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Key Documents

SAB4300128

Sigma-Aldrich

Anti-phospho-NOS3 (pSer1177) antibody produced in rabbit

affinity isolated antibody

Synonym(s):

ECNOS, NOS, NOSIII, eNOS

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About This Item

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

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

predicted mol wt 133 kDa

species reactivity

mouse, rat, human

concentration

1 mg/mL

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

phosphorylation (pSer1177)

Gene Information

human ... NOS3(4846)

Immunogen

Peptide sequence around phosphorylation site of serine 1177 (T-Q-S(p)-F-S), according to the protein NOS3.

Application

Recommended dilutions
Western Blot 1:500 - 1:1000

Optimal dilutions should be determined by the user.

Biochem/physiol Actions

Produces nitric oxide (NO) which is implicated in vascular smooth muscle relaxation through a cGMP-mediated signal transduction pathway. NO mediates vascular endothelial growth factor (VEGF)-induced angiogenesis in coronary vessels and promotes blood clotting through the activation of platelets.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physical form

Solution in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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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Yuki Hirano et al.
Cardiovascular research, 113(10), 1208-1218 (2017-05-05)
Although surfactant protein-D (SP-D) is a pneumoprotein that is predominantly synthesized by type II epithelial cells in the lung, individuals with increased circulating levels of SP-D are at an elevated risk of mortality from ischemic heart disease. Whether SP-D contributes
Naoyuki Otani et al.
Hypertension research : official journal of the Japanese Society of Hypertension, 41(11), 923-931 (2018-09-07)
This study was designed to investigate the effects of uric acid on vascular endothelial function in measurements carried out either at the bedside or the laboratory bench. First, we performed reactive hyperemia peripheral arterial tonometry using an EndoPAT 2000 device
Szabolcs Zahorán et al.
Antioxidants (Basel, Switzerland), 10(4) (2021-05-01)
Nitric oxide (NO) bioavailability is fundamental in the regulation of redox balance and functionality of the endothelium, especially in the case of the umbilical cord (UC), which has no innervation. The analysis of UC vessel-related complications could serve as a
Deok Hwa Nam et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 33(1), 711-721 (2018-07-20)
Coordinated changes in signaling pathways and gene expression in hearts subjected to prolonged stress maintain cardiac function. Loss of steroid receptor coactivator-2 (SRC-2) results in a reversal to the fetal gene program and disrupts the response to pressure overload, accompanied
David C Reineke et al.
European journal of medical research, 20, 59-59 (2015-06-25)
Definitive fate of the coronary endothelium after implantation of a drug-eluting stent remains unclear, but evidence has accumulated that treatment with rapamycin-eluting stents impairs endothelial function in human coronary arteries. The aim of our study was to demonstrate this phenomenon

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