Claudin 3 Rabbit Polyclonal Antibody

货号：

AWA41883

应用：

WB,IHC-P,IF-C

反应性：

Human,Mouse,Rat

来源：

Rabbit

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:

Rabbit

Reactivity:

Human, Mouse, Rat

Molecular Wt:

23 kDa

Clonality:

Polyclonal

Isotype:

IgG

Concentration:

1mg/ml

Other Names:

CLDN3; Cldn3; CLDN 3; CPE-receptor 2; C7orf1; Clostridium perfringens enterotoxin receptor 2; CPE-R 2; CPE R2; CPE-R2; CPETR 2; CPETR2; CPE-receptor 2; Rat ventral prostate.1 protein homolog; hRVP1; HRVP 1; HRVP1; RVP1; Claudin3; Claudin-3; Claudin 3

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-C 1:100-1:800
ELISA 1:40000

Immunogen
Information

Gene Name:

CLDN3

Protein Name:

Claudin-3

Gene ID:

1365 (Human)
12739 (Mouse)
65130 (Rat)

SwissPro:

O15551 (Human)
Q9Z0G9 (Mouse)
Q63400 (Rat)

Immunogen
Information

Subcellular Location:

Cell junction, tight junction. Cell membrane.

Immunogen:

Synthetic peptide within mouse Claudin 3. AA range: 206-219.

Specificity:

Claudin 3 Polyclonal Antibody detects endogenous levels of Claudin 3 protein.

Product images
	Fig: Immunocytochemistry analysis of MCF-7 cells labeling Claudin-3 with Rabbit anti-Claudin-3 antibody （AWA41883）at 1/150 dilution(Green). Cells were fixed in 4% paraformaldehyde for 10 minutes at 37 ℃, permeabilized with 0.03% Triton X-100 in PBS for 30 minutes, and then blocked with 5% BSA for 60 minutes at 37 ℃. Cells were then incubated with Rabbit anti-Claudin-3 antibody （AWA41883）at 1/150 dilution in 2% negative goat serum overnight at 4 ℃. Goat Anti-Rabbit IgG H&L (iFluor™ 488, AWS0005c) was used as the secondary antibody at 1/200 dilution for 60 minutes at 37 ℃. Nuclear DNA was labelled in blue with DAPI(AWC0291).

	Fig : Western blot analysis of Claudin 3 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 (AWA41883, 1/1000) was used in TBST at room temperature for 2 hours. Goat Anti-Rabbit IgG - HRP Secondary Antibody (AWS0002) at 1:5,000 dilution was used for 1 hour at room temperature. Positive control: Lane 1: SK-BR-3 cell Lane 2: Mouse pancreatic Predicted molecular weight:23 kDa Observed molecular weight:23 kDa

	Fig : Immunohistochemical analysis of paraffin-embedded Human-uterus tissue with Rabbit anti- Claudin 3 antibody （AWA41883） 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 （AWA41883） 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 : Immunohistochemical analysis of paraffin-embedded Rat-uterus tissue with Rabbit anti- Claudin 3 antibody （AWA41883） 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 （AWA41883） 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.

引用文献 (1)

BRAIN RESEARCH BULLETIN IF:3.7

TBX21 knockdown attenuates neuroinflammation induced by intracerebral hemorrhage via the SIRT1-WDR5-H3K4me3 axis

Neuroinflammation is a key contributor to the development of secondary brain injury (SBI) following intracerebral hemorrhage (ICH). This study aimed to elucidate the role and underlying mechanisms of T-box transcription factor 21 (TBX21), a known regulator of type I inflammatory responses, in ICH-induced neuroinflammation. An in vitro oxygen-glucose deprivation (OGD) model using BV2 microglia and an in vivo autologous blood injection-induced ICH rat model were used to modulate TBX21 and sirtuin 1 (SIRT1) expression. The results showed that TBX21 knockdown significantly suppressed the OGD-induced release of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), decreased levels of the oxidative stress marker malondialdehyde (MDA), and restored the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In addition, TBX21 knockdown reversed the OGD-induced upregulation of TBX21, WDR5, H3K4me3, cyclooxygenase-2 (COX2), and inducible nitric oxide synthase (iNOS), while enhancing SIRT1 expression. Mechanistically, TBX21 could directly bind to the promoter region of SIRT1 and suppress its transcription, and the protective effects of TBX21 knockdown were abolished by SIRT1 knockdown. In the ICH rat model, TBX21 knockdown or SIRT1 overexpression led to improvements in neurological severity scores, reductions in hematoma volume, and restoration of tight junction protein expression (occludin, claudin-3, and ZO-1). Collectively, these findings indicate that TBX21 promotes post-ICH neuroinflammation by repressing SIRT1, thereby enhancing WDR5-mediated H3K4me3 epigenetic modifications. TBX21 may therefore serve as a promising therapeutic target for mitigating SBI after ICH.

pubTime 2025-06-02

Application

Specie

Rat

Dilution