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TSG101 Antibody (monoclonal) (M01)
Mouse monoclonal antibody raised against a partial recombinant TSG101.
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC, IF, E |
|---|---|
| Primary Accession | Q99816 |
| Other Accession | NM_006292 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | IgG2a Kappa |
| Clone Names | 5B7 |
| Calculated MW | 43944 Da |
| Gene ID | 7251 |
|---|---|
| Other Names | Tumor susceptibility gene 101 protein, ESCRT-I complex subunit TSG101, TSG101 |
| Target/Specificity | TSG101 (NP_006283, 201 a.a. ~ 280 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. |
| Dilution | WB~~1:500~1000 |
| Format | Clear, colorless solution in phosphate buffered saline, pH 7.2 . |
| Storage | Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. |
| Precautions | TSG101 Antibody (monoclonal) (M01) is for research use only and not for use in diagnostic or therapeutic procedures. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene belongs to a group of apparently inactive homologs of ubiquitin-conjugating enzymes. The gene product contains a coiled-coil domain that interacts with stathmin, a cytosolic phosphoprotein implicated in tumorigenesis. The protein may play a role in cell growth and differentiation and act as a negative growth regulator. In vitro steady-state expression of this tumor susceptibility gene appears to be important for maintenance of genomic stability and cell cycle regulation. Mutations and alternative splicing in this gene occur in high frequency in breast cancer and suggest that defects occur during breast cancer tumorigenesis and/or progression.
References
1.Characterization of human thymic exosomes.Skogberg G, Gudmundsdottir J, van der Post S, Sandstrom K, Bruhn S, Benson M, Mincheva-Nilsson L, Baranov V, Telemo E, Ekwall OPLoS One. 2013 Jul 2;8(7):e67554. doi: 10.1371/journal.pone.0067554. Print 2013.
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