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