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AB3639

Sigma-Aldrich

Anti-Endonuclease G Antibody

Chemicon®, from rabbit

Synonyme(s) :

EndoG

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Forme d'anticorps

affinity purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

polyclonal

Produit purifié par

affinity chromatography

Espèces réactives

mouse, rat, human

Fabricant/nom de marque

Chemicon®

Technique(s)

western blot: suitable

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ENDOG(2021)
mouse ... Endog(13804)
rat ... Endog(362100)

Spécificité

Recognizes Endonuclease G (EndoG), a mitochondrion-specific nuclease that translocates to the nucleus and cleaves chromatin DNA during apoptosis. EndoG is specifically activated by apoptotic stimuli and is able to induce nucleosomal fragmentation of DNA independently of caspase and DFF/CAD (1,2).

Immunogène

Synthetic peptide corresponding to amino acids 55 to 70 of human EndoG (GGPRGPGELAKYGLP).

Application

Anti-Endonuclease G Antibody is an antibody against Endonuclease G for use in WB.
Research Category
Apoptosis & Cancer
Research Sub Category
Apoptosis - Additional
Western blotting (1-2μg/mL)

Optimal working dilutions must be determined by the end user.

Forme physique

Affinity purified immunoglobulin. Liquid in PBS containing 0.02% sodium azide.

Stockage et stabilité

Maintain at 2-8ºC for 12 months.

Autres remarques

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

Informations légales

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

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Shuangping Zhao et al.
Journal of neuroscience research, 88(8), 1727-1737 (2010-01-16)
We have shown that generalized seizures produce necrotic neurons with caspase-independent nuclear pyknosis and DNA fragmentation. In this study, we determined the time course of translocation of mitochondrial cytochrome c, apoptosis-inducing factor, endonuclease G, lysosomal cathepsins B and D, and
Tamara Azarashvili et al.
International journal of molecular sciences, 17(12) (2016-12-17)
The translocator protein (TSPO; 18 kDa) is a high-affinity cholesterol-binding protein located in the outer membrane of mitochondria. A domain in the C-terminus of TSPO was characterized as the cholesterol recognition/interaction amino acid consensus (CRAC). The ability of the CRAC
Sathivel Chinnathambi et al.
Cells, tissues, organs, 187(2), 131-140 (2007-10-17)
We examined how young and old keratinocytes died from heat stress in vitro. We found that keratinocyte cell death was not due to oxidative stress as neither Mn-SOD nor Cu-Zn-SOD was produced in either young or old heated keratinocytes. Instead
H-W Zheng et al.
Cell death & disease, 5, e1262-e1262 (2014-05-31)
Receptor-interacting protein (RIP) kinases promote the induction of necrotic cell death pathways. Here we investigated signaling pathways in outer hair cells (OHCs) of adult male CBA/J mice exposed to noise that causes permanent threshold shifts, with a particular focus on
Traumatic noise activates Rho-family GTPases through transient cellular energy depletion.
Chen, FQ; Zheng, HW; Hill, K; Sha, SH
The Journal of Neuroscience null

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