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Anti-IRG1 Rabbit Antibody [L17A13]

Catalog No.: F3470

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IP1:30

Application
WB, IP

Reactivity
Human, Mouse

Source
Rabbit

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 Observed MW
53 kDa 50 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	RAW 264.7 (LPS, 100 ng/ml, 4 h); THP-1 (PMA, 100 ng/ml, 72 h and LPS, 1 µg/ml, 16 h)
Negative Control	RAW 264.7; THP-1

Datasheet & SDS

Biological Description

Specificity
IRG1 Rabbit mAb detects endogenous levels of total IRG1 protein.

Clone
L17A13

Synonym(s)
IRG1, ACOD1, Cis-aconitate decarboxylase, CAD, Aconitate decarboxylase, Aconitate decarboxylase 1, Cis-aconitic acid decarboxylase, Immune-responsive gene 1 protein

Background
Immune-responsive gene 1 (IRG1) is among the most strongly upregulated genes in macrophages under proinflammatory conditions and is also highly expressed in the pregnant uterus during implantation. IRG1 encodes a cis-aconitate decarboxylase that catalyzes the conversion of cis-aconitic acid—an intermediate of the tricarboxylic acid (TCA) cycle—into itaconic acid. Itaconic acid acts as an endogenous inhibitor of succinate dehydrogenase, thereby linking metabolic reprogramming in macrophages to the regulation of inflammation. Functionally, IRG1 plays critical roles in embryonic implantation and neurodegeneration. In macrophages, it promotes endotoxin tolerance by enhancing A20 expression through the generation of reactive oxygen species (ROS). The cytoprotective enzyme heme oxygenase-1 (HO-1), which produces endogenous carbon monoxide (CO), is also expressed in the lung during lipopolysaccharide (LPS)-induced tolerance and cross-tolerance, highlighting a broader anti-inflammatory network in which IRG1 participates. During the early implantation phase—marked by high levels of inflammatory cytokine secretion—IRG1 expression in the uterus is particularly elevated. Dysregulation of IRG1 has been associated with autoimmune and inflammatory diseases. Localized predominantly to the mitochondria, IRG1 serves as a key link between immune and metabolic pathways. Notably, silencing IRG1 increases NF-κB and IRF3 activation, coupled with reduced A20 expression and diminished ROS production, further underscoring its regulatory role in inflammation.

Background

Immune-responsive gene 1 (IRG1) is among the most strongly upregulated genes in macrophages under proinflammatory conditions and is also highly expressed in the pregnant uterus during implantation. IRG1 encodes a cis-aconitate decarboxylase that catalyzes the conversion of cis-aconitic acid—an intermediate of the tricarboxylic acid (TCA) cycle—into itaconic acid. Itaconic acid acts as an endogenous inhibitor of succinate dehydrogenase, thereby linking metabolic reprogramming in macrophages to the regulation of inflammation. Functionally, IRG1 plays critical roles in embryonic implantation and neurodegeneration. In macrophages, it promotes endotoxin tolerance by enhancing A20 expression through the generation of reactive oxygen species (ROS). The cytoprotective enzyme heme oxygenase-1 (HO-1), which produces endogenous carbon monoxide (CO), is also expressed in the lung during lipopolysaccharide (LPS)-induced tolerance and cross-tolerance, highlighting a broader anti-inflammatory network in which IRG1 participates. During the early implantation phase—marked by high levels of inflammatory cytokine secretion—IRG1 expression in the uterus is particularly elevated. Dysregulation of IRG1 has been associated with autoimmune and inflammatory diseases. Localized predominantly to the mitochondria, IRG1 serves as a key link between immune and metabolic pathways. Notably, silencing IRG1 increases NF-κB and IRF3 activation, coupled with reduced A20 expression and diminished ROS production, further underscoring its regulatory role in inflammation.

References
https://pubmed.ncbi.nlm.nih.gov/23610393/ https://pubmed.ncbi.nlm.nih.gov/25640654/

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

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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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%