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Keratin 16

K16, keratin 16, cytokeratin 16, CK16
The protein encoded by this gene is a member of the keratin gene family. The keratins are intermediate filament proteins responsible for the structural integrity of epithelial cells and are subdivided into cytokeratins and hair keratins. Most of the type I cytokeratins consist of acidic proteins which are arranged in pairs of heterotypic keratin chains and are clustered in a region of chromosome 17q12-q21. This keratin has been coexpressed with keratin 14 in a number of epithelial tissues, including esophagus, tongue, and hair follicles. Mutations in this gene are associated with type 1 pachyonychia congenita, non-epidermolytic palmoplantar keratoderma and unilateral palmoplantar verrucous nevus. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: cytokeratin, CAN, K14, Involucrin, K10
Papers using K16 antibodies
Ashcroft Gillian S et al., In Genome Biology, 2002
... antibody (R&D Systems, Abingdon, UK), anti-LOR, anti-INV (Covance, Berkeley, CA, USA), JCMC (rabbit polyclonal anti-Dsc1), anti-K16, anti-ARG1 (Santa Cruz Biotechnology, Santa Cruz, CA, USA), ...
Monoclonal antibody analysis of keratin expression in epidermal diseasesa 48- and 56-kdalton keratin as molecular markers for hyperproliferative keratinocytes
Coulombe Pierre A. et al., In The Journal of Cell Biology, 1983
... Two K16-C14 and four K16 transgenic lines were generated with ...
Papers on K16
Decreased Expression of Caveolin-1 Contributes to the Pathogenesis of Psoriasiform Dermatitis in Mice.
Aihara et al., Yokohama, Japan. In J Invest Dermatol, Nov 2015
CAV1 silencing in keratinocytes in vitro revealed significant activation of STAT3, leading to increased expression of keratin 16 and several cytokine/chemokines, such as IL-6, C-X-C chemokine ligand 8 (CXCL8), CXCL9, and C-C chemokine ligand 20.
Downmodulation of key inflammatory cell markers with a topical Janus kinase 1/2 inhibitor.
Gottlieb et al., Boston, United States. In Br J Dermatol, Oct 2015
INCB018424 treatment reduced epidermal hyperplasia and dermal inflammation in most patient samples, with reductions in CD3, CD11c, Ki67 and keratin 16 observed by immunohistochemical analysis.
Differentiating confluent and reticulated papillomatosis from acanthosis nigricans.
Kim et al., Suwŏn, South Korea. In J Cutan Pathol, Sep 2015
In both group, increases in Ki-67 and keratin 16 expression were similar.
RNA sequencing atopic dermatitis transcriptome profiling provides insights into novel disease mechanisms with potential therapeutic implications.
Guttman-Yassky et al., Denmark. In J Allergy Clin Immunol, May 2015
The common AD transcriptome identified by using both techniques contained 217 genes, including inflammatory (S100A8/A9/A12, CXCL1, and 2'-5'-oligoadenylate synthetase-like [OASL]) and barrier (MKi67, keratin 16 [K16], and claudin 8 [CLDN8]) AD-related genes.
Canine aural cholesteatoma: a histological and immunohistochemical study.
Giudice et al., Milano, Italy. In Vet J, 2014
Immunohistochemically, the cholesteatoma epithelium was CK14- and CK16-positive, and CK8/18- and CK19-negative.
The changes in the expression levels of follicular markers in keratoacanthoma depend on the stage: keratoacanthoma is a follicular neoplasm exhibiting infundibular/isthmic differentiation without expression of CK15.
Narisawa et al., Saga, Japan. In J Cutan Pathol, 2014
CK1, CK10, CK16, CK17, CK15 (clone LHK15) and calretinin showed dynamic changes in their expression in KA depending on the stage.
Immunohistochemical monitoring of wound healing in antibiotic treated Buruli ulcer patients.
Pluschke et al., Basel, Switzerland. In Plos Negl Trop Dis, 2014
In addition, healing wounds revealed dermal tissue remodeling by apoptosis, and showed increased cytokeratin 16 expression in the epidermis.
Establishment and characterization of immortalized gingival epithelial and fibroblastic cell lines for the development of organotypic cultures.
Bostanci et al., Zürich, Switzerland. In Cells Tissues Organs, 2013
The expression levels of cell type-specific markers, i.e. cytokeratin (CK) 10, CK13, CK16, CK18, CK19 for HGEK-16 and Col I and Col II for GFB-16, were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR).
