Deuterium+oxide
Catalog Number:
(10282-058)
Supplier:
Bioss
Description:
ADH6 (alcohol dehydrogenase 6), also known as ADH-5, is a 368 amino acid member of the class V zinc-containing alcohol dehydrogenase family. This family of enzymes functions to metabolize a wide variety of substrates such as retinol, hydroxysteroids, ethanol, aliphatic alcohols and lipid peroxidation products. Localized to the cytoplasm and expressed in the stomach and liver, ADH6 catalyzes the reversible oxidation of alcohols to their corresponding aldehydes or ketones and is able to bind two zinc ions as cofactors. ADH6 contains a glucocorticoid response element upstream of its 5' UTR which is thought to be a steroid binding site, suggesting that expression of ADH6 may be under hormonal control. Multiple isoforms of ADH6 exist due to alternative splicing events.
Catalog Number:
(10802-952)
Supplier:
Rockland Immunochemical
Description:
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the reversible oxidative phosphorylation of glyceraldehyde-3-phosphate in the presence of inorganic phosphate and nicotinamide adenine dinucleotide (NAD), an important energy-yielding step in carbohydrate metabolism. Recent evidence suggests that it also is involved in a number of cellular processes such as membrane fusion, phosphotransferase activity, DNA replication and repair, and nuclear RNA export. GAPDH has also been implicated in playing a role in different pathologies such as cancer progression, apoptosis, and neuronal diseases such as Alzheimer's and Huntington's disease. GAPDH is constitutively expressed at high levels in almost all tissues and cell lines making it ideal for use as a loading control marker in immunoblots.
Catalog Number:
(10801-542)
Supplier:
Rockland Immunochemical
Description:
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) catalyzes the reversible oxidative phosphorylation of glyceraldehyde-3-phosphate in the presence of inorganic phosphate and nicotinamide adenine dinucleotide (NAD), an important energy-yielding step in carbohydrate metabolism. Recent evidence suggests that it also is involved in a number of cellular processes such as membrane fusion, phosphotransferase activity, DNA replication and repair, and nuclear RNA export. GAPDH has also been implicated in playing a role in different pathologies such as cancer progression, apoptosis, and neuronal diseases such as Alzheimer's and Huntington's disease. GAPDH is constitutively expressed at high levels in almost all tissues and cell lines making it ideal for use as a loading control marker in immunoblots.
Catalog Number:
(10287-550)
Supplier:
Bioss
Description:
In human liver cytosolic fractions, four forms of biliverdin reductase have been identified, including two biliverdin-IX Beta reductases and two biliverdin-IX Alpha reductases, designated isozymes I and II and isozymes III and IV, respectively. Biliverdin reductase A (BLVRA), also designated biliverdin-IX Alpha-reductase, belongs to the GFO/iIDH/MocA family and the biliverdin reductase subfamily. The gene that encodes this cytoplasmic protein maps to chromosome 7p14-cen. BLVRA reduces biliverdin IX ?(the ?methene bridge of the open tetrapyrrole) to bilirubin with the concomitant oxidation of an NADH or NADPH cofactor (bilirubin + NADP+ = biliverdin + NADPH). BLVRA is expressed primarily in liver.
Catalog Number:
(10284-630)
Supplier:
Bioss
Description:
In human liver cytosolic fractions, four forms of biliverdin reductase have been identified, including two biliverdin-IX Beta reductases and two biliverdin-IX Alpha reductases, designated isozymes I and II and isozymes III and IV, respectively. Biliverdin reductase A (BLVRA), also designated biliverdin-IX Alpha-reductase, belongs to the GFO/iIDH/MocA family and the biliverdin reductase subfamily. The gene that encodes this cytoplasmic protein maps to chromosome 7p14-cen. BLVRA reduces biliverdin IX ?(the ?methene bridge of the open tetrapyrrole) to bilirubin with the concomitant oxidation of an NADH or NADPH cofactor (bilirubin + NADP+ = biliverdin + NADPH). BLVRA is expressed primarily in liver.
Supplier:
Adipogen
Description:
Antibiotic. Shows antiviral, antifungal and antitumor properties. Immunosuppressive drug used to prevent rejection in organ transplantation, rheumatoid arthritis, and psoriasis. Potent reversible inhibitor of inosine-5'-monophosphate dehydrogenase (IMPDH), leading to depletion of GMP and interruption of the de novo synthesis of purine nucleotides necessary for B and T lymphocyte proliferation. Inhibits the type II IMPDH isoform (IMPDH-2) 5-fold more potently compared to type I isoform. Inhibits RNA and DNA synthesis. Inducible nitric oxide synthase (iNOS/NOS II) inhibitor. Apoptosis and necrosis inducer. Novel type of inhibitor against RNA guanylyltransferases. Inhibits TNF-alpha-stimulated MAPK/NF-kappaB and ROS generation.
