Keratin 17 (KRT17) ELISA Kits

Mouse (Murine) Keratin 17 (KRT17) interaction partners

1. Narrow-band ultraviolet B irradiation with doses of MED or higher could eliminate the imiquimod-induced psoriasis-like dermatitis and inhibit K17 expression via the ERK1/2 and STAT3 signaling pathways.

2. TGF-beta1-induced CK17 enhances cancer stem cell-like properties rather than epithelial-mesenchymal transition in promoting cervical cancer metastasis via the ERK1/2-MZF1 signaling pathway.

3. the data suggest that the loss of Krt17 may foster an overall protective environment for lesion-prone cervical tissue.

4. High KR17 expression is associated with oral cancer.

5. p53 operates as a direct Krt17 repressor that invites therapeutic targeting in radiodermatitis .

6. genetic loss of caspase-7 promotes solar-simulated light-induced skin carcinogenesis by blocking caspase-7-mediated cleavage of keratin-17.

7. Data indicate that keratin 17 (k17) regulates autoimmune regulator Aire to promote skin tumorigenesis.

8. These findings functionally integrate K17, hnRNP K, and gene expression along with RSK and CXCR3 signaling in a keratinocyte-autonomous axis and provide a potential basis for their implication in tumorigenesis

9. KRT17 is necessary for oncogenic transformation in Ewing sarcoma and accounts for much of the GLI1-mediated transformation function but via a mechanism independent of AKT signaling.

10. Cytochrome b5 and cytokeratin 17 are biomarkers in bronchoalveolar fluid signifying onset of acute lung injury.

11. IL-22 up-regulates K17 expression in keratinocytes in a dose-dependent manner through STAT3- and ERK1/2-dependent mechanisms.

12. Type I keratin 17 protein is phosphorylated on serine 44 by p90 ribosomal protein S6 kinase 1 (RSK1) in a growth- and stress-dependent fashion

13. Keratin 17 promotes epithelial proliferation and tumor growth by polarizing the immune response in skin.

14. Keratin 17 null mice exhibit age- and strain-dependent alopecia

15. Induction of K6 and K17 correlates with changes in epithelial cells at wound edge. Closure of embryonic wounds is delayed in K17 null embryos. Correlation between K6 and K17 expression and epithelial wound closure. Important for timeliness of process.

16. Gene located immediately 5' upstream from mK17 is functional and encodes a type I keratin protein highly analogous to mK17. Expression is highly restricted and most prevalent in nail bed and matrix, mK17n (n stands for nail). (K17n)

17. K6alpha, K6beta, and K17 have roles in normal development of the nail bed epithelium

18. sonic hedgehog participates in K17 regulation

19. These findings identify K17 and TNFalpha as two novel and interdependent regulators of hair cycling.

20. keratin 17, an intermediate filament protein rapidly induced in wounded stratified epithelia, regulates cell growth through binding to the adaptor protein 14-3-3sigma

Human Keratin 17 (KRT17) interaction partners

1. The c.275A>G (Asn92Ser) mutation of the KRT17 gene probably underlies pachyonychia congenital in a Chinese pedigree

2. The study findings suggest that the K17 protein likely acts as an autoantigen in psoriasis and that patients' risk genotype is strongly correlated with the magnitude of the response to this putative autoantigen.

3. this study shows that Trim21 ubiquitylates and stabilizes Keratin 17 to induce STAT3 activation in psoriasis

4. High KRT17 expression is associated with paclitaxel-induced resistance and migration in cervical cancer.

5. A report of a recurrent mutation in the KRT17 gene found in a family with severe SM, which provides further evidence that some factors such as modifiers, androgenic stimulation and/or environment influence the phenotypes, and other genetic or proteomic conditions might also influence the final manifestations of the disease.

6. High CK17 expression is associated with lymph node metastasis in oral squamous cell carcinoma.

7. High expression of KRT17 is frequent in Lung adenocarcinoma tissues.

8. Narrow-band ultraviolet B irradiation could downregulate K17 expression by inhibiting the ERK1/2 and STAT3 signaling pathways.

9. Our results highlight KRT17 as a possible biomarker in gastric cancer promoting tumor growth, motility, and invasion, and suggest that KRT17 can be a valuable molecular target for development of anti-gastric cancer-specific therapies

10. The findings suggest that CK17, although not specific for differentiated vulvar intraepithelial neoplasia (dVIN), when combined with histologic findings, Ki-67, and p53 immunohistochemistry, can be a marker of vulvar dysplasia and serve as an adjunct in the diagnosis of dVIN.

11. Krt17 was demonstrated to contribute to areca nut-induced oral malignancy

12. TGFbeta/SMAD/miR-486-3p signaling axis in keratinocytes regulated K17 expression and cell proliferation. We conclude that the loss of miR-486-3p in psoriatic epidermis leads to K17 protein overexpression and contributes to the pathogenesis of psoriasis.

13. inflammatory cytokines promoted Nrf2 nuclear translocation in psoriatic epidermis, which led to elevated expression of K6, K16, and K17, thus promoting keratinocyte proliferation and contributing to the pathogenesis of psoriasis.

14. KRT17 promotes tumor cell growth, at least partially, through its anti-apoptotic effect as a result of the KRT17 overexpression by GLIs in oral squamous cell carcinoma (OSCC)..

15. TGF-beta1-induced CK17 enhances cancer stem cell-like properties rather than epithelial-mesenchymal transition in promoting cervical cancer metastasis via the ERK1/2-MZF1 signaling pathway.

16. K17 is highly expressed in most cases of both invasive adenocarcinoma and in AIS and is a powerful, negative prognostic marker for patient survival.

17. the data suggest that the loss of Krt17 may foster an overall protective environment for lesion-prone cervical tissue.

18. High KR17 expression is associated with oral cancer.

19. K17 is expressed in a subset of triple-negative breast cancers, and is a marker of poor prognosis in patients with advanced stage and ER(-)/HER2(-) breast cancer.

20. MiR-138 may regulate K17 protein expression to affect cell proliferation and apoptosis by targeting hTERT gene in keratinocytes from psoriatic vulgaris patients.