Keratin 16 regulates innate immunity in response to epidermal barrier breach.
Coulombe et al., Baltimore, United States. In Proc Natl Acad Sci U S A, 2013
Mutations in the type I keratin 16 (Krt16) and its partner type II keratin 6 (Krt6a, Krt6b) cause pachyonychia congenita (PC), a disorder typified by dystrophic nails, painful hyperkeratotic calluses in glabrous skin, and lesions involving other epithelial appendages.
Suppression of molecular inflammatory pathways by Toll-like receptor 7, 8, and 9 antagonists in a model of IL-23-induced skin inflammation.
Krueger et al., New York City, United States. In Plos One, 2012
Both agents strongly decreased IL-17A expression (>12-fold reduction), normalized IL-17 induced genes such as beta-defensin and CXCL1, and normalized aberrant expression of keratin 16 (indicating epidermal hyperplasia).
Keratin 16-null mice develop palmoplantar keratoderma, a hallmark feature of pachyonychia congenita and related disorders.
Coulombe et al., Baltimore, United States. In J Invest Dermatol, 2012
we show that the loss of Krt16 function in mice causes the development of prominent calluses on the plantar side of front and hind paws, which significantly compromise mobility.
Pachyonychia congenita patients with mutations in KRT6A have more extensive disease compared with patients who have mutations in KRT16.
Tang et al., Stanford, United States. In Br J Dermatol, 2012
Phenotypic differences exist between KRT6A and KRT16 mutations support adoption of a new classification system.
Genotype-phenotype correlations among pachyonychia congenita patients with K16 mutations.
Tang et al., Stanford, United States. In J Invest Dermatol, 2011
Patients with p.Asn125Asp and p.Arg127Pro mutations in KRT16 exhibited more severe disease than patients carrying p.Asn125Ser and p.Arg127Cys mutations in terms of age of onset of symptoms, extent of nail involvement, and impact on daily quality of life.
Trichohyalin is a potential major autoantigen in human alopecia areata.
Tobin et al., Bradford, United Kingdom. In J Proteome Res, 2010
Data suggest that an immune response to trichohyalin and K16 may have a role in the pathogenesis of the enigmatic disorder.
Hyperproliferation markers in ear canal epidermis.
Ribeiro et al., São Paulo, Brazil. In Braz J Otorhinolaryngol, 2010
The most studied ones were cytokeratin 16, Ki-67 and PCNA.
Aberrant heterodimerization of keratin 16 with keratin 6A in HaCaT keratinocytes results in diminished cellular migration.
Onder et al., Salzburg, Austria. In Mech Ageing Dev, 2010
these data highlight the possibility of a physiological role for K6/K16 heterodimers in keratinocyte cell migration, in addition to the heterodimer's known functions in cell differentiation and mechanical resilience.
[Functional polymorphisms in clock genes and circadian rhythm sleep disorders].
Ebisawa, Tokyo, Japan. In Nihon Shinkei Seishin Yakurigaku Zasshi, 2007
Mutations in Per2 gene (S662G) or Casein Kinasel delta (CK16) gene (T44A) cause Familial advanced sleep phase syndrome.
Lessons learned from psoriatic plaques concerning mechanisms of tissue repair, remodeling, and inflammation.
Lingen et al., Maywood, United States. In J Investig Dermatol Symp Proc, 2006
We hypothesize saliva and chronic trauma contribute to a constitutive epithelial program where keratinocyte proliferation is more intense prior to differentiation, accompanied by keratin 16 expression in hard palate, thereby resembling plaques.
The aggressive nature of the odontogenic keratocyst: is it a benign cystic neoplasm? Part 3. Immunocytochemistry of cytokeratin and other epithelial cell markers.
Shear, Cape Town, South Africa. In Oral Oncol, 2002
With regard to OKC behaviour, it has been pointed out that there was strong reaction of OKC lining for keratin 16, a cytokeratin that has been associated with high proliferative activity.
Transition from symptomless to lesional psoriatic skin.
de Jong et al., Nijmegen, Netherlands. In Clin Exp Dermatol, 1996
The appearance of a predominantly lymphocytic infiltrate, in particular the extravasation of CD4+ T lymphocytes, and the suprabasal expression of keratin 16 are intermediary stages.
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