Description: This NJTEN3 monoclonal antibody reacts with the pro-form of mouse IL-1 beta, which is a proinflammatory cytokine expressed by monocytes, macrophages, and dendritic cells. It is synthesized in response to inflammatory stimuli as a 31 kDa inactive pro-form that accumulates in the cytosol. Cleavage of pro-IL-1 beta into the active 17 kDa protein requires the activation of inflammasomes, which are multi-protein complexes that respond to pathogens, stress conditions, and other danger signals. Inflammasome activation triggers the processing of the caspase-1 precursor into its active form, which in turn cleaves pro-IL-1 beta. IL-1 beta lacks a signal sequence peptide for classical ER/Golgi pathway and is instead secreted alongside caspase-1 via an alternate and incompletely understood mechanism. IL-1 beta signals through two receptors, IL-1RI and IL-1RII, both of which are shared with IL-1 alpha. These cytokines play important roles in innate host defense by triggering the production of other proinflammatory cytokines in target cells and initiating acute-phase responses. Their activity can be moderated by IL-1 Receptor Antagonist (IL-1RA), a protein produced by many cell types that blocks receptor binding through competitive inhibition. Elevated levels of IL-1 beta have been associated with many chronic inflammatory conditions, giving IL-RA or IL-1 beta neutralizing antibodies potential therapeutical value.The NJTEN3 antibody recognizes only the pro-form of mouse IL-1 beta and does not see the active (cleaved) form.