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- Bioss
- bs-3897P
- 2026年10月10日
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- 技术资料
- 规格：
500ug
| 产品编号 | bs-3897P |
| 英文名称 | TXNIP Antibody Blocking Peptide |
| 中文名称 | 硫氧还蛋白结合蛋白2封闭多肽 |
| 英文别名 | ;THIF; thioredoxin binding protein 2; thioredoxin interacting protein; Thioredoxin-binding protein 2; Thioredoxin-interacting protein; upregulated by 1,25-dihydroxyvitamin D-3; VDUP1; Vitamin D3 up-regulated protein 1; TXNIP_HUMAN. |
| 纯化方法 | HPLC |
| 研究领域 | Cancer > Cancer Metabolism > Cellular metabolic process Cancer > Cancer Metabolism > Metabolic signaling pathway > Metabolism of carbohydrates Cancer > Oncoproteins/suppressors > Tumor suppressors Cell Biology > Other Antibodies > Oxidative Stress Epigenetics and Nuclear Signaling > Nuclear Signaling Pathways > Nuclear Receptors > Co-activators/co-repressors Epigenetics and Nuclear Signaling > Transcription > Cancer susceptibility > Tumor Suppressors Metabolism > Pathways and Processes > Metabolic signaling pathways > Carbohydrate metabolism Metabolism > Pathways and Processes > Metabolic signaling pathways > Energy transfer pathways > Energy Metabolism Metabolism > Pathways and Processes > Redox metabolism > Oxidative stress Signal Transduction > Metabolism > Energy Metabolism |
| 亚基 | Interacts with TXN/thioredoxin through its redox-active site. Interacts with transcriptional repressors ZBTB16, ZBTB32 and HDAC1. Interacts (via C-terminus) with ITCH (via WW domains). Interacts with DDIT4. |
| 亚细胞定位 | Cytoplasm |
| 翻译后修饰 | Ubiquitinated; undergoes polyubiquitination catalyzed by ITCH resulting in proteasomal degradation. |
| 相似性 | Belongs to the arrestin family. |
| 功能 | 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). |
| 保存条件 | Shipped at 4℃. Stored at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事项 | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| 背景资料 | TXNIP may act as an oxidative stress mediator by inhibiting thioredoxin activity or by limiting its bioavailability. It interacts with COPS5 and restores COPS5-induced suppression of CDKN1B stability, blocking the COPS5-mediated translocation of CDKN1B from the nucleus to the cytoplasm. It 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. It is required for the maturation of natural killer cells (from SwissProt). |
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