Product Name: Cytokeratin5 Antibody [3E2F1]
Species Reactivity: Human
Tested Applications: ELISA, IHC, WB
Applications: Western Blot:1:500 – 1:2,000 IHC(P):1:500 – 1:2,000ELISA:Propose dilution 1:10,000.Determining optimal working dilutions by titration test.
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight:
Immunogen: Ni-NTA purified truncated recombinant CK5-Trx-His expressed in E. Coli strain BL21 (DE3).
Host Species: Mouse
Purification:
Physical State:
CAS NO.: 950762-95-5
Product: PCI-34051
Buffer: Ascitic fluid containing 0.03% sodium azide.
Concentration:
Storage Conditions: Cytokeratin 5 monoclonal antibody can be stored at -20˚C, stable for one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Clonality: Monoclonal
Conjugate: Unconjugated
Alternate Names: 58 kDa cytokeratin, CK-5, K5, CK5, DDD, DDD1, EBS2, KRT5A
Accession NO.: P13647
Protein Ino: 143811411
Official Symbol: KRT5
Geneid: 3852
Background: CK5 (keratin 5) is a member of the keratin gene family. Biochemically, most members of the CK family fall into one of two classes, type I (acidic polypeptides) and type II (basic polypeptides). The type II cytokeratins consist of basic or neutral proteins which are arranged in pairs of heterotypic keratin chains coexpressed during differentiation of simple and stratified epithelial tissues. This type II cytokeratin is specifically expressed in the basal layer of the epidermis with family member KRT14. The type II cytokeratins are clustered in a region of chromosome 12q12-q13. At least one member of the acidic family and one member of the basic family is expressed in all epithelial cells. Cytokeratin 5 is expressed in normal basal cells. Mutations of the Cytokeratin5 gene (KRT5) have been shown to result in the autosomal dominant disorderepidermolysis bullosa (EB). Defects in KRT5 are a cause of epidermolysis bullosa simplex.
PubMed ID:http://aac.asm.org/content/38/1/130.abstract
