InChI
1S/C46H75NO14/c1-13-16-34-28(7)37(58-38-22-33(48)43(31(10)57-38)60-45(47)53)23-46(54,61-34)30(9)41(51)29(8)42-35(55-11)18-15-17-24(3)19-26(5)39(49)32(14-2)40(50)27(6)20-25(4)21-36(56-12)44(52)59-42/h13,15-18,20-21,26-35,37-43,48-51,54H,14,19,22-23H2,1-12H3,(H2,47,53)/b16-13+,18-15+,24-17+,25-20+,36-21-/t26-,27-,28-,29+,30+,31-,32+,33-,34-,35+,37-,38+,39+,40-,41-,42-,43-,46-/m1/s1
InChI key
DJZCTUVALDDONK-HQMSUKCRSA-N
assay
≥90% (HPLC)
form
lyophilized solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
solubility
DMSO: soluble
shipped in
ambient
storage temp.
−20°C
Quality Level
General description
A highly sensitive and specific inhibitor of vacuolar-type H+-ATPase (V-type; Ki = 20 pM). Inhibits acidification of organelles, such as lysosomes and the Golgi apparatus. Also blocks cell surface expression of viral envelope glycoproteins without affecting their synthesis. Useful for studies of intracellular protein translocation. Exhibits cytotoxic effects on a number of cell lines in a cell viability assay.
Biochem/physiol Actions
Cell permeable: no
Primary Target
Vacuolar-type H+-ATPase
Vacuolar-type H+-ATPase
Product does not compete with ATP.
Reversible: no
Target Ki: 20 pM against vacuolar-type H+-ATPase
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 1 year at -20°C.
Further dilute with aqueous buffers just prior to use.
Other Notes
Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.
Kane, M.D., et al. 1999. J. Neurochem.72, 1939.
Nishihara, T., et al. 1995. Biochem. Biophys. Res. Commun.212, 255.
Muroi, M., et al. 1994. Biosci. Biotech. Biochem.58, 425.
Drose, S., et al. 1993. Biochemistry32, 3902.
Muroi, M., et al. 1993. Biochem. Biophys. Res. Commun.193, 999.
Muroi, M., et al. 1993. Cell Struct. Funct.18, 139.
Nishihara, T., et al. 1995. Biochem. Biophys. Res. Commun.212, 255.
Muroi, M., et al. 1994. Biosci. Biotech. Biochem.58, 425.
Drose, S., et al. 1993. Biochemistry32, 3902.
Muroi, M., et al. 1993. Biochem. Biophys. Res. Commun.193, 999.
Muroi, M., et al. 1993. Cell Struct. Funct.18, 139.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Highly Toxic (H)
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 1 Inhalation - Acute Tox. 2 Dermal - Acute Tox. 2 Oral - Eye Irrit. 2
存储类别
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Peter Göttle et al.
Frontiers in cellular neuroscience, 15, 777542-777542 (2021-12-11)
Myelin repair in the adult central nervous system (CNS) is driven by successful differentiation of resident oligodendroglial precursor cells (OPCs) and thus constitutes a neurodegenerative process capable to compensate for functional deficits upon loss of oligodendrocytes and myelin sheaths as
Michael J Rigby et al.
Communications biology, 4(1), 454-454 (2021-04-14)
Nε-lysine acetylation in the ER lumen is a recently discovered quality control mechanism that ensures proteostasis within the secretory pathway. The acetyltransferase reaction is carried out by two type-II membrane proteins, ATase1/NAT8B and ATase2/NAT8. Prior studies have shown that reducing
Jin Rui Liang et al.
Cell, 180(6), 1160-1177 (2020-03-12)
Selective autophagy of organelles is critical for cellular differentiation, homeostasis, and organismal health. Autophagy of the ER (ER-phagy) is implicated in human neuropathy but is poorly understood beyond a few autophagosomal receptors and remodelers. By using an ER-phagy reporter and
Keiji Ibata et al.
Neuron, 102(6), 1184-1198 (2019-05-11)
Synapse formation is achieved by various synaptic organizers. Although this process is highly regulated by neuronal activity, the underlying molecular mechanisms remain largely unclear. Here we show that Cbln1, a synaptic organizer of the C1q family, is released from lysosomes
我们的科学家团队拥有各种研究领域经验,包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持