IL-1β Antibody [J24M1] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IF1:200 - 1:800 FCM1:100 - 1:400

Application
WB, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
17 kDa, 31 kDa

Positive Control	THP-1 cells (LPS, 100 ng/ml, 3 h)
Negative Control	THP-1 cells

Datasheet & SDS

Biological Description

Specificity
IL-1β Antibody [J24M1] detects endogenous levels of total IL-1β protein.

Clone
J24M1

Synonym(s)
Catabolin; Interleukin-1 beta; IL-1 beta; IL1B; IL1F2

Background
Interleukin-1β (IL-1β), the mature pro-inflammatory cytokine cleaved from its 31 kDa precursor by caspase-1 at Asp116-Ala117, functions as a master regulator of innate immunity by binding to IL-1R1 and recruiting IL-1RAcP to form a high-affinity signaling complex that activates MyD88-dependent pathways, primarily IRAK4 and IRAK1, leading to TRAF6 ubiquitination and divergent activation of NF-κB (driving pro-inflammatory gene expression) and MAPK/AP-1 cascades (JNK/p38/ERK, promoting cytokine production). IL-1β adopts a β-trefoil fold with 12 β-strands forming receptor-binding interfaces, where Lys93, Lys94, and Lys117 create a basic patch for IL-1R1 docking and Pro68, Tyr68 stabilize receptor ternary complex formation. IL-1β amplifies acute inflammation by inducing fever through PGE2/COX-2 production acting on hypothalamic EP3R, promoting neutrophil recruitment and survival, stimulating acute phase protein synthesis (CRP, SAA, fibrinogen) in hepatocytes, and driving Th17 polarization while synergizing with IL-6 and TNF-α to sustain chronic inflammation. IL-1β coordinates host defense against infection and injury, whereas pathologically, constitutive activation, often due to NLRP3 inflammasome hyperactivity, drives rheumatoid arthritis (synovial inflammation), type 2 diabetes (β-cell apoptosis), atherosclerosis (plaque instability), and neurodegeneration (microglial activation).

Background

Interleukin-1β (IL-1β), the mature pro-inflammatory cytokine cleaved from its 31 kDa precursor by caspase-1 at Asp116-Ala117, functions as a master regulator of innate immunity by binding to IL-1R1 and recruiting IL-1RAcP to form a high-affinity signaling complex that activates MyD88-dependent pathways, primarily IRAK4 and IRAK1, leading to TRAF6 ubiquitination and divergent activation of NF-κB (driving pro-inflammatory gene expression) and MAPK/AP-1 cascades (JNK/p38/ERK, promoting cytokine production). IL-1β adopts a β-trefoil fold with 12 β-strands forming receptor-binding interfaces, where Lys93, Lys94, and Lys117 create a basic patch for IL-1R1 docking and Pro68, Tyr68 stabilize receptor ternary complex formation. IL-1β amplifies acute inflammation by inducing fever through PGE2/COX-2 production acting on hypothalamic EP3R, promoting neutrophil recruitment and survival, stimulating acute phase protein synthesis (CRP, SAA, fibrinogen) in hepatocytes, and driving Th17 polarization while synergizing with IL-6 and TNF-α to sustain chronic inflammation. IL-1β coordinates host defense against infection and injury, whereas pathologically, constitutive activation, often due to NLRP3 inflammasome hyperactivity, drives rheumatoid arthritis (synovial inflammation), type 2 diabetes (β-cell apoptosis), atherosclerosis (plaque instability), and neurodegeneration (microglial activation).

References
https://pubmed.ncbi.nlm.nih.gov/18650393/ https://pubmed.ncbi.nlm.nih.gov/18806223/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%