Key features and details
- Guinea pig polyclonal to Cytokeratin 14
- Reacts with: Mouse, Cow, Human
- Isotype: IgG
Product nameAnti-Cytokeratin 14 antibody
See all Cytokeratin 14 primary antibodies
DescriptionGuinea pig polyclonal to Cytokeratin 14
Host speciesGuinea pig
Species reactivityReacts with: Mouse, Cow, Human
Recombinant full length protein corresponding to Human Cytokeratin 14 aa 1-472. (NP_000517.2)
MTTCSRQFTSSSSMKGSCGIGGGIGGGSSRISSVLAGGSCRAPSTYGGGL SVSSSRFSSG GACGLGGGYGGGFSSSSSSFGSGFGGGYGGGLGAGLGG GFGGGFAGGDGLLVGSEKVTMQ NLNDRLASYLDKVRALEEANADLEVK IRDWYQRQRPAEIKDYSPYFKTIEDLRNKILTAT VDNANVLLQIDNAR LAADDFRTKYETELNLRMSVEADINGLRRVLDELTLARADLEMQIE SL KEELAYLKKNHEEEMNALRGQVGGDVNVEMDAAPGVDLSRILNEMRDQYE KMAEKNRK DAEEWFFTKTEELNREVATNSELVQSGKSEISELRRTMQN LEIELQSQLSMKASLENSLE ETKGRYCMQLAQIQEMIGSVEEQLAQLR CEMEQQNQEYKILLDVKTRLEQEIATYRRLLE GEDAHLSSSQFSSGSQ SSRDVTSSSRQIRTKVMDVHDGKVVSTHEQVLRTKN
Database link: P02533
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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 long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.09% Sodium azide
Constituent: 0.5% BSA
Concentration information loading...
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
ab192694 has been referenced in 3 publications.
- Yeo AJ et al. Increased susceptibility of airway epithelial cells from ataxia-telangiectasia to S. pneumoniae infection due to oxidative damage and impaired innate immunity. Sci Rep 9:2627 (2019). PubMed: 30796268
- Shaalan A & Proctor G Salivary glands require Aurora Kinase B for regeneration after transient innate immune-mediated injury. Sci Rep 9:11339 (2019). PubMed: 31383943
- Schagen J et al. Characterizing well-differentiated culture of primary human nasal epithelial cells for use in wound healing assays. Lab Invest 98:1478-1486 (2018). PubMed: 30089850