Anti-CANX monoclonal antibody (DCABH-8501)

Mouse anti-Human CANX monoclonal antibody for FC, ICC/IF, IP, WB, IHC-P

Specifications


Host Species
Mouse
Antibody Isotype
IgG1
Clone
BG29
Species Reactivity
Mouse, Human
Immunogen
Focus cells (human hepatoma cell line)
Conjugate
Unconjugated

Applications


Application Notes
Flow Cyt: 1μg/106 cells; ICC/IF: 1 μg/ml; WB: 5 μg/ml; IHC-P: 1 μg/ml.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
CANX; calnexin; CNX; IP90; major histocompatibility complex class I antigen binding protein p88; P90
Entrez Gene ID
UniProt ID

Product Background


Pathway
Adaptive Immune System, organism-specific biosystem; Antigen Presentation: Folding, assembly and peptide loading of class I MHC, organism-specific biosystem; Antigen processing and presentation, organism-specific biosystem; Antigen processing and presentation, conserved biosystem; Asparagine N-linked glycosylation, organism-specific biosystem; Assembly of Viral Components at the Budding Site, organism-specific biosystem; Calnexin/calreticulin cycle, organism-specific biosystem;

Citations


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Custom Antibody Labeling


We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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References


Compilation and evaluation of a Paso del Norte emission inventory

SCIENCE OF THE TOTAL ENVIRONMENT

Authors: Funk, TH; Chinkin, LR; Roberts, PT; Saeger, M; Mulligan, S; Figueroa, VHP; Yarbrough, J

Emission inventories of ozone precursors are routinely used as input to comprehensive photochemical air quality models. Photochemical model performance and the development of effective control strategies rely on the accuracy and representativeness of an underlying emission inventory. This paper describes the tasks undertaken to compile and evaluate an ozone precursor emission inventory for the El Paso/Ciudad Juarez/Southern Dona Ana region. Point, area and mobile source emission data were obtained from local government agencies and were spatially and temporally allocated to a gridded domain using region-specific demographic and land-cover information. The inventory was then processed using the US Environmental Protection Agency (EPA) recommended Emissions Preprocessor System 2.0 (UAM-EPS 2.0) which generates emissions files compatible with the Urban Airshed Model (UAM). A top-down evaluation of the emission inventory was performed to examine how well the inventory represented ambient pollutant compositions. The top-down evaluation methodology employed in this study compares emission inventory ratios of non-methane hydrocarbon (NMHC)/nitrogen oxide (NOx) and carbon monoxide (CO)/NOx ratios to corresponding ambient ratios. Detailed NMHC species comparisons were made in order to investigate the relative composition of individual hydrocarbon species in the emission inventory and in the ambient data. The emission inventory compiled during this effort has since been used to model ozone in the Paso del Norte airshed (Emery et at., CANx modeling of ozone and carbon monoxide in the Paso del Norte airshed. In: Proc of Ninety-Third Annual Meeting of Air & Waste Management Association, 18-22 June 2000, Air & Waste Management Association, Pittsburgh, PA, 2000). (C) 2001 Elsevier Science B.V. All rights reserved.

Endoplasmic reticulum stress activation in adipose tissue induces metabolic syndrome in individuals with familial partial lipodystrophy of the Dunnigan type

DIABETOLOGY & METABOLIC SYNDROME

Authors: Foss-Freitas, Maria C.; Ferraz, Rafael C.; Monteiro, Luciana Z.; Gomes, Patricia M.; Iwakura, Ricardo; de Freitas, Luiz Carlos C.; Foss, Milton C.

Background: Familial partial lipodystrophy of the Dunnigan type is one of the most common inherited lipodystrophies variables. These individuals have important metabolic disorders that cause predisposition to various diseases. In this study we aimed to demonstrate the relation between the metabolic abnormalities, inflammatory profile and the expression of genes involved in the activation of the endoplasmic reticulum stress (ERS) in subjects with FPLD. Methods: We evaluated 14 female FPLD patients and compared with 13 female healthy individuals. The subjects were paired with their respective BMI and age and categorized into two groups: Familial partial lipodystrophy of the Dunnigan type (FPLD) and control. Patients were fasted for 12 h before blood collection for measurement of HbA1c, glucose, insulin, lipids and inflammatory markers. Subcutaneous adipose tissue was collected by puncture aspiration of submental region during ambulatorial surgical aesthetic procedure. Results: We demonstrate that patients with FPLD show increased HbA1c (p < 0.01), fasting glucose (p < 0.002) and triglycerides (p < 0.005) while HDL/cholesterol (p < 0.001) was lower when compared to healthy individuals. We found that 64.2% FPLD patients had metabolic syndrome according to International Diabetes Federation definition. We also observe increased AUC of glucose (p < 0.001) and insulin during oGTT, featuring a frame of hyperglycemia and hyperinsulinemia, suggesting insulin resistance. Also we found hyperactivation of several genes responsible for ERS such as ATF-4 (p < 0.01), ATF-6 (p < 0.01), EIF2 alpha 3K (p < 0.005), CCT4 (p < 0.001), CHOP (p < 0.01), CALR (p < 0.001) and CANX (p < 0.005), that corroborate the idea that diabetes mellitus and metabolic syndrome are associated with direct damage to the endoplasmic reticulum homeostasis. Ultimately, we note that individuals with lipodystrophy have an increase in serum interleukins, keys of the inflammatory process, as IL-1 beta, TNF-alpha and IL-6 (p < 0.05 all), compared with healthy individuals, which can be the trigger to insulin resistance in this population. Conclusion: Individuals with FPLD besides having typical dysfunctions of metabolic syndrome, show a hyperactivation of ERS associated with increased systemic inflammatory profile, which together may explain the complex clinical aspect of this diseases.

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