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B8437

Sigma-Aldrich

Anti-Biliverdin Reductase A antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Sinónimos:

Anti-BLVR, Anti-BLVRA, Anti-BVR, Anti-BVRA

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~35 kDa

species reactivity

human

technique(s)

immunoprecipitation (IP): 5-10 μL using human HeLa cell lysates
western blot: 1:250-1:500 using whole extracts of human HepG2 cells

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... BLVRA(644)

Categorías relacionadas

General description

Biliverdin reductase A (BVRA) contains a domain that acts as a serine/ threonine/ tyrosine kinase and belongs to the insulin receptor substrate family. Whereas most tyrosine kinase activity is membrane-bound, BVR is a soluble protein. BVRA gene is mapped to human chromosome 7p13.

Specificity

Anti-Biliverdin Reductase A recognizes human Biliverdin Reductase A.

Immunogen

human biliverdin reductase A recombinant protein.

Application

Anti-Biliverdin Reductase A antibody produced in rabbit may be used in western blotting and immunoprecipitation.

Biochem/physiol Actions

Biliverdin reductase A (BVR, BLVRA) catalyzes the conversion of biliverdin to bilirubin in the presence of nicotinamide adenine dinucleotide phosphate (NADPH) or nicotinamide adenine dinucleotide (NADH). Biliverdin reductase A is also considered as a major physiologic cytoprotectant and may have other protective properties in disease states. It has been shown to suppress experimental autoimmune encephalomyelitis in rats. The depletion of the enzyme leads to the accumulation of cellular oxidants and augmented cell death. Mutation in the BVRA gene is implicated in hyperbiliverdinaemia or green jaundice.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Storage and Stability

Store at -20 °C. For continuous use, the product may be stored at 2-8 °C for up to one month.For extended storage, freeze at -20 °C in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution bycentrifugation before use. Working dilution samples should be discard if not used within 12 hours.

Disclaimer

Unless otherwise stated in our catalog, our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable


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Nidhi Sharma et al.
Neurobiology of disease, 125, 176-189 (2019-02-10)
Hyper-active GSK-3β favors Tau phosphorylation during the progression of Alzheimer's disease (AD). Akt is one of the main kinases inhibiting GSK-3β and its activation occurs in response to neurotoxic stimuli including, i.e., oxidative stress. Biliverdin reductase-A (BVR-A) is a scaffold
Urszula M Florczyk et al.
Pharmacological reports : PR, 60(1), 38-48 (2008-02-16)
Biliverdin reductase (BVR) was known for a long time solely as an enzyme converting biliverdin to bilirubin, the major physiological antioxidant. Recent years revealed unique features of this protein which are not related to its reductase activity. The most intriguing
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Liver international : official journal of the International Association for the Study of the Liver, 29(7), 1116-1124 (2009-07-08)
Hyperbiliverdinaemia is a poorly defined clinical sign that has been infrequently reported in cases of liver cirrhosis or liver carcinoma, usually indicating a poor long-term prognosis. To clarify the pathogenesis of hyperbiliverdinaemia in an extended case report. A 64-year-old man
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Free radical biology & medicine, 91, 127-142 (2015-12-25)
Clinical studies suggest a link between peripheral insulin resistance and cognitive dysfunction. Interestingly, post-mortem analyses of Alzheimer disease (AD) subjects demonstrated insulin resistance in the brain proposing a role for cognitive deficits observed in AD. However, the mechanisms responsible for

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