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Keratin 17/19 (D32D9) XP® Rabbit mAb #3984

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  • WB
  • IHC
Western Blotting Image 1: Keratin 17/19 (D32D9) XP® Rabbit mAb
Western blot analysis of extracts of HeLa, A549 and A431 cells using Keratin 17/19 (D32D9) XP® Rabbit mAb. As expected, keratin 17 is detected in HeLa and A431 cells while keratin 19 is found in A549 cells.

To Purchase # 3984

Cat. # Size Qty. Price
3984T 20 µl
$168
3984S 100 µl
$371

Supporting Data

REACTIVITY H M R Mk
SENSITIVITY Endogenous
MW (kDa) 48/41
Source/Isotype Rabbit IgG
Application Key:
  • WB-Western Blotting 
  • IHC-Immunohistochemistry 
Species Cross-Reactivity Key:
  • H-Human 
  • M-Mouse 
  • R-Rat 
  • Mk-Monkey 
  • Related Products

Product Information

Product Usage Information

Application Dilution
Western Blotting 1:1000
Immunohistochemistry (Paraffin) 1:300

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

For a carrier free (BSA and azide free) version of this product see product #88848.

Protocol

Specificity / Sensitivity

Keratin 17/19 (D32D9) XP® Rabbit mAb detects endogenous levels of keratin 17 and keratin 19 proteins.

Species Reactivity:

Human, Mouse, Rat, Monkey

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to amino acids near the amino terminus of human keratin 17 and human keratin 19.

Background

Keratins (cytokeratins) are intermediate filament proteins that are mainly expressed in epithelial cells. Keratin heterodimers composed of an acidic keratin (or type I keratin, keratins K9-K28) and a basic keratin (or type II keratin, keratins K1-K8 and K71-K80) assemble to form filaments. Keratin isoforms demonstrate tissue- and differentiation-specific profiles that make them useful as research and clinical biomarkers (1,2).

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 is involved in wound healing and cell growth, two processes that require rapid cytoskeletal remodeling (7). Keratinocytes deficient in keratin 17 exhibit abnormal Akt/mTOR signaling and fail to produce an increase in translation, cell size, or growth; these cells also exhibit abnormal 14-3-3σ localization. As 14-3-3σ typically associates with keratin 17, these results imply that Akt/mTOR signaling results in sequestration of 14-3-3σ with keratin 17 in the cytosol, which is required for translation and cell growth. Phosphorylation of keratin 17 on Ser44 may provide a docking site for 14-3-3σ binding (8).
For Research Use Only. Not For Use In Diagnostic Procedures.
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