Product Pathways - TGF-beta/Smad Signaling
ID3 (D16D10) Rabbit mAb #9837
PhosphoSitePlus® protein, site, and accession data: ID3
| Applications | Reactivity | Sensitivity | MW (kDa) | Isotype |
|---|---|---|---|---|
| W IP IF-IC F | H (Dg) | Endogenous | 13 | Rabbit IgG |
Applications Key:
W=Western Blotting
IP=Immunoprecipitation
IF-IC=Immunofluorescence (Immunocytochemistry)
F=Flow Cytometry
Reactivity Key:
H=Human
Dg=Dog
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
Specificity / Sensitivity
ID3 (D16D10) Rabbit mAb recognizes endogenous levels of total ID3 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human ID3 protein.
Western Blotting
Western blot analysis of extracts from various cell lines using ID3 (D16D10) Rabbit mAb.
Flow Cytometry
Flow cytometric analysis of Raji cells using ID3 (D16D10) Rabbit mAb compared to concentration-matched Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (red).
IF-IC
Confocal immunofluorescent analysis of HeLa (positive; left) and HCT-15 (negative; right) cells using ID3 (D16D10) Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red).
Background
Inhibitor of DNA-binding/Differentiation (ID) proteins are a family of proteins that function to repress the activity of basic helix-loop-helix (bHLH) transcription factors. There are four known ID proteins in humans (ID1-4), all of which contain a helix-loop-helix domain, but lack a basic DNA binding domain. Heterodimerization with bHLH transcription factors therefore functions to sequester bHLH proteins and prevent their binding to DNA (1). ID proteins play important functional roles in development, primarily by inhibiting premature differentiation of stem/progenitor cells (1,2). ID3 plays an important role in immune system development, where it has been shown to repress E2A-mediated differentiation of T cells (3). Studies in mouse models have shown that homozygous deletion of ID3 disrupts regulatory T cell differentation (4), and leads to development of γδ T cell lymphoma (5). Outside of the hematopoietic compartment, ID3 was shown to repress MyoD, implicating ID3 in TGFβ-mediated muscle repair (6). Similarly, research studies have shown that ID3 suppresses p21 in colon cancer cells, a function that is purported to promote the self-renewal capacity of putative cancer-initiating cells (7).
- Yokota, Y. (2001) Oncogene 20, 8290-8.
- Hong, S.H. et al. (2011) J Cell Sci 124, 1445-52.
- Miyazaki, M. et al. (2011) Nat Immunol 12, 992-1001.
- Maruyama, T. et al. (2011) Nat Immunol 12, 86-95.
- Li, J. et al. (2010) Blood 116, 5615-21.
- Clever, J.L. et al. (2010) Am J Physiol Cell Physiol 298, C1087-99.
- O'Brien, C.A. et al. (2012) Cancer Cell 21, 777-92.
Application References
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For Research Use Only. Not For Use In Diagnostic Procedures.