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TXNIP Blocking Peptide(N-term)
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9H3M7 |
|---|---|
| Other Accession | Q5M7W1, Q8BG60, NP_006463.3 |
| Gene ID | 10628 |
|---|---|
| Other Names | Thioredoxin-interacting protein, Thioredoxin-binding protein 2, Vitamin D3 up-regulated protein 1, TXNIP, VDUP1 |
| Target/Specificity | The synthetic peptide sequence is selected from aa 14-27 of HUMAN TXNIP |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | TXNIP |
|---|---|
| Synonyms | VDUP1 |
| Function | May act as an oxidative stress mediator by inhibiting thioredoxin activity or by limiting its bioavailability. Interacts with COPS5 and restores COPS5-induced suppression of CDKN1B stability, blocking the COPS5-mediated translocation of CDKN1B from the nucleus to the cytoplasm. Functions as a transcriptional repressor, possibly by acting as a bridge molecule between transcription factors and corepressor complexes, and over-expression will induce G0/G1 cell cycle arrest. Required for the maturation of natural killer cells. Acts as a suppressor of tumor cell growth. Inhibits the proteasomal degradation of DDIT4, and thereby contributes to the inhibition of the mammalian target of rapamycin complex 1 (mTORC1). |
| Cellular Location | Cytoplasm. |
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Provided below are standard protocols that you may find useful for product applications.
Background
TXNIP may act as an oxidative stress mediator by inhibiting thioredoxin activity or by limiting its bioavailability. Interacts with COPS5 and restores COPS5-induced suppression of CDKN1B stability, blocking the COPS5-mediated translocation of CDKN1B from the nucleus to the cytoplasm. Functions as a transcriptional repressor, possibly by acting as a bridge molecule between transcription factors and corepressor complexes, and over-expression will induce G0/G1 cell cycle arrest. Required for the maturation of natural killer cells.
References
Zhuo de, X., et al. J. Biol. Chem. 285(41):31491-31501(2010)
Kwon, H.J., et al. J. Immunol. 185(7):3980-3989(2010)
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Yu, F.X., et al. J. Biol. Chem. 285(33):25822-25830(2010)
Cadenas, C., et al. Breast Cancer Res. 12 (3), R44 (2010) :
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