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主要文件

MAB3194

Sigma-Aldrich

Anti-Glutathione: N-ethylmaleimide adduct Antibody, clone 8.1GSH

clone 8.1GSH, Chemicon®, from mouse

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About This Item

分類程式碼代碼:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物源

mouse

品質等級

抗體表格

purified antibody

抗體產品種類

primary antibodies

無性繁殖

8.1GSH, monoclonal

物種活性(以同源性預測)

mammals

製造商/商標名

Chemicon®

技術

ELISA: suitable
flow cytometry: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable

同型

IgG1

運輸包裝

wet ice

目標翻譯後修改

unmodified

特異性

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

應用

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
Research Category
Neuroscience
Research Sub Category
Oxidative Stress

外觀

Format: Purified
Liquid in 0.02M PBS pH 7.6, 0.25M NaCl containing 0.1% sodium azide.

儲存和穩定性

Maintain at 2-8°C in undiluted.

其他說明

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

法律資訊

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

免責聲明

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.

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儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 2

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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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
Gobinath Shanmugam et al.
Antioxidants & redox signaling, 32(18), 1293-1312 (2020-02-18)
Aims: Redox homeostasis is tightly controlled and regulates key cellular signaling pathways. The cell's antioxidant response provides a natural defense against oxidative stress, but excessive antioxidant generation leads to reductive stress (RS). This study elucidated how chronic RS, caused by
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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