Specificityab106035 is primarily directed against mature, 17,000 MW Mouse IL1 beta. It will recognize 10% of the non-denatured (native) precursor 31,000 MW Mouse IL1 beta containing samples but will primarily detect all of the 17,000 MW mature molecule.
ab106034 does not detect IL1 alpha.
Use at an assay dependent concentration. It is recommended to incubate the sample with a dilution of the antibody for at least 4 hours before being tested.
Use at an assay dependent concentration. .
Use at an assay dependent concentration. Caution should be exhibited as the F(c) domain of the rabbit IgG molecule may interact with cells non-specifically.
ab200208-Rabbit polyclonal IgG, is suitable for use as an isotype control with this antibody.
Use at an assay dependent concentration. Preclearing the preparation with a non-specific Rabbit IgG to reduce background is suggested.
1/1000 - 1/5000.
FunctionPotent proinflammatory cytokine. Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production. Promotes Th17 differentiation of T-cells.
Tissue specificityExpressed in activated monocytes/macrophages (at protein level).
Sequence similaritiesBelongs to the IL-1 family.
Post-translational modificationsActivation of the IL1B precursor involves a CASP1-catalyzed proteolytic cleavage. Processing and secretion are temporarily associated.
Cellular localizationCytoplasm, cytosol. Lysosome. Secreted, exosome. Cytoplasmic vesicle, autophagosome. Secreted. The precursor is cytosolic. In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted. IL1B lacks any known signal sequence and the pathway(s) of its secretion is(are) not yet fully understood (PubMed:24201029). On the basis of experimental results, several unconventional secretion mechanisms have been proposed. 1. Secretion via secretory lysosomes: a fraction of CASP1 and IL1B precursor may be incorporated, by a yet undefined mechanism, into secretory lysosomes that undergo Ca(2+)-dependent exocytosis with release of mature IL1B (PubMed:15192144). 2. Secretory autophagy: IL1B-containing autophagosomes may fuse with endosomes or multivesicular bodies (MVBs) and then merge with the plasma membrane releasing soluble IL1B or IL1B-containing exosomes (PubMed:24201029). However, autophagy impacts IL1B production at several levels and its role in secretion is still controversial. 3. Secretion via exosomes: ATP-activation of P2RX7 leads to the formation of MVBs containing exosomes with entrapped IL1B, CASP1 and other inflammasome components. These MVBs undergo exocytosis with the release of exosomes. The release of soluble IL1B occurs after the lysis of exosome membranes (By similarity). 4. Secretion by microvesicle shedding: activation of the ATP receptor P2RX7 may induce an immediate shedding of membrane-derived microvesicles containing IL1B and possibly inflammasome components. The cytokine is then released in the extracellular compartment after microvesicle lysis (PubMed:11728343). 5. Release by translocation through permeabilized plasma membrane. This may occur in cells undergoing pyroptosis due to sustained activation of the inflammasome (By similarity). These mechanisms may not be not mutually exclusive.