TRIM33 (E1N2Z) Rabbit mAb #13387
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 150 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
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
In contrast, the ubiquitous nuclear protein TRIM33 does not interact with either HP1 family members or chromatin-remodeling/modifying complexes. Rather, TRIM33 plays a pivotal role in signaling cascades driven by the TGF-β superfamily of ligands (7-9). A research study suggests that TRIM33 and Smad4 compete for binding to receptor phosphorylated Smad2/3 and that TRIM33-Smad2/3 and Smad4-Smad2/3 complexes complement one another in the TGF-β-dependent control of hematopoietic cell fate (9). Other studies, however, demonstrate that TRIM33 functions to repress signal relay by the TGF-β superfamily (7-8,10). Indeed, knockout of murine Trim33 results in embryonic lethality due to upregulated Nodal signaling (10). Mechanistically, TRIM33 functions as an E3-ubiquitin ligase and promotes monoubiquitination of Smad4, a modification that impairs its ability to associate with phospho-Smad2 (8). This negative regulatory mechanism is further substantiated by the discovery that TRIM33 disrupts transcriptionally competent Smad complexes on the promoter/enhancer regions of TGF-β-responsive genes by associating with specific epigenetic marks on histone H3, which is a requirement for activating TRIM33's monoubiquitin ligase activity toward Smad4 (11). In line with the ability of TRIM33 to regulate the development of different blood cell lineages, it was shown that loss of TRIM33 expression due to epigenetic silencing of its promoter contributes to the pathogenesis of chronic myelomonocytic leukemia (12).
- Meroni, G. and Diez-Roux, G. (2005) Bioessays 27, 1147-57.
- Jain, A.K. and Barton, M.C. (2009) Cell Cycle 8, 3668-74.
- Underhill, C. et al. (2000) J Biol Chem 275, 40463-70.
- Schultz, D.C. et al. (2001) Genes Dev 15, 428-43.
- Groner, A.C. et al. (2010) PLoS Genet 6, e1000869.
- Khetchoumian, K. et al. (2004) J Biol Chem 279, 48329-41.
- Dupont, S. et al. (2005) Cell 121, 87-99.
- Dupont, S. et al. (2009) Cell 136, 123-35.
- He, W. et al. (2006) Cell 125, 929-41.
- Morsut, L. et al. (2010) Development 137, 2571-8.
- Agricola, E. et al. (2011) Mol Cell 43, 85-96.
- Aucagne, R. et al. (2011) J Clin Invest 121, 2361-70.
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