iNOS, inflammation, and apoptosis

All the tools you need to study the role of inducible nitric oxide synthase (iNOS) in inflammation and apoptosis.


Figure 1. Schematic of Sirt1 S-nitrosylation-dependent activation (acetylation) of NF-κB and p53, leading to inflammation and apoptosis.

Key targets involved




​Expression of iNOS is induced in response to cytokines and other agents. Once expressed, iNOS generates high concentration of nitric oxide (NO).

Figure 2. Anti-iNOS antibody [EPR16635] (ab178945). Western blot of RAW 264.7 whole cell lysate. Lane 1 – untreated, Lane 2 – treatment with LPS.

Protein S-nitrosylation is the attachment of NO to reactive cysteine thiols and a major mediator of NO actions. S-nitrosylation of SIRT1 inhibits SIRT1’s deacetylation abilities.

Figure 3. Anti-S-nitrosocysteine antibody [HY8E12] (ab94930). Western blot using Anti-S-nitrosocysteine on mouse tissue lysate (melanoma cancer).


Deacetylation by SIRT1 inhibits p53 and NF-κB activities, suppressing apoptosis and inflammation.

Figure 4. Anti-SIRT1 antibody [E104] (ab32441). Western blot using anti-SIRT1 antibody on cell lysates; Lane 1 – Jurkat, Lane 2 – HeLa, Lane 3 – HEK293, Lane 4 – A549, Lane 5 – SW480.

p65/NK-kB, a transcription factor, is a key mediator of the inflammatory response.

Figure 5. Anti-NF-kB p65 antibody (ab16502). Immunocytochemistry of HeLa cells stained with anti-NF-kB p65 antibody.


p53 stimulates a wide network of signals that act through the extrinsic and intrinsic apoptosis pathways.

Figure 6. Anti-p53 antibody [PAb 240] (ab26). Immunocytochemistry of A431 cells stained with anti-p53 antibody.

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