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N2280

Sigma-Aldrich

Monoclonal Anti-Nitric Oxide Synthase, Brain (1-181) antibody produced in mouse

clone NOS-B1, ascites fluid

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Synonym(s):
Anti-bNOS
MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

ascites fluid

antibody product type

primary antibodies

clone

NOS-B1, monoclonal

mol wt

antigen 150-160 kDa

contains

15 mM sodium azide

species reactivity

rat, goat, pig, human

technique(s)

microarray: suitable
western blot: 1:3,000 using fresh rat cerebellum extract

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... NOS1(4842)
rat ... Nos1(24598)

General description

Monoclonal Anti-Nitric Oxide Synthase-Brain (bNOS) (mouse IgG1 isotype) is derived from the NOS-B1 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from immunized BALB/c mice. Nitric oxide synthase (NOS) has been localized in many different cell types. Type I NOS is found in neurons. It is a 150-160 kDa protein, also called NOS-1, neuronal NOS (nNOS), brain NOS (bNOS), cerebral NOS, constitutive NOS or Ca2+- regulated NOS (cNOS). bNOS is present also in skeletal muscle, where it is complexed with dystrophin, and is absent in Duchenne′s muscular dystrophy, which perhaps accounts for symptoms of the disease.

Specificity

Monoclonal Anti-Nitric Oxide Synthase, Brain (1-181) antibody is specific for nitric oxide synthase (NOS) derived from brain (bNOS, 150-160 kDa and several breakdown products of lower M.W.). The product does not bind to NOS derived from macrophages (mNOS) and endothelial cells (eNOS). This antibody is specific for bNOS in humans, goats, pigs and rats.

Immunogen

recombinant neuronal NOS fragment (amino acids 1-181) from rat brain.

Application

Monoclonal Anti-Nitric Oxide Synthase, Brain (1-181) antibody produced in mouse has been used in:
  • western blot analysis
  • immunocytochemistry
  • double immunofluorescence
  • immunofluorescence staining
  • enzyme-linked immunosorbent assay (ELISA)
  • dot blot immunoassay
  • immunohistochemical staining

Biochem/physiol Actions

Nitric oxide synthase is an enzyme that catalyzes the formation of nitric oxide. Nitric oxide is responsible for regulating several biochemical functions such as hemostasis, neurotransmission and vascular injury response . Mutations in nitric oxide synthase gene have been associated with diabetic nephropathy.

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.

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Chadd M Funk et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 37(38), 9132-9148 (2017-08-20)
During non-rapid eye-movement (NREM) sleep, cortical and thalamic neurons oscillate every second or so between ON periods, characterized by membrane depolarization and wake-like tonic firing, and OFF periods, characterized by membrane hyperpolarization and neuronal silence. Cortical slow waves, the hallmark
Elevated expression of CAPON and neuronal nitric oxide synthase in the sciatic nerve of rats following constriction injury
Cui Z, et al.
The Veterinary Journal, 187(3), 374-380 (2011)
The distribution of nitric oxide synthase in the inferior colliculus of guinea pig
Coote EJ, et al.
Neuroscience, 154(1), 218-225 (2008)
The complex contribution of NOS interneurons in the physiology of cerebrovascular regulation
Duchemin S, et al.
Frontiers in Neural Circuits, 6 (2012)
Anna Steinberg et al.
The journal of headache and pain, 17(1), 78-78 (2016-09-03)
Migraine and Cluster Headache (CH) are two primary headaches with severe disease burden. The disease expression and the mechanisms involved are poorly known. In some attacks of migraine and in most attacks of CH, there is a release of vasoactive

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