GPR17 is thought to play a role in mediating neuronal death, remodeling brain circuitries by microglia and initiating remyelination in damaged neurons. Two named isoforms of GPR17 exist as a result of alternative splicing events.

UOM: 1 * 100 µl

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Artikel-Nr: (PRSI30-136)

Lieferant: ProSci Inc.

Hersteller Artikel Nummer : 30-136

Beschreibung: DUT is an essential enzyme of nucleotide metabolism. This protein forms a ubiquitous, homotetrameric enzyme that hydrolyzes dUTP to dUMP and pyrophosphate. This reaction serves two cellular purposes: providing a precursor (dUMP) for the synthesis of thymine nucleotides needed for DNA replication, and limiting intracellular pools of dUTP. Elevated levels of dUTP lead to increased incorporation of uracil into DNA, which induces extensive excision repair mediated by uracil glycosylase. This repair process, resulting in the removal and reincorporation of dUTP, is self-defeating and leads to DNA fragmentation and cell death.This gene encodes an essential enzyme of nucleotide metabolism. The encoded protein forms a ubiquitous, homotetrameric enzyme that hydrolyzes dUTP to dUMP and pyrophosphate. This reaction serves two cellular purposes: providing a precursor (dUMP) for the synthesis of thymine nucleotides needed for DNA replication, and limiting intracellular pools of dUTP. Elevated levels of dUTP lead to increased incorporation of uracil into DNA, which induces extensive excision repair mediated by uracil glycosylase. This repair process, resulting in the removal and reincorporation of dUTP, is self-defeating and leads to DNA fragmentation and cell death. Alternative splicing of this gene leads to different isoforms that localize to either the mitochondrion or nucleus. A related pseudogene is located on chromosome 19.

UOM: 1 * 100 µG

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Artikel-Nr: (BOSSBS-8288R-FITC)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-FITC

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

Sale

Artikel-Nr: (BOSSBS-8288R-A680)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-8288R-A680

Beschreibung: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterised by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.

UOM: 1 * 100 µl

Sale

Artikel-Nr: (BOSSBS-13521R-CY7)

Lieferant: Bioss

Hersteller Artikel Nummer : BS-13521R-CY7

Beschreibung: G protein-coupled receptor 17, GPR17, also known as uracil nucleotide/cysteinyl leukotriene receptor or P2Y-like receptor (P2YL), is a 367 amino acid member of the G-protein coupled receptor 1 family of proteins. While GPR17 is expressed in kidney, heart and umbilical vein endothelial cells, it is expressed in the highest levels in the brain. Upon brain injury, the extracellular concentrations of nucleotides and cysteinyl leukotrienes (CysLTs), two families of endogenous signaling molecules, increase significantly at the site of damage. In some neurons, GPR17, a membrane receptor for uracil nucleotide and CysLTs, is upregulated as well, infiltrating the lesioned area. GPR17 is thought to play a role in mediating neuronal death, remodeling brain circuitries by microglia and initiating remyelination in damaged neurons. Two named isoforms of GPR17 exist as a result of alternative splicing events.

UOM: 1 * 100 µl

Sale