产品: N Cadherin 抗体
货号: AF5239
描述: Rabbit polyclonal antibody to N Cadherin
应用: WB IHC IF/ICC
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
蛋白ID: P19022
RRID: AB_2837725

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   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

货期: 当天发货

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IF/ICC 1:100-1:500, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
N Cadherin Antibody detects endogenous levels of total N Cadherin.
RRID:
AB_2837725
引用格式: Affinity Biosciences Cat# AF5239, RRID:AB_2837725.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

CADH2_HUMAN; Cadherin 2; Cadherin 2 N cadherin neuronal; Cadherin 2 type 1; Cadherin 2 type 1 N cadherin neuronal; Cadherin 2, type 1, N-cadherin (neuronal); Cadherin-2; Cadherin2; Calcium dependent adhesion protein neuronal; CD325; CD325 antigen; CDH2; CDHN; CDw325; CDw325 antigen; N cadherin 1; N-cadherin; NCAD; Neural cadherin; OTTHUMP00000066304; OTTHUMP00000067378;

抗原和靶标

免疫原:

A synthesized peptide derived from human N Cadherin, corresponding to a region within C-terminal amino acids.

基因/基因ID:
描述:
Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types. CDH2 may be involved in neuronal recognition mechanism. In hippocampal neurons, may regulate dendritic spine density

研究领域

· Environmental Information Processing > Signaling molecules and interaction > Cell adhesion molecules (CAMs).   (View pathway)

· Human Diseases > Cardiovascular diseases > Arrhythmogenic right ventricular cardiomyopathy (ARVC).

文献引用

1). OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026 (PubMed: 41560298) [IF=15.1]

2). Copper Depletion Nanoparticles Potentiate Cancer Immunotherapy by Avoiding Innate and Adaptive Immune Resistance. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026 (PubMed: 41926649) [IF=15.1]

3). METTL13 Mediates the Translation of Snail in Head and Neck Squamous Cell Carcinoma. International Journal of Oral Science, 2020 (PubMed: 34381012) [IF=10.8]

4). Enhanced oral nanomedicine utilizing biomineralized oncolytic virus for synergistic gastrointestinal cancer therapy. Materials today. Bio, 2025 (PubMed: 41377584) [IF=8.7]

5). Prolyl hydroxylase-2 (EGLN1) mediates TGF-β1 pathway regulated epithelial–mesenchymal transition in yak kidneys. International Journal of Biological Macromolecules, 2025 [IF=8.5]

6). SB431542 partially inhibits high glucose-induced EMT by restoring mitochondrial homeostasis in RPE cells. Cell communication and signaling : CCS, 2024 (PubMed: 38183022) [IF=8.4]

7). Deprivation of methionine inhibits osteosarcoma growth and metastasis via C1orf112-mediated regulation of mitochondrial functions. Cell death & disease, 2024 (PubMed: 38769167) [IF=8.1]

8). BRD7 inhibits enhancer activity and expression of BIRC2 to suppress tumor growth and metastasis in nasopharyngeal carcinoma. Cell Death & Disease, 2023 (PubMed: 36788209) [IF=8.1]

Application: WB    Species: Human    Sample: 5-8 F and HNE1 cells

Fig. 5 Restoration of BIRC2 expression reverses the inhibitory effect of BRD7 on cell migration and invasion. A Scratch wound healing analysis of cell migration in 5-8 F and HNE1 cells stably with BRD7 overexpression, BRD7 and BIRC2 simultaneous overexpression or control. Quantification of the wound recovery rate of the three groups (right). B Matrigel invasion analysis of cell invasive capabilities in 5-8 F and HNE1 cells stably with BRD7 overexpression, BRD7 and BIRC2 simultaneous overexpression or control. C Significantly differently expressed proteins involved in EMT progression (E-cadherin, N-cadherin, Vimentin, ZO-1) in BRD7 overexpression, BIRC2 overexpression and BIRC2 restoration cells, respectively. GAPDH served as an internal control. Error bars represent the mean ± SD. *P 

