CABT-BL7742

antibody from Creative Diagnostics
Targeting: IL1B IL-1B, IL1-BETA, IL1F2
Provider product page for CABT-BL7742
Flow cytometry

Antibody data

Product number
CABT-BL7742 - Provider product page
Provider
Creative Diagnostics
Product name
Anti-IL1B Monoclonal antibody, clone C-B26 [FITC]
Antibody type
Monoclonal
Description
Interleukin-1 beta (IL-1 beta) 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. Although IL-1 beta is most often secreted in its active form, secretion of the uncleaved protein may be detectable under some biological conditions.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.
Reactivity
Human
Host
Mouse
Conjugate
Green dye
Isotype
IgG
Antibody clone number
C-B26
Vial size
100 tests
Concentration
10ul/Test
Storage
4°C
IL1B protein structure - CABT-BL7742 shown in red.