Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

Invitrogen™ iNOS Polyclonal Antibody

Rabbit Polyclonal Antibody

Supplier:  Invitrogen™ PA1036

Catalog No. PA1036


Only null left
Edge
Add to Cart

Description

Description

PA1-036 detects inducible nitric oxide synthase (iNOS) from human, mouse and rat tissues and cells as well as recombinant human and mouse iNOS. This antibody does not detect other NOS isoforms. PA1-036 has been successfully used in Western blot and immunofluorescence procedures. By Western blot, this antibody detects an ~135 kDa protein representing mouse iNOS from LPS stimulated RAW 264.7 cells. The PA1-036 immunogen is a synthetic peptide corresponding to residues D(17) L K E E K D I N N N V K K T(31) of mouse iNOS.

iNOS (Inducible Nitric oxide, NO, NOS) is an inorganic, gaseous free radical that carries a variety of messages between cells. Vasorelaxation, neurotransmission and cytotoxicity can all be potentiated through cellular response to NO. NO production is mediated by members of the nitric oxide synthase (NOS) family. iNOS is expressed in liver and inducible by a combination of lipopolysaccharide and certain cytokines. NOS catalyzes the oxidization of L-arginine to produce L-citrulline and NO. Two constitutive isoforms, brain or neuronal NOS (b or nNOS, type I) and endothelial cell NOS (eNOS, type III), and one inducible isoform (iNOS, type II), have been cloned. All NOS isoforms contain calmodulin, nicotinamide adenine dinucleotide phosphate (NADPH), flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN) binding domains. iNOS is found in a variety of cell types including macrophages, hepatocytes, synoviocytes, and smooth muscle cells. Cytokines such as interferon-gamma (IFN), tumor necrosis factor (TNF), interleukin-1 and -2, and lipopolysaccarides (LPS) cause an increase in iNOS mRNA, protein, and activity levels. Protein kinase C-stimulating agents exhibit the same effect on iNOS activity. After cytokine induction, iNOS exhibits a delayed activity response which is then followed by a significant increase in NO production over a long period of time. Three related iNOS pseudogenes are located within the Smith-Magenis syndrome region on chromosome 17. Diseases associated with iNOS dysfunction include achalasia and impotence.
TRUSTED_SUSTAINABILITY
Specifications

Specifications

iNOS
Polyclonal
Unconjugated
Nos2
Hepatocyte NOS; hepatocytes; HEP-NOS; inducible nitric oxide synthase; inducible NO synthase; Inducible NOS; iNos; i-NOS; Inosl; MAC-NOS; macrophage NOS; nitric oxide synthase 2; nitric oxide synthase 2, inducible; nitric oxide synthase 2, inducible, macrophage; nitric oxide synthase 2A (inducible, hepatocytes); nitric oxide synthase, inducible; nitric oxide synthase, macrophage; nitric oxide synthase-inducible; NOS; NOS type II; NOS, type II; Nos2; Nos-2; Nos2a; NOS-II; OTTMUSP00000000202; peptidyl-cysteine S-nitrosylase NOS2
Rabbit
Ammonium sulfate precipitation
RUO
18126, 24599, 4843
-20°C, Avoid Freeze/Thaw Cycles
Liquid
Immunohistochemistry (Paraffin), Western Blot, Immunocytochemistry
4 mg/mL
PBS with 1mg/mL BSA and 0.05% sodium azide
P29477, P35228, Q06518
Nos2
Synthetic peptide corresponding to residues D(17) L K E E K D I N N N V K K T(31) of mouse iNOS.
200 μL
Primary
Human, Mouse, Rat
Antibody
IgG
Product Suggestions

Product Suggestions

Videos
Safety and Handling

Safety and Handling

WARNING: Cancer - www.P65Warnings.ca.gov
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

Your input is important to us. Please complete this form to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Your feedback has been submitted: Thank you for helping us improve our website.