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Submit ReviewXIE62-1004 is an inducer of p62-LC3 interaction. Binds to the ZZ domain of p62, leading to p62 self-aggregation and interaction with LC3 on autophagosome membranes; facilitates delivery of cargo proteins to the autophagosome for degradation. Active in vitro and in vivo in a concentration- and time-dependent manner and is specific for wild type p62. Induces degradation of mutant huntingtin in vitro. Can also be used in AUTAC protein degradation systems to induce autophagy through p62 self-aggregation and LC3 interaction.
分子量 | 399.91 |
公式 | C23H25NO3.HCl |
储存 | Store at -20°C |
纯度 | ≥98% (HPLC) |
CAS Number | 2421146-32-7 |
PubChem ID | 126601715 |
InChI Key | ROURICFSUKPJOO-UHFFFAOYSA-N |
Smiles | Cl.OCCNCC1=CC=C(OCC=2C=CC=CC2)C(OCC=3C=CC=CC3)=C1 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
溶剂 | 最高浓度 mg/mL | 最高浓度 mM | |
---|---|---|---|
溶解性 | |||
DMSO | 8 | 20 |
以下数据基于产品分子量 399.91。 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
浓度/溶剂体积/质量 | 1 mg | 5 mg | 10 mg |
---|---|---|---|
0.2 mM | 12.5 mL | 62.51 mL | 125.03 mL |
1 mM | 2.5 mL | 12.5 mL | 25.01 mL |
2 mM | 1.25 mL | 6.25 mL | 12.5 mL |
10 mM | 0.25 mL | 1.25 mL | 2.5 mL |
参考文献是支持产品生物活性的出版物。
Zhang et al (2018) ZZ-dependent regulation of p62/SQSTM1 in autophagy. Nat.Commun. 9 4373 PMID: 30349045
Cha-Molstad et al (2017) p62/SQSTM1/Sequestosome-1 is an N-recognin of the N-end rule pathway which modulates autophagosome biogenesis. Nat.Commun. 8 102 PMID: 28740232
If you know of a relevant reference for XIE62-1004, please let us know.
关键词: XIE62-1004, XIE62-1004 supplier, XIE621004, p62, LC3, p62zz, zz, domain, autophagosome, degrader, degradation, degrade, degrades, mutant, AUTAC, huntingtin, Autophagy, Protein, Dimerizers, 7878, Tocris Bioscience
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There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.