E. coli-derived Human KRT6A/Cytokeratin6A fragment
Preparation
Produced in rabbits immunized with E. coli-derived Human KRT6A/Cytokeratin6A fragment, and purified by antigen affinity chromatography.
Source
Polyclonal Rabbit IgG
Purification
Protein A & Antigen Affinity
Formulation
PBS, pH7.0 with 0.03% Proclin300
Conjugate
Unconjugated
Form
Liquid
Shipping
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Avoid repeated freeze-thaw cycles.
Anti-KRT6A rabbit polyclonal antibody at 1:10000 dilution Lane A: A431 Whole Cell Lysate Lysates/proteins at 30 μg per lane. Secondary Goat Anti-Rabbit IgG (H+L)/HRP at 1/10000 dilution. Developed using the ECL technique. Performed under reducing conditions. Predicted band size:60 kDa Observed band size:60 kDa (We are unsure as to the identity of these extra bands.)
Anti-KRT6A rabbit polyclonal antibody at 1:10000 dilution Lane A: A431 Whole Cell Lysate Lysates/proteins at 30 μg per lane. Secondary Goat Anti-Rabbit IgG (H+L)/HRP at 1/10000 dilution. Developed using the ECL technique. Performed under reducing conditions. Predicted band size:60 kDa Observed band size:60 kDa (We are unsure as to the identity of these extra bands.)
Image 2 Alt Text
Human KRT6A/Cytokeratin6A Immunohistochemistry(IHC) 23222
Mutations in the KRT6A or KRT16 gene cause pachyonychia congenita type 1 (PC-1), while mutations in KRT16 or KRT6C underlie focal palmoplantar keratoderma (FPPK). Pachyonychia congenita (PC) is an autosomal dominant, very rare keratin disorder caused by mutations in any of at least four genes (KRT6A, KRT6B, KRT16, or KRT17), which can lead to hypertrophic nail dystrophy and palmoplantar keratoderma, among other manifestations. A de novo missense mutation in the KRT6A gene, I462S, has been found in a sporadic PC-1 patient. The identification of this novel mutation in the KRT6A gene provides further evidence that mutation in the KRT6A gene causes PC-1 phenotype.