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Key Documents

AB1529

Sigma-Aldrich

Anti-Nitric Oxide Synthase I Antibody

serum, Chemicon®

Synonym(s):

NOS I, bNOS, nNOS

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

sheep

Quality Level

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

species reactivity

rabbit, rat, guinea pig

manufacturer/tradename

Chemicon®

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

guinea pig ... Nos1(100729682)
rabbit ... Nos1(100009243)
rat ... Nos1(24598)

Specificity

bNOS (neuronal). Not yet tested for cross-reactivity to iNOS or eNOS. See reference below.

Immunogen

A 21 amino acid peptide (1409-1429) of the neuronal form of NOS from rat cerebellum, coupled to KLH. The sequence is H-RSESIAFIEESKKDADEVFSS-NH2.

Application

Detect Nitric Oxide Synthase I using this Anti-Nitric Oxide Synthase I Antibody validated for use in WB, IH.
Immunohistochemistry: 1:500-1,000

Immunoblotting

Optimal working dilutions must be determined by end user.
Research Category
Neuroscience
Research Sub Category
Oxidative Stress

Physical form

Sheep serum. Lyophilized, no preservatives. Reconstitute with 100 μL of sterile distilled water. Centrifuge to remove any residue.

Storage and Stability

Maintain at -20 to -70°C in undiluted aliquots for up to 12 months. Avoid repeated freeze/thaw cycles. Glycerol (1:1) can be added for additional stability.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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

11 - Combustible Solids

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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Viviana Filpa et al.
American journal of physiology. Gastrointestinal and liver physiology, 312(4), G374-G389 (2017-02-06)
Neuronal and inducible nitric oxide synthase (nNOS and iNOS) play a protective and damaging role, respectively, on the intestinal neuromuscular function after ischemia-reperfusion (I/R) injury. To uncover the molecular pathways underlying this dichotomy we investigated their possible correlation with the
Siomara Hernandez et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 33(5), 6168-6184 (2019-02-23)
Gulf War illness (GWI) is a chronic multisymptom disorder that is prominent in Gulf War veterans. Major unexplained symptoms of GWI include functional gastrointestinal disorders and undiagnosed illnesses, including neurologic disorders. Exposure to the antinerve gas drug pyridostigmine bromide (PB)
Eileen S Rodriguez-Tapia et al.
Experimental physiology, 102(3), 299-313 (2016-12-23)
What is the central question of this study? Subtypes of enteric neurons are coded by the neurotransmitters they synthesize, but it is not known whether enteric neuron subtypes might also be coded by other proteins, including calcium channel subtypes controlling
Isola A M Brown et al.
American journal of physiology. Gastrointestinal and liver physiology, 314(1), G39-G52 (2017-09-09)
Enteric glia play an important neuroprotective role in the enteric nervous system (ENS) by producing neuroprotective compounds such as the antioxidant reduced glutathione (GSH). The specific cellular pathways that regulate glial production of GSH and how these pathways are altered
Rebecca K Bubenheimer et al.
Frontiers in cellular neuroscience, 10, 73-73 (2016-04-06)
Gut inflammation contributes to the development of gut motility disorders in part by disrupting the function and survival of enteric neurons through mechanisms that involve oxidative stress. How enteric neurons regulate oxidative stress is still poorly understood. Importantly, how neuron

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