Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H, R||ICC, IF, IHC, WB||M||Ascites||Monoclonal Antibody|
|Description||Anti-Cytokeratin 17 Antibody, clone E3|
|Presentation||Ascites with no preservatives.|
|Safety Information according to GHS|
|Material Size||100 µL|
|MOUSE ANTI-KERATIN 17 -2545377||2545377|
|MOUSE ANTI-KERATIN 17 -2638873||2638873|
|MOUSE ANTI-KERATIN 17 -2664452||2664452|
|Reference overview||Pub Med ID|
|The use of polyethylenimine-DNA to topically deliver hTERT to promote hair growth. |
H-M Jan,M-F Wei,C-L Peng,S-J Lin,P-S Lai,M-J Shieh
Gene therapy 19 2012
The present study investigates the efficacy of polyethylenimine (PEI)-DNA complex that expressed human telomerase reverse transcriptase (hTERT) to transfect hair follicle stem cells and produce sufficient hTERT to stimulate hair growth. Transfection with pLC-hTERT-DNA-PEI complex (D+P group) in vitro induced expression of proliferating cell nuclear antigen in 35.8% of the purified stem cell population, suggesting enhanced cell proliferation. In vivo transfection efficiency of rat dorsal skin was determined by staining for β-gal activity. Cells positive for β-gal were located in the bulge region and dermal sheath of hair follicles. The follicles in the hTERT-transfected region entered anagenon day 15 after transfection, whereas non-transfected (Neg) controls remained in telogen. The similar effect was observed in 50-day-old rat dorsal skin. D+P group displayed a specific expression of hTERT and sufficient to initiate a transition to the anagen phase and promote new hair synthesis 18 days after the transfection. hTERT promoted follicle neogenesis following wounding. In all, 60 days after wounding, tissues of the D+P group showed more newly regenerating hair follicles (83±52 regenerated follicles per rat) in contrast to control group tissues (15±15 regenerated follicles per rat). These studies provide a potential approach for gene therapy of skin disease.
|Patterns of expression of keratin 17 in human epithelia: dependency on cell position. |
Troyanovsky, S M, et al.
J. Cell. Sci., 93 ( Pt 3): 419-26 (1989) 1989
By immunomorphology, using keratin 17-specific monoclonal antibody, it has been shown that this keratin is expressed only in the basal cells of a group of complex epithelia: glandular epithelium with myoepithelial component, transitional and pseudostratified epithelia. Immunolocalization of keratin 17 provides evidence that the expression of this keratin strongly depends on the cell position within epithelial structures. The topographical character of the keratin expression suggests that these proteins may be implicated in the generation of spatial organization of epithelial tissues.
|Monoclonal antibody mapping of keratins 8 and 17 and of vimentin in normal human mammary gland, benign tumors, dysplasias and breast cancer. |
Guelstein, V I, et al.
Int. J. Cancer, 42: 147-53 (1988) 1988
The distribution of keratins 8 and 17 and of vimentin in 28 normal human mammary tissue samples, 16 benign tumors, 26 fibrocytic diseases and 52 malignant breast tumors have been studied using monoclonal antibodies HI, E3 and NT30, respectively. Three cell populations in normal mammary epithelium have been identified: luminal epithelium containing keratin 8, myoepithelium of the lobular structures positive for vimentin, and myoepithelium of extralobular ducts positive for keratin 17. In different kinds of benign tumor and dysplastic proliferation a mosaic of cells with all normal phenotypes has been observed. The majority of cells co-expressed keratins 8 and 17 or vimentin. In the overwhelming majority of carcinomas, cells did not contain myoepithelial markers (keratin 17 and vimentin) but expressed only keratin 8 specific to normal luminal epithelium.
|Anti-Cytokeratin 17, clone E3 - Data Sheet|