anti-Keratin 14 (KRT14) Antikörper

Human Keratin 14 (KRT14) Interaktionspartner

1. we summarized the various aspects of the presence of KRT5 and KRT14 in the epidermis, their relation to the incidence and severity of epidermolysis bullosa simplex phenotypes, and the processes with which these proteins can affect them.

2. Recessive KRT14 epidermolysis bullosa simplex (EBS) should be clinically differentiated from other EB forms, and also from epidermolytic ichthyosis due to the presence of hyperkeratotic lesions in addition to blisters

3. Data indicate keratins K5/K14 and p53 homolog p63 as markers of breast epithelial stem cells.

4. High CK14 expression is associated with lymph node metastasis in oral squamous cell carcinoma.

5. Efficient homology-directed repair of a dominant negative KRT14 mutation via CRISPR/Cas9 nickases in epidermolysis bullosa simplex patients' keratinocytes has been reported.

6. Immunocytochemical staining using cocktail antibody targeting p63/CK14 was useful for the differential diagnosis of FA and DCIS in FNAC of the breast.

7. the findings show that squamous and micropapillary bladder cancers have different expression patterns of CK14 and FOXA1 and suggest that they arise from distinct precursors.

8. PADI4 contributes to gastric tumorigenesis by upregulating CXCR2, KRT14 and TNF-alpha expression.

9. this study adds a further 10 novel mutations to the catalogued genotype-phenotype correlations in epidermolysis bullosa simplex and demonstrates a potential modifying effect of SNPs on the phenotype. We therefore support the notion of full DNA sequencing of both KRT5 and KRT14 genes so as to not miss any variants in the genes contributing to the phenotype.

10. The novel c.1234A>G(p.Ile412Val) mutation of the KRT14 gene is probably responsible for the disease.

11. Keratin14/p63-positive epithelial proliferations suggest benign breast disease.

12. K14 was coexpressed with alphav-integrin in fetal and adult corneas and cultured corneolimbal epithelium, and colony-forming efficiency (an indicator of stem cell activity) was similar in cells from both sources.

13. Loss of keratin 14 is associated with epidermolysis bullosa.

14. contributes to collective invasion of salivary adenoid cystic carcinoma and may be a biomarker of worse prognosis

15. vimentin regulates the differentiation switch via modulation of K5/K14 expression. Moreover, because there was a significant correlation between high vimentin-K14 expression and recurrence/poor survival in oral cancer patients, vimentin-K14 together may prove to be the novel markers for the prognostication of human oral cancer.

16. We concluded that smoking habits were capable of inducing changes in global DNA methylation, miR-9-3 methylation status and K19 expression.

17. data demonstrates that keratinocyte migration requires the interaction between vimentin and keratins at the -YRKLLEGEE- sequence at the helical 2B domain of viment

18. Immunocytochemistry using this antibody cocktail comprises five antibodies recognising p63, and cytokeratins ( 7, 18, 5 and 14) showed good sensitivity and specificity for diagnosing breast cancers. Thus, this method is useful for mammary cytology using FNA

19. identification of 29 different mutations in KRT5 and KRT14, 11 of which were novel, in a Polish cohort of epidermolysis bullosa simplex patients

20. findings reveal K14 as a key regulator of metastasis and establish the concept that K14(+) epithelial tumor cell clusters disseminate collectively to colonize distant organs

Mouse (Murine) Keratin 14 (KRT14) Interaktionspartner

1. keratin 1 (K1) is essential for the persistent infection caused by LCMV strain MX, and its absence very effectively slows down the course of infection

2. Cumulatively, these data indicate that altered CK14 (high) and CK18 (low) expression is perhaps an early event in bladder cancer tumorigenesis in females at least and is characteristic of both urothelial superficial pre-neoplastic and neoplastic lesions.

3. KRT14 is expressed in a subpopulation of bladder basal cells with pivotal role in regeneration and tumorigenesis.

4. CDK1, Aurora-B, and Rho-kinase phosphorylate keratin 5/14.

5. RA regulates Krt5 and Krt14 expression independently of stem cell character in developing salivary epithelium. The stem cell gene Kit is regulated inversely from Krt5/Krt14 by RA signaling.

6. Analysis of K14 variants with single or multiple substitutions of cysteine residues points to a spatial and temporal hierarchy in how Cys-4/Cys-40 and Cys-367 regulate keratin assembly in vitro and filament dynamics in live keratinocytes

7. Disulfide bonding is a novel and important mechanism regulating the assembly, intracellular organization, and dynamics of K14-containing intermediate filaments in skin keratinocytes.

8. K14-VEGF transgenic mouse a valuable model to study novel immunotherapies for psoriasis

9. autoantibodies in Scurfy mice and patients with IPEX target keratin 14

10. nipple connective tissue and its development: insights from the keratin 14-PTHrP mouse

11. The keratin-14 IL-4 transgenic (Tg) mouse model of atopic dermatitis (AD) is characterized by skin infiltration of T cells, early up-regulation of T(h)2 cytokines and late surge of T(h)1 cytokines.

12. These studies provide a potential mechanism by which deltaNp63 directly governs the expression of K14 in a keratinocyte-specific manner.

13. Study describes the expression profile of claudins and keratin markers in the accelerated epidermal permeability barrier formation of K14-CaSR transgenic mice during development as compared to the wild type from E12.5 to newborn stages.

14. IL-6 and IFN-gamma stimulated VEGF-A mRNA production in the skin and in primary keratinocytes of keratin 14 IL-4 transgenic mice

15. DeltaNp63 alone can restore the expression of the basal keratins and reinitiate the failed epidermal differentiation program in the skin of p63 null animals.

Xenopus laevis Keratin 14 (KRT14) Interaktionspartner

1. findings indicate that ouro1 and ouro2 participate in the process of tail regression as immune antigens and highlight the possibility that the acquired immune system contributes not only to self-defense but also to remodeling processes in morphogenesis.