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E166

Sigma-Aldrich

Monoclonal Anti-Endothelin-1 antibody produced in mouse

clone TR.ET.48.5, purified antibody

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified antibody

antibody product type

primary antibodies

clone

TR.ET.48.5, monoclonal

species reactivity

rat, human, sheep

technique(s)

immunocytochemistry: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:250
radioimmunoassay: 1:25,000
western blot: suitable

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... EDN1(1906)

Related Categories

General description

Endothelin consists of a family of potent vasoconstrictor peptides, which include four structurally related isoforms, ET-1, ET-2, ET-3 and vasointestinal contractor (VIC, β -ET)

Specificity

The antibody shows little cross-reactivity to related peptides and no known cross-reactivity to non-related peptides.

Immunogen

endothelin-1 (ET-1) conjugated to KLH

Application

Monoclonal Anti-Endothelin-1 antibody produced in mouse is suitable for immunoblotting and immunocytochemistry.It is also suitable for radioimmunoassay (RIA) at a working dilution of 1:25,000 and for immunohistochemistry at 1:250 working dilution using formalin-fixed, paraffin-embedded tissue sections.

Biochem/physiol Actions

ET-1, a 21 amino acid peptide, is produced by vascular endothelial cells. It is a potent vasoconstrictor and plays an important role in the homeostasis of the circulatory system. It is also important in pathogenesis of cardiovascular diseases. It is also involved in contraction of airway and intestinal smooth muscle. It releases vasodilator prostaglandins and nitric oxide (NO). It also plays a role in mitogenic effects on vascular smooth muscle cells and fibroblasts, stimulation of atrial natriuretic peptide secretion from atrial cardiocytes and inhibition of renin release. ET-1 is expressed in the spinal cord and dorsal root ganglia, where it may serve as a neurotransmitter/neuromodulator.

Physical form

Solution in phosphate buffered saline, containing 0.05% 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 Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Aykut Gram et al.
Reproduction (Cambridge, England), 150(5), 405-415 (2015-08-05)
Luteal development is regulated by many locally produced mediators, e.g., prostaglandins and angiogenic factors. However, the role and function of vasoactive factors in the canine corpus luteum (CL) remain largely unknown. Consequently, expression of the endothelin (ET) receptors-A and -B
M W MacCumber et al.
Proceedings of the National Academy of Sciences of the United States of America, 87(6), 2359-2363 (1990-03-01)
We have explored the cellular loci of endothelin (ET) actions and formation in the brain, using cerebellar mutant mice as well as primary and continuous cell cultures. A glial role is favored by several observations: (i) mutant mice lacking neuronal
Leryn J Reynolds et al.
Journal of applied physiology (Bethesda, Md. : 1985), 122(1), 38-47 (2016-11-01)
Increased endothelin-1 (ET-1) and reduced endothelial nitric oxide phosphorylation (peNOS) are hypothesized to reduce insulin-stimulated blood flow in type 2 diabetes (T2D), but studies examining these links in humans are limited. We sought to assess basal and insulin-stimulated endothelial signaling
Hany S Abed et al.
Heart rhythm, 10(1), 90-100 (2012-10-16)
Obesity is associated with atrial fibrillation (AF); however, the mechanisms by which it induces AF are unknown. To examine the effect of progressive weight gain on the substrate for AF. Thirty sheep were studied at baseline, 4 months, and 8
H Rakugi et al.
Biochemical and biophysical research communications, 155(3), 1244-1247 (1988-09-30)
The effect of endothelin on renin release from isolated rat glomeruli was examined. Endothelin inhibited basal renin release in a dose-dependent manner with an IC50 of 1.0 x 10(-9) M. Endothelin also inhibited renin release stimulated by isoproterenol (10(-5) M).

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