N7782
Anti-Nitric Oxide Synthase, Inducible antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
Synonym(s):
Anti-iNOS
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 130 kDa
species reactivity
rat, mouse
technique(s)
microarray: suitable
western blot: 1:10,000 using cells extract of murine RAW 264.7 macrophages activated with LPS and IFN-γ.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
mouse ... Nos2(18126)
rat ... Nos2(24599)
General description
Anti-Nitric Oxide Synthase, inducible is specific for nitric oxide synthase (NOS), derived from activated mouse macrophage RAW 264.7 cells (iNOS, 130 kDa), but does not recognize NOS derived from brain tissue (bNOS) and endothelial cells (eNOS). The NOS isoform characterized in macrophages is a 130 kDa protein, also known as macrophage NOS (macNOS; mNOS), NOS2, or inducible NOS (iNOS). iNOS is an interferon (IFN)-γ-inducible protein. This gene is located on human chromosome 17q11.
Specificity
Anti-Nitric Oxide Synthase, Inducible is specific for nitric oxide synthase (NOS), derived from activated mouse macrophage RAW 264.7 cells (iNOS, 130 kDa), but does not recognize NOS derived from brain tissue (bNOS) and endothelial cells (eNOS). By immunoblotting of an activated mouse macrophage RAW 264.7 cells extract, the staining of the iNOS band is specifically inhibited by the immunizing peptide.
Immunogen
synthetic peptide corresponding to amino acids 1126-1144 of nitric oxide synthase (NOS) of mouse macrophage origin (iNOS, also termed macNOS) conjugated to KLH. The immunogen sequence is highly conserved in rat iNOS and diverges from the human iNOS.
Application
Anti-Nitric Oxide Synthase, Inducible antibody produced in rabbit has been used in immunoblotting and immunohistochemistry.
Biochem/physiol Actions
Inducible nitric oxide synthase (NOS2) produces nitric oxide (NO), which is expected to be lethal to malaria parasites in vitro.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM 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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Product No.
Description
Pricing
Storage Class Code
10 - Combustible liquids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Inducible nitric oxide synthase is a key host factor for toxoplasma GRA15-dependent disruption of the gamma interferon-induced antiparasitic human response
Bando H, et al.
mBio, 9(5), e01738-e01718 (2018)
Yu-Lun Wang et al.
Molecular medicine reports, 14(4), 3559-3564 (2016-08-31)
Tormentic acid (TA) is a triterpene isolated from the stem bark of the plant Vochysia divergens and has been reported to exhibit anticancer, anti‑inflammatory and anti‑atherogenic properties. However, the functions of TA in hydrogen peroxide (H2O2)‑induced oxidative stress and inflammation in
Localization of the human gene for inducible nitric oxide synthase (NOS2) to chromosome 17q11. 2-q12
Marsden PA, et al.
Genomics, 19(1) (1994)
Saleem S Qader et al.
American journal of physiology. Endocrinology and metabolism, 292(5), E1447-E1455 (2007-02-01)
Chronic exposure of pancreatic islets to elevated plasma lipids (lipotoxicity) can lead to beta-cell dysfunction, with overtime becoming irreversible. We examined, by confocal microscopy and biochemistry, whether the expression of islet inducible nitric oxide synthase (iNOS) and the concomitant inhibition
Heterotrimeric G protein-dependent WNT-5A signaling to ERK1/2 mediates distinct aspects of microglia proinflammatory transformation
Halleskog C, et al.
Journal of Neuroinflammation, 9(1), 111-111 (2012)
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