IκB-α Recombinant Mouse Monoclonal Antibody

货号：

AWA00605

应用：

WB,IHC-P,IF-T,IP,FCM

反应性：

Human,Mouse,Rat

来源：

Mouse

规格 价格 库存
20μL ¥620 1-3个工作日
50μL ¥1250 1-3个工作日
100μL ¥2200 1-3个工作日

产品概述

Product Details

Host Species:

Mouse

Reactivity:

Human, Mouse, Rat

Molecular Wt:

Predicted MW: 36 kDa
Observed MW: 36 kDa

Clonality:

Monoclonal

Isotype:

IgG2a

Concentration:

1mg/ml

Other Names:

IKBA; NFKBIA; Ikβ-α; IkB-alpha; MAD-3; NFKBI; EDAID2; IκBα; IκB α; IκB-α

Formulation:

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Purification:

Affinity-chromatography

Storage:

Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20°C storage.

Applications

WB 1:1000-1:10000
IHC-P 1:100-1:1000
IF-T 1:100-1:1000
IP 1:100-1:300
FCM 1:50-1:200

Immunogen
Information

Gene Name:

NFKBIA

Protein Name:

NF-kappa-B inhibitor alpha

Gene ID:

4792 (Human)
18035 (Mouse)
25493 (Rat)

SwissPro:

P25963 (Human)
Q9Z1E3 (Mouse)
Q63746 (Rat)

Immunogen
Information

Subcellular Location:

Cytoplasm. Nucleus.

Immunogen:

Synthetic peptide within human IκB-α. AA range: 1-50.

Specificity:

IκB-α Monoclonal Antibody detects endogenous levels of IκB-α protein.

Product images
	Fig : Immunohistochemical analysis of paraffin-embedded Mouse-kidney tissue with Mouse anti- IκB-α antibody (AWA00605 ) at 1/200 dilution. The section was pre-treated using heat mediated antigen retrieval with Sodium citrate buffer (pH 6.0) for 20 minutes. The tissues were blocked in 3% H₂O₂ for 15 minutes at room temperature, washed with ddH2O and PBS, and then probed with the primary antibody (AWA00605 ) at 1/200 dilution for 1 hour at room temperature. The detection was performed using an HRP conjugated compact polymer system(ABIOWELL, AWI0629). DAB was used as the chromogen. Tissues were counterstained with hematoxylin and mounted with DPX.

	Fig : Western blot analysis of IκB-α on different lysates. Proteins were transferred to a NC membrane and blocked with 5% NF-Milk in TBST for 1 hour at room temperature. The primary antibody (AWA00605, 1/1000) was used in TBST at room temperature for 2 hours. Goat Anti-Mouse IgG - HRP Secondary Antibody (AWS0001) at 1:5,000 dilution was used for 1 hour at room temperature. Positive control: Lane 1: C6 cell Lane 2: HSC-T6 cell Lane 3: SHZ-88 cell Predicted molecular weight:36 kDa Observed molecular weight:36 kDa

引用文献 (1)

NEUROCHEMISTRY INTERNATIONAL IF:4

METTL3/IGF2BP2/IκBα axis participates in neuroinflammation in Alzheimer's disease by regulating M1/M2 polarization of microglia

Background Microglia-mediated neuroinflammation is closely related to the development of Alzheimer's disease (AD). This study further elucidated the regulatory mechanism of microglia polarization in AD. Method Microglia polarization was assessed using RT-qPCR, ELISA, and immunofluorescence (IF). Western blot (WB) analyzed inflammation-related, p-tau, and apoptosis-related proteins. Neuronal damage was evaluated by immunofluorescence, and neuronal apoptosis by flow cytometry and TUNEL assay. METTL3 and IκBα expression were detected using RT-qPCR and WB. N 6 -methyladenosine (m 6 A) levels were quantified with a colorimetric assay. RNA pull-down assay examined METTL3, IGF2BP2, and IκBα mRNA binding. IGF2BP expression was assessed by RT-qPCR. Learning and memory abilities were evaluated using morris water maze (MWM) test and novel object recognition (NOR) test. Inflammation-related proteins were detected using IF. Results Stimulation with Aβ 1-42 led to microglia M1 polarization, upregulation of inflammation-related proteins, and exacerbation of neuronal injury and apoptosis, along with increased p-tau expression in neurons. METTL3/IGF2BP2 modulated IκBα m 6 A modification through binding to IκBα mRNA, enhancing its expression. Enhanced METTL3 or IGF2BP2 expression suppressed M1 polarization, inflammation, and neuronal apoptosis in microglia, reversed by knockdown of IκBα. AD model mice exhibited cognitive impairments, neuroinflammation, and elevated M1 polarization. METTL3 or IGF2BP2 overexpression improved cognitive function, reduced neuroinflammation, and inhibited M1 polarization, and this effect was similarly reversed by knockdown of IκBα. Conclusion Our study demonstrates that the METTL3/IGF2BP2/IκBα axis is involved in neuroinflammation in AD by modulating microglia M1/M2 polarization, which sheds light on the treatment of AD.

pubTime 2025-03-17

Application

Specie

Mouse

Dilution

1:1000