Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- HRP Rabbit monoclonal [EP1612Y] to Cytokeratin 14
- Suitable for: WB, IHC-P
- Reacts with: Human
- Conjugation: HRP
Product nameHRP Anti-Cytokeratin 14 antibody [EP1612Y]
See all Cytokeratin 14 primary antibodies
DescriptionHRP Rabbit monoclonal [EP1612Y] to Cytokeratin 14
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Human
Synthetic peptide within Human Cytokeratin 14 aa 400-500 (C terminal). The exact sequence is proprietary.
- WB: A431 cell lysate. IHC-P: FFPE human skin tissue sections.
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In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle. Store In the Dark.
Storage bufferpH: 7.40
Preservative: 0.1% 10% Proclin 300 Solution
Constituents: 30% Glycerol, 1% BSA, PBS
Concentration information loading...
PurityProtein A purified
- Alexa Fluor® 488 Anti-Cytokeratin 14 antibody [EP1612Y] (ab192055)
- Alexa Fluor® 647 Anti-Cytokeratin 14 antibody [EP1612Y] (ab192056)
- PE Anti-Cytokeratin 14 antibody [EP1612Y] (ab210414)
- Alexa Fluor® 555 Anti-Cytokeratin 14 antibody [EP1612Y] (ab214391)
- Anti-Cytokeratin 14 antibody [EP1612Y] - BSA and Azide free (ab243907)
- Alexa Fluor® 555 Anti-Cytokeratin 14 antibody [EP1612Y] (ab275112)
- Anti-Cytokeratin 14 antibody [EP1612Y] (ab51054)
Our Abpromise guarantee covers the use of ab192081 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/5000. Detects a band of approximately 52 kDa (predicted molecular weight: 52 kDa).|
FunctionThe 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.
Tissue specificityDetected 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 diseaseDefects 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.
Sequence similaritiesBelongs to the intermediate filament family.
Cellular localizationCytoplasm. Nucleus. Expressed in both as a filamentous pattern.
- Information by UniProt
- CK 14 antibody
- CK-14 antibody
- ck14 antibody
HRP Anti-Cytokeratin 14 antibody [EP1612Y] (ab192081) at 1/5000 dilution + A431 (Human epithelial carcinoma cell line) Whole Cell Lysate at 10 µg
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 52 kDa
Observed band size: 52 kDa
Exposure time: 90 seconds
This blot was produced using a 4-12% Bis-tris gel under the MOPS buffer system. The gel was run at 200V for 50 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 2% Bovine Serum Albumin before being incubated with ab192081 overnight at 4°C. Antibody binding was visualised using ECL development solution ab133406.
IHC image of Cytokeratin 14 staining in human skin formalin fixed paraffin embedded tissue section*. The section was pre-treated using pressure cooker heat mediated antigen retrieval with sodium citrate buffer (pH6) for 30 mins. The section was incubated with an HRP-conjugated primary, ab192081 at a working dilution of 1 in 100 overnight at +4°C. The section was counterstained with haematoxylin and mounted with DPX.
*Tissue obtained from the Human Research Tissue Bank, supported by the NIHR Cambridge Biomedical Research Centre
ab192081 has not yet been referenced specifically in any publications.