9). Targeting the MDK/c-Myc complex to overcome temozolomide resistance in glioma. Clinical and translational medicine, 2025 (PubMed: 40468625) [IF=7.9]

Application: WB    Species: Mouse    Sample:

FIGURE 4 MDK affects the ubiquitination modification of c-Myc and the Wnt/β-catenin signalling pathway. (A–C) Results from proteomic analysis indicated that MDK affected the Wnt/β-catenin signalling pathway and protein ubiquitination. The raw data are shown in Table S8. (A) Volcano plot analysis results showed differentially expressed proteins (Table S9). The red dots represent upregulated expression in the siMDK group compared with the control group, and the yellow dots represent downregulated expression in the siMDK group compared with the control group. (B) Cluster analysis results showed similarities and differences among the groups (control vs. siMDK) and the stability of the mass spectrometry results of the three repeated experiments (Table S10). (C) KEGG pathway enrichment analysis revealed the signalling pathway affected by MDK knockdown (Table S11). (D) After treatment with 10 mM MG132 for 4 h, siMDK-U118MG and siMDK-SF126 cell lysates were immunoprecipitated with c-Myc and immunoblotted with ubiquitination antibodies. (E) After treatment with 10 mM MG132 for 4 h, OE-MDK-SHG44 and OE-MDK-U87 cell lysates were immunoprecipitated with c-Myc and immunoblotted with ubiquitination antibodies. (F–G) 50 mg/mL cycloheximide was added (at different time points: 0, 2, 4, 6, and 8 h) to glioma cells transfected with siRNA to block protein synthesis. The expression of c-Myc was then detected by Western blot. (H) MDK knockdown was performed on SF126, U118MG, and U251, and then a Western blot was used to detect the Wnt/β-catenin signalling pathway and EMT pathway markers. (I) MDK was overexpressed in U87, BT325, and SHG44, and Western blot was used to detect the Wnt/β-catenin signalling pathway and EMT pathway markers.

Application: WB    Species: Mouse    Sample:

FIGURE 4 MDK affects the ubiquitination modification of c-Myc and the Wnt/β-catenin signalling pathway. (A–C) Results from proteomic analysis indicated that MDK affected the Wnt/β-catenin signalling pathway and protein ubiquitination. The raw data are shown in Table S8. (A) Volcano plot analysis results showed differentially expressed proteins (Table S9). The red dots represent upregulated expression in the siMDK group compared with the control group, and the yellow dots represent downregulated expression in the siMDK group compared with the control group. (B) Cluster analysis results showed similarities and differences among the groups (control vs. siMDK) and the stability of the mass spectrometry results of the three repeated experiments (Table S10). (C) KEGG pathway enrichment analysis revealed the signalling pathway affected by MDK knockdown (Table S11). (D) After treatment with 10 mM MG132 for 4 h, siMDK-U118MG and siMDK-SF126 cell lysates were immunoprecipitated with c-Myc and immunoblotted with ubiquitination antibodies. (E) After treatment with 10 mM MG132 for 4 h, OE-MDK-SHG44 and OE-MDK-U87 cell lysates were immunoprecipitated with c-Myc and immunoblotted with ubiquitination antibodies. (F–G) 50 mg/mL cycloheximide was added (at different time points: 0, 2, 4, 6, and 8 h) to glioma cells transfected with siRNA to block protein synthesis. The expression of c-Myc was then detected by Western blot. (H) MDK knockdown was performed on SF126, U118MG, and U251, and then a Western blot was used to detect the Wnt/β-catenin signalling pathway and EMT pathway markers. (I) MDK was overexpressed in U87, BT325, and SHG44, and Western blot was used to detect the Wnt/β-catenin signalling pathway and EMT pathway markers.

10). Targeted demethylation of the BRD7 promoter based on CRISPR/dCas9 system inhibits the malignant progression of nasopharyngeal carcinoma. Clinical and translational medicine, 2026 (PubMed: 41510594) [IF=7.9]

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