The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Biological Activity: Activates the NF-kB pathway.
< 0.100 Eu/µg
>90% by SDS-PAGE.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at -20ºC.
Constituent: 99% PBS
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Reconstitute with 100µl sterile water to a concentration of 0.1 mg/ml. After reconstitution, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
IL 1 beta
Interleukin 1 beta
Preinterleukin 1 beta
Pro interleukin 1 beta
Potent 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.
Expressed in activated monocytes/macrophages (at protein level).
Belongs to the IL-1 family.
Activation of the IL1B precursor involves a CASP1-catalyzed proteolytic cleavage. Processing and secretion are temporarily associated.
Cytoplasm, 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.
Functional Studies - IL1 beta protein (Active) (ab157280)
IL1 beta activity was assessed by its ability to induce the activation of the NF-kB pathway. IkBa degradation was detected by Western blotting.
HeLa cells were grown to confluence in 6 well plates. IL-1b was diluted at the indicated concentrations in 500µl DMEM/Nut.Mix.F-12 10% fetal calf serum and added to the wells after being washed once with the same media. Cells were collected after 30 min and lysed. 100µg of cellular extract were separated on a SDS-PAGE and transferred on a nitrocellulose membrane. IkBa degradation was detected with a rabbit polyclonal antibody to IkBa and a goat anti-rabbit HRP-conjugated secondary antibody. Degradation of IkBa was detected at 10pg/µl IL1 beta, under these conditions.
has not yet been referenced specifically in any publications.
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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"
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