The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/10 - 1/50.
ab171870 - Rabbit polyclonal IgG, is suitable for use as an isotype control with this antibody.
1/50 - 1/100. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
1/1000. Predicted molecular weight: 52 kDa.
The nonhelical tail domain is involved in promoting KRT5-KRT14 filaments to self-organize into large bundles and enhances the mechanical properties involved in resilience of keratin intermediate filaments in vitro.
Detected in the basal layer, lowered within the more apically located layers specifically in the stratum spinosum, stratum granulosum but is not detected in stratum corneum. Strongly expressed in the outer root sheath of anagen follicles but not in the germinative matrix, inner root sheath or hair. Found in keratinocytes surrounding the club hair during telogen.
Involvement in disease
Defects in KRT14 are a cause of epidermolysis bullosa simplex Dowling-Meara type (DM-EBS) [MIM:131760]. DM-EBS is a severe form of intraepidermal epidermolysis bullosa characterized by generalized herpetiform blistering, milia formation, dystrophic nails, and mucous membrane involvement. Defects in KRT14 are a cause of epidermolysis bullosa simplex Weber-Cockayne type (WC-EBS) [MIM:131800]. WC-EBS is a form of intraepidermal epidermolysis bullosa characterized by blistering limited to palmar and plantar areas of the skin. Defects in KRT14 are a cause of epidermolysis bullosa simplex Koebner type (K-EBS) [MIM:131900]. K-EBS is a form of intraepidermal epidermolysis bullosa characterized by generalized skin blistering. The phenotype is not fundamentally distinct from the Dowling-Meara type, although it is less severe. Defects in KRT14 are the cause of epidermolysis bullosa simplex autosomal recessive (AREBS) [MIM:601001]. AREBS is an intraepidermal epidermolysis bullosa characterized by localized blistering on the dorsal, lateral and plantar surfaces of the feet. Defects in KRT14 are the cause of Naegeli-Franceschetti-Jadassohn syndrome (NFJS) [MIM:161000]; also known as Naegeli syndrome. NFJS is a rare autosomal dominant form of ectodermal dysplasia. The cardinal features are absence of dermatoglyphics (fingerprints), reticular cutaneous hyperpigmentation (starting at about the age of 2 years without a preceding inflammatory stage), palmoplantar keratoderma, hypohidrosis with diminished sweat gland function and discomfort provoked by heat, nail dystrophy, and tooth enamel defects. Defects in KRT14 are the cause of dermatopathia pigmentosa reticularis (DPR) [MIM:125595]. DPR is a rare ectodermal dysplasia characterized by lifelong persistent reticulate hyperpigmentation, noncicatricial alopecia, and nail dystrophy.
Belongs to the intermediate filament family.
Cytoplasm. Nucleus. Expressed in both as a filamentous pattern.
Immunohistochemical analysis of formalin-fixed and paraffin-embedded human breast carcinoma labeling Cytokeratin 14 with ab175549 at 1/25 dilution. Tissue was fixed with formaldehyde and blocked with 3% BSA for 0.5 hour at 38°C. Antigen retrieval was heat mediation with a citrate buffer (pH6). Samples were incubated with primary antibody (1/25) for 1 hours at 37°C. A Peroxidase-conjugated goat anti-rabbit polyclonal (ready to use) was used as the secondary antibody.
Overlay histogram showing MDA-MB431 cells stained with ab175549 (green line). The cells were fixed with paraformaldehyde and then permeabilized with 90% methanol for 10 min. The cells were then incubated in 3% BSA to block non-specific protein-protein interactions followed by the antibody (ab175549, 1µg/1x106 cells) for 60 min at 37ºC. The secondary antibody used was FITC conjugated goat anti-rabbit antibodies at 1/200 dilution for 40 min at room temperature. Blank control (blue line) was used under the same conditions. Acquisition of >10,000 events was performed.