Sie suchten nach: Fu\u00DFst\u00FCtzen

Lieferant: Biotium

Beschreibung: This antibody recognizes a protein of 36 kDa, identified as Thymidylate Synthase (TS) (EC 2.1.1.45). TS converts deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), which is essential for DNA biosynthesis. TS is also a critical target for the fluoropyrimidines, an important group of antineoplastic drugs that are widely used in the treatment of solid tumors. Both 5-FU and fluorodeoxyuridine are converted in tumor cells to FdUMP which inactivates TS by formation of a ternary covalent complex in the presence of the folate cofactor 5,10-methylenetetrahydrofolate. Expression of TS protein is associated with response to 5-fluorouracil (5-FU) in human colorectal, gastric, head and neck, and breast carcinomas.

Artikel-Nr: (BTIUBNUM0714-50)

Lieferant: Biotium

Beschreibung: This antibody recognizes a protein of 36 kDa, identified as Thymidylate Synthase (TS) (EC 2.1.1.45). TS converts deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), which is essential for DNA biosynthesis. TS is also a critical target for the fluoropyrimidines, an important group of antineoplastic drugs that are widely used in the treatment of solid tumors. Both 5-FU and fluorodeoxyuridine are converted in tumor cells to FdUMP which inactivates TS by formation of a ternary covalent complex in the presence of the folate cofactor 5,10-methylenetetrahydrofolate. Expression of TS protein is associated with response to 5-fluorouracil (5-FU) in human colorectal, gastric, head and neck, and breast carcinomas.

VE: 1 * 50 µl

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Lieferant: Biotium

Beschreibung: This antibody recognizes a protein of 36 kDa, identified as Thymidylate Synthase (TS) (EC 2.1.1.45). TS converts deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), which is essential for DNA biosynthesis. TS is also a critical target for the fluoropyrimidines, an important group of antineoplastic drugs that are widely used in the treatment of solid tumors. Both 5-FU and fluorodeoxyuridine are converted in tumor cells to FdUMP which inactivates TS by formation of a ternary covalent complex in the presence of the folate cofactor 5,10-methylenetetrahydrofolate. Expression of TS protein is associated with response to 5-fluorouracil (5-FU) in human colorectal, gastric, head and neck, and breast carcinomas.

Artikel-Nr: (BTIUBNUM0715-50)

Lieferant: Biotium

Beschreibung: This antibody recognizes a protein of 36 kDa, identified as Thymidylate Synthase (TS) (EC 2.1.1.45). TS converts deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), which is essential for DNA biosynthesis. TS is also a critical target for the fluoropyrimidines, an important group of antineoplastic drugs that are widely used in the treatment of solid tumors. Both 5-FU and fluorodeoxyuridine are converted in tumor cells to FdUMP which inactivates TS by formation of a ternary covalent complex in the presence of the folate cofactor 5,10-methylenetetrahydrofolate. Expression of TS protein is associated with response to 5-fluorouracil (5-FU) in human colorectal, gastric, head and neck, and breast carcinomas.

VE: 1 * 50 µl

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Artikel-Nr: (USBI042773-FITC)

Lieferant: US Biological

Beschreibung: Anti-TFPT Rabbit Polyclonal Antibody (FITC (Fluorescein Isothiocyanate))

VE: 1 * 200 µl

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Artikel-Nr: (USBI030973-APC)

Lieferant: US Biological

Beschreibung: Anti-FUCA2 Mouse Monoclonal Antibody (APC (Allophycocyanin)) [clone: 234CT20.2.1]

VE: 1 * 200 µl

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Artikel-Nr: (USBI030973-PE)

Lieferant: US Biological

Beschreibung: Anti-FUCA2 Mouse Monoclonal Antibody (PE (Phycoerythrin)) [clone: 234CT20.2.1]

VE: 1 * 200 µl

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Artikel-Nr: (USBI035795)

Lieferant: US Biological

Beschreibung: Anti-SRSF10 Rabbit Polyclonal Antibody

VE: 1 * 200 µl

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Artikel-Nr: (USBI030973-FITC)

Lieferant: US Biological

Beschreibung: Anti-FUCA2 Mouse Monoclonal Antibody (FITC (Fluorescein Isothiocyanate)) [clone: 234CT20.2.1]

VE: 1 * 200 µl

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Artikel-Nr: (BOSSBS-8288R)

Lieferant: Bioss

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.

VE: 1 * 100 µl

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

Lieferant: Bioss

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.

VE: 1 * 100 µl

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

Lieferant: Bioss

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.

VE: 1 * 100 µl

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

Lieferant: Bioss

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.

VE: 1 * 100 µl

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

Lieferant: Bioss

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.

VE: 1 * 100 µl

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

Lieferant: Bioss

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.

VE: 1 * 100 µl

Sale!

Artikel-Nr: (BOSSBS-8288R-A555)

Lieferant: Bioss

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.

VE: 1 * 100 µl

Sale!