Catalog Number:
(10297-730)
Supplier:
Bioss
Description:
GLUD2 is both mitochondrial matrix enzymes belonging to the Glu/Leu/Phe/Val dehydrogenases family. Exisiting as homohexamers, GLUD1 catalyzes the oxidative deamination of glutamate to ?ketoglutarate and ammonia while GLUD2 is involved in the recycling of glutamate during neurotransmission. GLUD1 is critical for regulating amino acid induced insulin secretion and is allosterically activated by ADP and inhibited by GTP and ATP. Mutations in the gene encoding GLUD1 causes hyperinsulinism-hyperammonemia syndrome (HHS), which is an inherited condition characterized by high insulin and ammonia levels in the blood. GLUD1 may also be involved in learning and memory reactions by increasing the turnover of the excitatory neurotransmitter glutamate. GLUD2 is expressed in testis and retina, with lower levels found in brain.
Catalog Number:
(10364-182)
Supplier:
Bioss
Description:
Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Also involved in LPS-independent inflammatory responses triggered by free fatty acids, such as palmitate. In complex with TLR6, promotes sterile inflammation in monocytes/macrophages in response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42. In this context, the initial signal is provided by oxLDL- or amyloid-beta 42-binding to CD36. This event induces the formation of a heterodimer of TLR4 and TLR6, which is rapidly internalized and triggers inflammatory response, leading to the NF-kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion.
Catalog Number:
(10364-164)
Supplier:
Bioss
Description:
Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Also involved in LPS-independent inflammatory responses triggered by free fatty acids, such as palmitate. In complex with TLR6, promotes sterile inflammation in monocytes/macrophages in response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42. In this context, the initial signal is provided by oxLDL- or amyloid-beta 42-binding to CD36. This event induces the formation of a heterodimer of TLR4 and TLR6, which is rapidly internalized and triggers inflammatory response, leading to the NF-kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion.
Catalog Number:
(10256-866)
Supplier:
Bioss
Description:
The Cpt1 family of proteins are outer mitochondrial membrane proteins that regulate the entry into, and oxidation of fatty acids by, mitochondria. Malonyl-CoA, an intermediate in fatty acid synthesis, has been implicated as a regulatory component of the energy sensing system that feeds into hypothalmic neurons to impart energy homeostasis. Malonyl-CoA levels in the hypothalamus are dynamically regulated by fasting and feeding, altering subsequent feeding behaviour. Cpt1c, the brain-specific carnitine O-palmitoyltransferase 1, is thought to relay information about malonyl-CoA levels in hypothalamic neurons that express orexigenic and anorexigenic neuropeptides that regulate food intake and peripheral energy expenditure. Unlike other Cpt1 proteins, Cpt1c binds Malonyl-CoA but does not catalyse the transfer of the malonyl group from CoA to carnitine.
Catalog Number:
(10255-260)
Supplier:
Bioss
Description:
The Cpt1 family of proteins are outer mitochondrial membrane proteins that regulate the entry into, and oxidation of fatty acids by, mitochondria. Malonyl-CoA, an intermediate in fatty acid synthesis, has been implicated as a regulatory component of the energy sensing system that feeds into hypothalmic neurons to impart energy homeostasis. Malonyl-CoA levels in the hypothalamus are dynamically regulated by fasting and feeding, altering subsequent feeding behaviour. Cpt1c, the brain-specific carnitine O-palmitoyltransferase 1, is thought to relay information about malonyl-CoA levels in hypothalamic neurons that express orexigenic and anorexigenic neuropeptides that regulate food intake and peripheral energy expenditure. Unlike other Cpt1 proteins, Cpt1c binds Malonyl-CoA but does not catalyse the transfer of the malonyl group from CoA to carnitine.
Supplier:
Adipogen
Description:
Activation of cells by LPS is mediated by the Toll-like receptor 4 (TLR4). For optimal interaction with LPS, TLR4 requires association with myeloid differentiation protein 2 (MD-2). According to current consensus activation of TLR4 is preceded by the transfer of LPS to membrane-bound (m) or soluble (s) CD14 by LPS-binding protein (LBP). Re-form LPS and lipid A, but not S-form LPS, are capable of inducing TNF-alpha responses also in the absence of CD14. LPS, synthesized by most wild-type (WT) Gram-negative bacteria (S-form LPS), consists of three regions, the O-polysaccharide chain, which is made up of repeating oligosaccharide units, the core oligosaccharide and the lipid A, which harbors the endotoxic activity of the entire molecule. R-form LPS synthesized by the so-called rough (R) mutants of Gram-negative bacteria lacks the O-specific chain. Furthermore, the core-oligosaccharide may be present in different degrees of completion, depending on the class (Ra to Re) to which the mutant belongs. LPS are amphipathic molecules whose hydrophobicity decreases with increasing length of the sugar part. Based upon these differences, S- and R-form LPS show marked differences in the kinetics of their blood clearance and cellular uptake as well as in the ability to induce oxidative burst in human granulocytes and to activate the host complement system.
Catalog Number:
(10364-176)
Supplier:
Bioss
Description:
Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Also involved in LPS-independent inflammatory responses triggered by free fatty acids, such as palmitate. In complex with TLR6, promotes sterile inflammation in monocytes/macrophages in response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42. In this context, the initial signal is provided by oxLDL- or amyloid-beta 42-binding to CD36. This event induces the formation of a heterodimer of TLR4 and TLR6, which is rapidly internalized and triggers inflammatory response, leading to the NF-kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion.
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