DBeQ

Discontinued Product

4417 has been discontinued.

View all p97 ATPase products.
说明: Selective and reversible p97 ATPase inhibitor
化学名: N2,N4-Bis(phenylmethyl)-2,4-quinazolinediamine
纯度: ≥99% (HPLC)
说明书
引用文献 (2)
评论 (1)
文献 (1)

生物活性 for DBeQ

DBeQ is a selective and reversible inhibitor of p97 ATPase (VCP, IC50 = 1.5 μM). Induces executioner caspases (caspase-3 and caspase-7) rapidly. Blocks the degradation of endoplasmic reticulum-associated degradation (ERAD) reporters; also blocks autophagosome maturation and promotes accumulation of LC3-II.

化合物库 for DBeQ

DBeQ is also offered as part of the Tocriscreen 2.0 Max. 了解 Tocris 化合物库的更多信息。

技术数据 for DBeQ

分子量 340.42
公式 C22H20N4
储存 Store at +4°C
纯度 ≥99% (HPLC)
CAS Number 177355-84-9
PubChem ID 676352
InChI Key QAIMUUJJAJBPCL-UHFFFAOYSA-N
Smiles C12=CC=CC=C1N=C(NCC4=CC=CC=C4)N=C2NCC3=CC=CC=C3

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.

参考文献 for DBeQ

参考文献是支持产品生物活性的出版物。

Chou et al (2011) Reversible inhibitor of p97, DBeQ, impairs both ubiquitin-dependent and autophagic protein clearance pathways. Proc.Natl.Acad.Sci.USA 108 4834 PMID: 21383145

Chou and Deshaies (2011) Development of p97 AAA ATPase inhibitors. Autophagy 7 1091 PMID: 21606684

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关键词: DBeQ, DBeQ supplier, DBeQ, aaa, atpases, p97, reversible, reversibly, selective, inhibitors, inhibits, autophagy, erad, endoplasmic-reticulum, associated, protein, degradation, Autophagy, Other, ER, stress/UPR, ATPase, Translocation, 4417, Tocris Bioscience

2 篇 DBeQ 的引用文献

引用文献是使用了 Tocris 产品的出版物。 DBeQ 的部分引用包括:

Keith et al (2022) Compounds activating VCP D1 ATPase enhance both autophagic and proteasomal neurotoxic protein clearance. Nat Commun 13 4146 PMID: 35842429

Tiwari et al (2016) Caveolin-1 is an aggresome-inducing protein. Sci Rep 6 38681 PMID: 27929047


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DbeQ on Dictyostelium mTORC1 signalling.
By Eleanor Warren on 05/23/2019
分析类型: In Vitro
种属: Other

Treated Dictyostelium cells with DbeQ at 15 uM and 1.5 uM concentrations for 1 hour or 24 hours, and monitored p-4E-BP1 levels as a readout for mTORc1 activity. Did not see any significant difference from control

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