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Anti-IκBα Mouse Antibody [L13L21]

Catalog No.: F3539

Application: Reactivity: Human, Mouse, Rat, Monkey, Bovine, Pig

Usage Information

Dilution
WB1:1000 IP1:50 IHC1:50 - 1:200 IF1:200 - 1:800 FCM1:400 - 1:1600

Application
WB, IP, IHC, IF, FCM

Reactivity
Human, Mouse, Rat, Monkey, Bovine, Pig

Source
Mouse

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
39 kDa

Positive Control	Human leiomyoma; Human lung carcinoma; Human renal adenocarcinma; THP-1 (differentiated with TPA, 80 nM, 24h; LPS, 1 μg/ml, 4 - 24 h); NIH/3T3; HeLa; Karpas 299; Neuro 2A; A20; C6
Negative Control

Datasheet & SDS

Biological Description

Specificity
IκBα Mouse mAb detects endogenous levels of total IκBα protein.

Clone
L13L21

Synonym(s)
NF-kappa-B inhibitor alpha; I-kappa-B-alpha; IkB-alpha; IkappaBalpha; Major histocompatibility complex enhancer-binding protein MAD3; NFKBIA; IKBA; MAD3; NFKBI

Background
IκBα (Inhibitor of kappa B alpha) is a key cytoplasmic inhibitor of the NF-κB signaling pathway, which regulates genes involved in inflammation, immunity, apoptosis, and cell proliferation. It binds to NF-κB dimers, such as p65/p50, masking their nuclear localization signals and retaining them in an inactive state in the cytoplasm. Upon stimulation by pro-inflammatory signals like TNF-α, IL-1β, or microbial components, IκB kinase (IKK) phosphorylates IκBα at specific serine residues, leading to its ubiquitination and subsequent degradation by the proteasome. This degradation releases NF-κB, allowing its translocation to the nucleus where it activates transcription of genes involved in immune responses and cell survival. Newly synthesized IκBα later enters the nucleus, removes NF-κB from DNA, and returns it to the cytoplasm, forming a negative feedback loop that ensures timely termination of the signal. IκBα contains ankyrin repeats for NF-κB binding and a C-terminal PEST domain that regulates its degradation. Dysregulation of IκBα results in sustained NF-κB activation and is implicated in chronic inflammatory diseases and autoimmune disorders.

Background

IκBα (Inhibitor of kappa B alpha) is a key cytoplasmic inhibitor of the NF-κB signaling pathway, which regulates genes involved in inflammation, immunity, apoptosis, and cell proliferation. It binds to NF-κB dimers, such as p65/p50, masking their nuclear localization signals and retaining them in an inactive state in the cytoplasm. Upon stimulation by pro-inflammatory signals like TNF-α, IL-1β, or microbial components, IκB kinase (IKK) phosphorylates IκBα at specific serine residues, leading to its ubiquitination and subsequent degradation by the proteasome. This degradation releases NF-κB, allowing its translocation to the nucleus where it activates transcription of genes involved in immune responses and cell survival. Newly synthesized IκBα later enters the nucleus, removes NF-κB from DNA, and returns it to the cytoplasm, forming a negative feedback loop that ensures timely termination of the signal. IκBα contains ankyrin repeats for NF-κB binding and a C-terminal PEST domain that regulates its degradation. Dysregulation of IκBα results in sustained NF-κB activation and is implicated in chronic inflammatory diseases and autoimmune disorders.

References
https://pubmed.ncbi.nlm.nih.gov/21203422/ https://pubmed.ncbi.nlm.nih.gov/26157801/

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

Tel: +1-832-582-8158 Ext:3
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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%