Human DDOST (Dolichyl-diphosphooligosaccharide--protein glycosyltransferase 48 kDa subunit) ELISA Kit (DEIA-FN382)

Regulatory status: For research use only, not for use in diagnostic procedures.

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serum, plasma, cell culture supernatants, tissue homogenate
Species Reactivity
Intended Use
For quantitative detection of Human DDOST (Dolichyl-diphosphooligosaccharide--protein glycosyltransferase 48 kDa subunit) in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy
Store the unopened product at 2 - 8 °C. Do not use past expiration date.
Intra-Assay: CV<8%
Inter-Assay: CV<10%
Detection Range
0.312-20 ng/mL
0.188 ng/mL
Standard Curve


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Increased liver AGEs induce hepatic injury mediated through an OST48 pathway


Authors: Zhuang, Aowen; Yap, Felicia Yt.; Bruce, Clinton; Leung, Chris; Plan, Manuel R.; Sullivan, Mitchell A.; Herath, Chandana; McCarthy, Domenica; Sourris, Karly C.; Kantharidis, Phillip; Coughlan, Melinda T.; Febbraio, Mark A.; Hodson, Mark P.; Watt, Matthew J.; Angus, Peter; Schulz, Benjamin L.; Forbes, Josephine M.

The protein oligosaccharyltransferase-48 (OST48) is integral to protein N-glycosylation in the endoplasmic reticulum (ER) but is also postulated to act as a membrane localised clearance receptor for advanced glycation end-products (AGE). Hepatic ER stress and AGE accumulation are each implicated in liver injury. Hence the objective of this study was to increase the expression of OST48 and examine the effects on hepatic function and structure. Groups of 8 week old male mice (n = 10-12/group) over-expressing the gene for OST48, dolichyl-diphosphooligosaccharide- protein glycosyltransferase (DDOST+/-), were followed for 24 weeks, while randomised to diets either low or high in AGE content. By week 24 of the study, either increasing OST48 expression or consumption of high AGE diet impaired liver function and modestly increased hepatic fibrosis, but their combination significantly exacerbated liver injury in the absence of steatosis. DDOST+/- mice had increased both portal delivery and accumulation of hepatic AGEs leading to central adiposity, insulin secretory defects, shifted fuel usage to fatty and ketoacids, as well as hepatic glycogen accumulation causing hepatomegaly along with hepatic ER and oxidative stress. This study revealed a novel role of the OST48 and AGE axis in hepatic injury through ER stress, changes in fuel utilisation and glucose intolerance.

Advanced Glycated apoA-IV Loses Its Ability to Prevent the LPS-Induced Reduction in Cholesterol Efflux-Related Gene Expression in Macrophages


Authors: Okuda, Ligia Shimabukuro; Iborra, Rodrigo Tallada; Ramos, Paula; Machado, Ubiratan Fabres; Correa-Giannella, Maria Lucia; Pickford, Russell; Woods, Tom; Brimble, Margaret Anne; Rye, Kerry-Anne; Passarelli, Marisa

We addressed how advanced glycation (AGE) affects the ability of apoA-IV to impair inflammation and restore the expression of genes involved in cholesterol efflux in lipopolysaccharide- (LPS-) treated macrophages. Recombinant human apoA-IV was nonenzymatically glycated by incubation with glycolaldehyde (GAD), incubated with cholesterol-loaded bone marrow-derived macrophages (BMDMs), and then stimulated with LPS prior to measurement of proinflammatory cytokines by ELISA. Genes involved in cholesterol efflux were quantified by RT-qPCR, and cholesterol efflux was measured by liquid scintillation counting. Carboxymethyllysine (CML) and pyrraline (PYR) levels, determined by Liquid Chromatography-Mass Spectrometry (LC-MS/MS), were greater in AGE-modified apoA-IV (AGE-apoA-IV) compared to unmodified-apoA-IV. AGE-apoA-IV inhibited expression of interleukin 6 (Il6), TNF-alpha (Tnf), IL-1 beta (Il1b), toll-like receptor 4 (Tlr4), tumor necrosis factor receptor-associated factor 6 (Traf6), Janus kinase 2/signal transducer and activator of transcription 3 (Jak2/Stat3), nuclear factor kappa B (Nfkb), and AGE receptor 1 (Ddost) as well as IL-6 and TNF-alpha secretion. AGE-apoA-IV alone did not change cholesterol efflux or ABCA-1 levels but was unable to restore the LPS-induced reduction in expression of Abca1 and Abcg1. AGE-apoA-IV inhibited inflammation but lost its ability to counteract the LPS-induced changes in expression of genes involved in macrophage cholesterol efflux that may contribute to atherosclerosis.

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