Phospho-Keratin 17 (Ser44) Antibody #3519
- WB
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 49 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Flow Cytometry (Fixed/Permeabilized) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Source / Purification
Background
Dysregulation/mutations in keratin genes can lead to a variety of disorders affecting the skin, hair, nails, and other epithelial tissues (3). While expression of keratins can be variable, immunohistochemical staining of keratins is widely used to help in the identification and classification of epithelial tumors, and may also provide prognostic information.
Keratins 8 and 18 (K8/K18) are expressed in simple epithelia of normal tissue, as well as in adenocarcinomas of the breast, lung, ovary, and gastrointestinal tract. Keratin 17 is expressed in basal keratinocytes of stratified epithelia, hair follicles, and sebaceous glands. Onset of keratin 17 expression coincides with the definition of major epithelial lineages during skin development (4). Keratin 14 (K14) is expressed in basal cells of stratified epithelia, and in basal-like subtypes of breast cancer and squamous cell carcinomas. Keratin 19 (K19) is expressed in glandular epithelia, including the liver, gallbladder, and pancreas, as well as in adenocarcinomas of the breast, thyroid, and bile duct. Keratin 20 (K20) is expressed in gastrointestinal epithelium, urothelium, and Merkel cells in the skin, as well as in colorectal carcinomas and some urothelial carcinomas. Keratin 5/6 (K5/6) is expressed in basal cells of stratified epithelia, including the skin, prostate, and breast, as well as in basal-like breast cancers, squamous cell carcinomas, and some lung carcinomas. Keratin 7 (K7) is expressed in glandular epithelia, such as those in the lung, breast, and female reproductive tract, as well as in adenocarcinomas of the lung, breast, and ovary (5,6).
Keratins, particularly K8, K18, and K19, serve as biomarkers for identification of circulating tumor cells (CTCs) (5).
Post-translational modifications, including phosphorylation, acetylation, ubiquitylation, sumoylation, glycosylation, and transamidation, have been shown to affect the functions of keratins in normal and disease states (6). Understanding the molecular mechanisms underlying these PTMs may provide insights into cancer pathogenesis.
Keratin 17 has been shown to be involved in wound healing, a process that requires rapid remodelling of the cytoskeleton (7). Another process that requires cytoskeletal remodelling is cell growth. It has been shown that in keratin 17 keratinocytes that signaling through the Akt/mTOR pathway fails to produce an increase in translation, cell size or growth, and that this defect is associated with abnormal localization of 14-3-3σ. Since in normal cells, 14-3-3σ associates with keratin 17, a model has been proposed whereby signaling through Akt/mTOR produces a sequestration of 14-3-3σ in the cytosol via its interaction with keratin 17, and this sequestration by keratin 17 is required for translation and cell growth. Phosphorylation of keratin 17 on Ser 44 is thought to provide a docking site for 14-3-3σ binding (8).
- Chang, L. and Goldman, R.D. (2004) Nat Rev Mol Cell Biol 5, 601-13.
- Schweizer, J. et al. (2006) J Cell Biol 174, 169-74.
- Sarma, A. (2022) Int J Biol Macromol 219, 395-413.
- McGowan, K.M. and Coulombe, P.A. (1998) J Cell Biol 143, 469-86.
- Werner, S. et al. (2020) Mol Aspects Med 72, 100817.
- Dmello, C. et al. (2019) J Biosci 44, 33.
- Paladini, R.D. et al. (1996) J Cell Biol 132, 381-97.
- Kim, S. et al. (2006) Nature 441, 362-5.
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