BDB563571
CD324 Mouse anti-Human, Alexa Fluor 647, Clone: 67A4, BD
Manufacturer: BD Biosciences
Select a Size
| Pack Size | SKU | Availability | Price |
|---|---|---|---|
| Each of 1 | BDB563571-Each-of-1 | In Stock | ₹ 20,915.00 |
BDB563571 - Each of 1
In Stock
Quantity
1
Base Price: ₹ 20,915.00
GST (18%): ₹ 3,764.70
Total Price: ₹ 24,679.70
Antigen
CD324
Classification
Monoclonal
Conjugate
Alexa Fluor 647
Formulation
Aqueous buffered solution containing BSA, protein stabilizer, and ≤0.09% sodium azide.
Immunogen
Human Breast Tumor Cell Line
Quantity
50 Tests
Primary or Secondary
Primary
Content And Storage
Store undiluted at 4°C and protected from prolonged exposure to light. Do not freeze.
Applications
Flow Cytometry
Clone
67A4
Description
E-cadherin
Host Species
Mouse
Purification Method
Affinity Purified
Regulatory Status
RUO
Target Species
Human
Isotype
IgG1 κ
Related Products
Description
- The 67A4 monoclonal antibody recognizes the extracellular domain of human E-Cadherin (CD324)
- E-Cadherin is a 120-kDa transmembrane glycoprotein that is localized in the adherens junctions of epithelial cells
- There it interacts with the cytoskeleton through the associated cytoplasmic catenin proteins
- In addition to being a calcium-dependent adhesion molecule, E-Cadherin is also a critical regulator of epithelial junction formation
- Its association with catenins is necessary for cell-to-cell adhesion
- These E-Cadherin/catenin complexes associate with cortical actin bundles at both the zonula adherens and the lateral adhesion plaques
- Tyrosine phosphorylation can disrupt these complexes, leading to changes in cell adhesion properties
- E-Cadherin expression is often down-regulated in highly invasive, poorly differentiated carcinomas
- Increased expression of E-Cadherin in these cells reduces their invasiveness
- Thus, loss of expression or function of E-Cadherin appears to be an important step in tumorigenic progression
- Pluripotent stem cells express E-Cadherin
- Upon differentiation, an epithelial to mesenchymal transition results in the loss of E-cadherin expression and a gain in the expression of N-cadherin.