Esta buscando: toxic

Proveedor: Biotium

Descripción: This antibody neutralizes TNF alpha biological activities. It prevents TNF alpha induced apoptosis in Jurkat cells. It also neutralizes HurTNFamediated cytotoxicity of L929 cells and inhibits tumor growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.

Proveedor: ENZO LIFE SCIENCES

Descripción: The Screen-Well® cardiotoxicity library is a focused collection of 130 compounds with defined and diverse cardiotoxicity, including ion channel blockage, mitochondrial toxicity, arrhythmia, fibrosis, and many more. A variety of structurally and mechanistically different compound classes are included, as well as nontoxic controls. The compounds are dissolved in DMSO at 10 mM and aliquoted into deep-well plates. The library is an essential tool for predictive toxicology screening and assay development.

Proveedor: CleanAir by Baker

Descripción: BioVanguard Greenline B is a class II cabinet range which offers simplicity, robustness and high reliability ensuring the highest level of protection for operator, product and the environment, minimising hazards inherent to working with agents assigned to biosafety levels 1, 2 and 3. BioVanguard B is designed for high risk microbiological and high toxic applications, such as the production of cytotoxic medicines.

Numero del catalogo: (BOSSBS-8288R-CY5.5)

Proveedor: Bioss

Descripción: 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

Promoción

Numero del catalogo: (BOSSBS-8288R-A488)

Proveedor: Bioss

Descripción: 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

Promoción

Proveedor: ENZO LIFE SCIENCES

Descripción: The Screen-Well® hepatotoxicity library is a focused collection of 238 compounds with defined and diverse hepatotoxicity, including steatosis, mitochondrial toxicity, Mallory body formation, cholestatic effects, and many more. A variety of structurally and mechanistically different compound classes are included, as well as nontoxic controls. The compounds are dissolved in DMSO at 10 mM and aliquoted into deep-well plates. The library is an essential tool for predictive toxicology screening and assay development.

Numero del catalogo: (BOSSBS-12862R)

Proveedor: Bioss

Descripción: The B subunit of cholera toxin (CtxB) binds to a GM1-ganglioside receptor, a ubiquitous glycolipid cell surface receptor. This binding is widely accepted to initiate toxin action by triggering uptake and delivery of the toxin A subunit into cells. The beta chain has no toxic activity by itself. The holotoxin consists of a pentameric ring of B subunits whose central pore is occupied by the A subunit. The A subunit contains two chains, A1 and A2, linked by a disulfide bridge. The A subunit (and Cholera toxin) activates the adenylate cyclase enzyme in cells of the intestinal mucosa leading to increased levels of intracellular cAMP.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-12862R-A350)

Proveedor: Bioss

Descripción: The B subunit of cholera toxin (CtxB) binds to a GM1-ganglioside receptor, a ubiquitous glycolipid cell surface receptor. This binding is widely accepted to initiate toxin action by triggering uptake and delivery of the toxin A subunit into cells. The beta chain has no toxic activity by itself. The holotoxin consists of a pentameric ring of B subunits whose central pore is occupied by the A subunit. The A subunit contains two chains, A1 and A2, linked by a disulfide bridge. The A subunit (and Cholera toxin) activates the adenylate cyclase enzyme in cells of the intestinal mucosa leading to increased levels of intracellular cAMP.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-12862R-A488)

Proveedor: Bioss

Descripción: The B subunit of cholera toxin (CtxB) binds to a GM1-ganglioside receptor, a ubiquitous glycolipid cell surface receptor. This binding is widely accepted to initiate toxin action by triggering uptake and delivery of the toxin A subunit into cells. The beta chain has no toxic activity by itself. The holotoxin consists of a pentameric ring of B subunits whose central pore is occupied by the A subunit. The A subunit contains two chains, A1 and A2, linked by a disulfide bridge. The A subunit (and Cholera toxin) activates the adenylate cyclase enzyme in cells of the intestinal mucosa leading to increased levels of intracellular cAMP.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-12862R-FITC)

Proveedor: Bioss

Descripción: The B subunit of cholera toxin (CtxB) binds to a GM1-ganglioside receptor, a ubiquitous glycolipid cell surface receptor. This binding is widely accepted to initiate toxin action by triggering uptake and delivery of the toxin A subunit into cells. The beta chain has no toxic activity by itself. The holotoxin consists of a pentameric ring of B subunits whose central pore is occupied by the A subunit. The A subunit contains two chains, A1 and A2, linked by a disulfide bridge. The A subunit (and Cholera toxin) activates the adenylate cyclase enzyme in cells of the intestinal mucosa leading to increased levels of intracellular cAMP.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (HACH2597200)

Proveedor: Hach

Descripción: Use the toxtrak™ toxicity reagent set to analyze your water or wastewater samples for toxicity.

UOM: 1 * 1 SET

Promoción

Proveedor: Biotium

Descripción: This antibody neutralizes TNF alpha biological activities. It prevents TNF alpha induced apoptosis in Jurkat cells. It also neutralizes HurTNFamediated cytotoxicity of L929 cells and inhibits tumor growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.

Numero del catalogo: (BOSSBS-2332R-HRP)

Proveedor: Bioss

Descripción: Catalyzes the terminal and only committed step in triacylglycerol synthesis by using diacylglycerol and fatty acyl CoA as substrates. In contrast to DGAT2 it is not essential for survival. May be involved in VLDL (very low density lipoprotein) assembly. In liver, plays a role in esterifying exogenous fatty acids to glycerol. Functions as the major acyl-CoA retinol acyltransferase (ARAT) in the skin, where it acts to maintain retinoid homeostasis and prevent retinoid toxicity leading to skin and hair disorders.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-4200R-A488)

Proveedor: Bioss

Descripción: Selenium is an essential trace element that confers tolerance to toxicity arising through exposure to heavy metals or other reactive xenobiotics. Selenium exhibits potent anticarcinogenic properties, and deficiency of selenium may cause certain neurologic diseases. Both effects are attributed to selenium-binding proteins. Selenium binding protein 1 is down-regulated in lung adenocarcinoma, colorectal cander and ovarian cancer. It is two-fold upregulated in the brains of patients suffering from schizophrenia, and is therefore a biomarker for this disease.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-4200R-CY5)

Proveedor: Bioss

Descripción: Selenium is an essential trace element that confers tolerance to toxicity arising through exposure to heavy metals or other reactive xenobiotics. Selenium exhibits potent anticarcinogenic properties, and deficiency of selenium may cause certain neurologic diseases. Both effects are attributed to selenium-binding proteins. Selenium binding protein 1 is down-regulated in lung adenocarcinoma, colorectal cander and ovarian cancer. It is two-fold upregulated in the brains of patients suffering from schizophrenia, and is therefore a biomarker for this disease.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-8288R-FITC)

Proveedor: Bioss

Descripción: 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

Promoción