background:
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).
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).
Subunit:
Interacts with TXN/thioredoxin through its redox-active site. Interacts with transcriptional repressors ZBTB16, ZBTB32 and HDAC1. Interacts (via SLCterminus) with ITCH (via WW domains). Interacts with DDIT4.
Subcellular Location:
Cytoplasm
Post-translational modifications:
Ubiquitinated; undergoes polyubiquitination catalyzed by ITCH resulting in proteasomal degradation.
Similarity:
Belongs to the arrestin family.
Database links:
UniProtKB/Swiss-Prot: Q9H3M7.1
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
硫氧还蛋白结合蛋白-2 (TRX-binding protein-2，TBP-2)又称:维生素D3上调蛋白1(Vitamin D3 up-regulated protein 1，VDUP1)或称硫氧还蛋白相互作用蛋白(Thioredoxin-interacting protein，Txnip)。
TBP-2与硫氧还蛋白(thioredoxin，TRX)的活性部位结合，抑制其活性，除了参与多种氧化应激反应，还具有多种生物学功能。
有学者认为：TBP-2与肿瘤密切相关，有些肿瘤组织中，TBP-2表达降低或缺失。TBP-2表达增高时，细胞周期停滞，肿瘤细胞繁殖受到抑制。目前已成为肿瘤研究的重要靶点。
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