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特异性
Reactive with thiol-modified glutatione. Does not react with oxidized glutathione (GSSG) or glutathione (GSH) in mixed disulfide linkage with proteins. MAB3194 is specific to the glutathione:N-ethylmaleimide adduct; thus it is useful for quantification of reduced glutathione (GSH) after reaction with N-ethylmaleimide. For use in ELISA or flow cytometry, sample must first be reacted with NEM.
免疫原
GS-NEM conjugated to KLH
应用
Detect the Glutathione: N-ethylmaleimide adduct protein using this Anti-Glutathione: N-ethylmaleimide adduct, clone 8.1GSH validated for use in ELISA, Flow, ICC, IHC & WB.
Immunohistochemistry: 1:100 (paraformaldehyde fixation)
Immunocytochemistry: 1:100 - 1:500 for assessment of intracellular GSH distribution.
ELISA: 1:100,000 - 1:200,000 to quantify GSH at >2 mM in biological specimens.
Flow cytometry: 1:100 - 1:1,000
Cells were fixed with cold 1% PFA for 5 min and vortexed into methanol (-20°C) containing 5mM NEM (10 min on dry ice) or 10 μM NEM (N-ethyl maleimide) for 30 min at RT.
Optimal working dilutions must be determined by end user.
Positive Control: Peripheral blood mononuclear cells (PBMC) treated with NEM
Immunocytochemistry: 1:100 - 1:500 for assessment of intracellular GSH distribution.
ELISA: 1:100,000 - 1:200,000 to quantify GSH at >2 mM in biological specimens.
Flow cytometry: 1:100 - 1:1,000
Cells were fixed with cold 1% PFA for 5 min and vortexed into methanol (-20°C) containing 5mM NEM (10 min on dry ice) or 10 μM NEM (N-ethyl maleimide) for 30 min at RT.
Optimal working dilutions must be determined by end user.
Positive Control: Peripheral blood mononuclear cells (PBMC) treated with NEM
Research Category
Neuroscience
Neuroscience
Research Sub Category
Oxidative Stress
Oxidative Stress
外形
Format: Purified
Liquid in 0.02M PBS pH 7.6, 0.25M NaCl containing 0.1% sodium azide.
储存及稳定性
Maintain at 2-8°C in undiluted.
其他说明
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
法律信息
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), 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.
WGK
WGK 2
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Mohammad Nizam Uddin et al.
Cell stress & chaperones, 28(2), 201-217 (2023-02-17)
Oxidative stress including decreased antioxidant enzyme activities, elevated lipid peroxidation, and accumulation of advanced glycation end products in the blood from children with autism spectrum disorders (ASD) has been reported. The mechanisms affecting the development of ASD remain unclear; however
Carole Escartin et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(20), 7392-7401 (2011-05-20)
Astrocytes support neuronal antioxidant capacity by releasing glutathione, which is cleaved to cysteine in brain extracellular space. Free cysteine is then taken up by neurons through excitatory amino acid transporter 3 [EAAT3; also termed Slc1a1 (solute carrier family 1 member
Gobinath Shanmugam et al.
Frontiers in physiology, 8, 268-268 (2017-05-19)
Nuclear factor erythroid 2 related factor 2 (Nrf2) signaling maintains the redox homeostasis and its activation is shown to suppress cardiac maladaptation. Earlier we reported that acute endurance exercise (2 days) evoked antioxidant cytoprotection in young WT animals but not
Reiko Satow et al.
Gastroenterology, 142(3), 572-581 (2011-12-14)
Loss of promyelocytic leukemia protein (PML) nuclear body (NB) formation has been reported in colorectal and other solid tumors. However, genetic alteration of PML is rarely observed in these tumors; the exact mechanisms that mediate loss of PML function are
Radhakrishnan Rajesh Kumar et al.
Journal of translational medicine, 14, 86-86 (2016-04-07)
Anomalies in myocardial structure involving myocyte growth, hypertrophy, differentiation, apoptosis, necrosis etc. affects its function and render cardiac tissue more vulnerable to the development of heart failure. Although oxidative stress has a well-established role in cardiac remodeling and dysfunction, the
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