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Merck

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號碼:
分類程式碼代碼:
12352203
NACRES:
NA.41

生物源

mouse

品質等級

共軛

unconjugated

抗體表格

purified antibody

抗體產品種類

primary antibodies

無性繁殖

TR.ET.48.5, monoclonal

物種活性

rat, human, sheep

技術

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

同型

IgG1

UniProt登錄號

運輸包裝

dry ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... EDN1(1906)

一般說明

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)

特異性

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

免疫原

endothelin-1 (ET-1) conjugated to KLH

應用

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.

生化/生理作用

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.

外觀

Solution in phosphate buffered saline, containing 0.05% sodium azide

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)

nwg

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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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
I Komuro et al.
FEBS letters, 238(2), 249-252 (1988-10-10)
Recently, a potent vasoconstrictor peptide, endothelin (EDT), was isolated from vascular endothelial cells. We examined its effect on rat vascular smooth muscle cells (VSMCs). EDT induced the elevation of intracellular calcium, which was dependent on extracellular calcium and inhibited by
Y Fukuda et al.
Biochemical and biophysical research communications, 155(1), 167-172 (1988-08-30)
Using cultured neonatal rat atrial cardiocytes, we have studied the effect of synthetic porcine endothelin (pET), a novel potent vasoconstrictor isolated from endothelial cells, on the release of immunoreactive (IR) rat atrial natriuretic peptide (rANP). pET stimulated IR-rANP secretion in
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
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

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