推荐产品
生物源
rabbit
共軛
unconjugated
抗體表格
IgG fraction of antiserum
抗體產品種類
primary antibodies
無性繁殖
polyclonal
形狀
buffered aqueous solution
分子量
antigen ~35 kDa
物種活性
human
技術
immunoprecipitation (IP): 5-10 μL using human HeLa cell lysates
western blot: 1:250-1:500 using whole extracts of human HepG2 cells
UniProt登錄號
運輸包裝
dry ice
儲存溫度
−20°C
目標翻譯後修改
unmodified
基因資訊
human ... BLVRA(644)
一般說明
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.
特異性
Anti-Biliverdin Reductase A recognizes human Biliverdin Reductase A.
免疫原
human biliverdin reductase A recombinant protein.
應用
Anti-Biliverdin Reductase A antibody produced in rabbit may be used in western blotting and immunoprecipitation.
生化／生理作用
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.
外觀
0.01M 磷酸缓冲盐溶液，pH 7.4，含 15mM 叠氮化钠。
儲存和穩定性
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.
免責聲明
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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儲存類別代碼
10 - Combustible liquids
閃點（°F）
Not applicable
閃點（°C）
Not applicable
Mats Gåfvels et al.
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
Flavia Agata Cimini et al.
Biochimica et biophysica acta. Molecular basis of disease, 1865(6), 1490-1501 (2019-03-04)
Biliverdin reductase-A (BVR-A) is a serine/threonine/tyrosine kinase involved in the regulation of insulin signaling. In vitro studies have demonstrated that BVR-A is a substrate of the insulin receptor and regulates IRS1 by avoiding its aberrant activation, and in animal model
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
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
Damian Klóska et al.
Archives of biochemistry and biophysics, 678, 108182-108182 (2019-11-11)
Endothelial dysfunction accompanied by the loss of endothelial cell phenotype plays an essential role in cardiovascular diseases. Here, we report that knockdown of biliverdin reductase (BVR), the enzyme of the heme degradation pathway converting biliverdin to bilirubin, shifts endothelial phenotype
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