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#28029 Anti- Smad3L (Ser 208/213 Phosphorylated) Rabbit IgG Affinity Purify

  • 28029_28031_A
  • 28029_28031_C
  • Colon Cancer
Intended Use:
Research reagents
Application:
WB, IP, IHC
Package Size1:
50 μg
Package Size2:
5 μg
Note on Application Abbreviations
WB:Western Blotting
IP:Immunoprecipitation
IHC:Immunohistochemistry

※ The product indicated as "Research reagents" in the column Intended Use cannot be used
  for diagnostic nor any medical purpose.
※ The datasheet listed on this page is sample only. Please refer to the datasheet
  enclosed in the product purchased before use.

Product Overview

Product Overview

Product Code 28029
Product Name Anti- Smad3L (Ser 208/213 Phosphorylated) Rabbit IgG Affinity Purify
Intended Use Research reagents
Application WB, IP, IHC
Immunizing antigen Synthetic peptide of phosphorylated Smad3L (Ser 208/213)
Purification Method Purified with antigen peptide
Specificity Reacts with phosphorylated Smad3L (Ser 208/213) of human, rat and mouse.
Not react with phosphorylated Smad3L (Ser 204), phosphorylated Smad2L (Ser 245/250/255) and non-phosphorylated Smad3.
Package Form Lyophilized product from PBS containing 1% BSA and 0.05% NaN3
Storage Condition 2 - 8℃
Poisonous and Deleterious Substances Applicable
Cartagena Not Applicable
Package Size 1 50 μg
Package Size 2 5 μg
Remarks1 The commercial use of products without our permission is prohibited. Please make sure to contact us and obtain permission.

Product Description

Product Description

Smads are critical mediators conveying signals from the TGF-β-superfamily members to the nucleus. Activated TGF-β type I receptor (TβRI) and c-Jun N-terminal kinase (JNK) differentially phosphorylate Smad3 to convert two distinctive phosphoisoforms: C-terminally phosphorylated Smad3 (pSmad3C) and linker-phosphorylated Smad3 (pSmad3L). Reversible shifting of Smad-dependent signaling between tumor suppression and oncogenesis in hyperactive Ras-expressing cells indicates that pSmad3C transmits a tumor-suppressive TGF-β signal in mature epithelial cells, while oncogenic activities such as cell proliferation and invasion are promoted by the pSmad3L pathway. Notably, pSmad3L-mediated signaling in activated mesenchymal cells promotes fibrosis by stimulating extracellular matrix deposition. As neoplasia progresses from normal epithelial cells through adenoma to cancer, the cells undergo transition from the tumor-suppressive pSmad3C pathway, which is characteristic of mature epithelial cells, to the JNK/pSmad3L pathway, which appears to favor the state of flux shown by the activated mesenchymal cells. Analysis of domain-specific phosphorylation states of Smad3 with the Abs should enhance understanding of TGF-β signaling in cancer and fibrosis, and help many researchers seek for new treatments of such diseases.