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E5654

Sigma-Aldrich

Anti-Endonuclease G antibody produced in rabbit

1 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-EndoG

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About This Item

MDL number:
UNSPSC Code:
12352203

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~35 kDa

species reactivity

rat, mouse, human

concentration

1 mg/mL

technique(s)

ELISA: suitable
immunohistochemistry: suitable
western blot: suitable

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

Immunogen

synthetic peptide corresponding to amino acids 55-70 of human EndoG.

Application

Anti-Endonuclease G antibody produced in rabbit is suitable for western blotting at a dilution of 2μg/mL.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)

Biochem/physiol Actions

Endonuclease G, mitochondrial is an enzyme encoded by the ENDOG gene in humans. It is mapped to human chromosomes 9q34.1. EndoG a member of DNA/RNA nonspecific ββα-Me-finger nucleases that is involved in apoptosis and normal cellular proliferation. EndoG is localized in the mitochondria of young cells, but relocalizes to the nucleus upon senescence. It plays an important role in the senescence program of human endothelial cells. ENDOG is alo involved in mitochondrial-mediated apoptotic signaling in older human muscle.

Physical form

Solution in phosphate buffered saline containing 0.02% sodium azide.

Disclaimer

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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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Shih-Lu Wu et al.
Journal of biomedical science, 16, 6-6 (2009-03-11)
Endonuclease G (EndoG), a member of DNA/RNA nonspecific betabetaalpha-Me-finger nucleases, is involved in apoptosis and normal cellular proliferation. In this study, we analyzed the critical amino acid residues of EndoG and proposed the catalytic mechanism of EndoG. To identify the
Thomas Diener et al.
Experimental gerontology, 45(7-8), 638-644 (2010-03-10)
Mitotic cells in culture show a limited replicative potential and after extended subculturing undergo a terminal growth arrest termed cellular senescence. When cells reach the senescent phenotype, this is accompanied by a significant change in the cellular phenotype and massive
Gilles Gouspillou et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 28(4), 1621-1633 (2013-12-29)
Mitochondrial dysfunction is implicated in skeletal muscle atrophy and dysfunction with aging, with strong support for an increased mitochondrial-mediated apoptosis in sedentary rodent models. Whether this applies to aged human muscle is unknown, nor is it clear whether these changes
Núria Bahi et al.
The Journal of biological chemistry, 281(32), 22943-22952 (2006-06-07)
Differentiated cardiomyocytes are resistant to caspase-dependent cell death; however, the mechanisms involved are still uncertain. We previously reported that low Apaf1 expression partially accounts for cardiomyocyte resistance to apoptosis. Here, we extend the knowledge on the molecular basis of cardiac
Takumi Kudo et al.
Cancer research, 72(11), 2901-2911 (2012-05-18)
RASSF3 is the smallest member of the RASSF family of proteins that function as tumor suppressors. Unlike other members of this important family, the mechanisms through which RASSF3 suppresses tumor formation remain unknown. Here, we show that RASSF3 expression induces

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