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239805

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Cyclopiazonic Acid, Penicillium cyclopium

A cell-permeable, reversible inhibitor of sarcoplasmic reticulum Ca2+-ATPase that releases Ca2+ from the same intracellular pools as Thapsigargin.

Synonyme(s) :

Cyclopiazonic Acid, Penicillium cyclopium, CPA

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About This Item

Formule empirique (notation de Hill):
C20H20N2O3
Numéro CAS:
Poids moléculaire :
336.38
Numéro MDL:
Code UNSPSC :
12352200

Niveau de qualité

Pureté

≥97% (TLC)

Forme

solid

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze

Couleur

off-white

Solubilité

DMSO: 1 mg/mL
chloroform: 10 mg/mL

Conditions d'expédition

ambient

Température de stockage

−20°C

InChI

1S/C20H20N2O3/c1-9(23)14-18(24)17-16-11-8-21-13-6-4-5-10(15(11)13)7-12(16)20(2,3)22(17)19(14)25/h4-6,8,12,16-17,21,25H,7H2,1-3H3/t12-,16+,17+/m1/s1

Clé InChI

RLOAZVAJNNPPDI-DQYPLSBCSA-N

Description générale

A cell-permeable, reversible inhibitor of endoplasmic reticulum Ca2+-ATPase that releases Ca2+ from the same intracellular pools as thapsigargin. Mobilizes Ca2+ without increasing the levels of Ins(1,4,5)P3. Also known to inhibit sarcoplasmic reticular Ca2+-ATPase that is distinct from actomyosin ATPase. Bay K 8644 (Cat. No. 196878) can reverse the inhibitory effect of cyclopiazonic acid on the refilling of Ca2+ pools that have been depleted by repetitive stimulation with acetylcholine.
A cell-permeable, reversible inhibitor of sarcoplasmic reticulum Ca2+-ATPase that releases Ca2+ from the same intracellular pools as Thapsigargin (Cat. No. 586005). Inhibits Ca2+ uptake in cultured arterial smooth muscle cells (IC50 = 560 nM). Also known to inhibit sarcoplasmic reticular Ca2+-ATPase that is distinct from actomyosin ATPase.

Actions biochimiques/physiologiques

Cell permeable: yes
Primary Target
Ca2+ uptake in cultured arterial musclue cells
Product does not compete with ATP.
Reversible: yes
Target IC50: 560 nM inhibiting Ca2+ uptake in cultured arterial smooth muscle cells

Avertissement

Toxicity: Toxic (F)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Autres remarques

Badaoui, A., et al. 1995. J. Mol. Cell. Cardiol. 27, 2495.
Elmoselli, A.B., et al. 1995. Mol. Cell. Biochem. 151, 149.
Schaefer, A., et al. 1994. J. Biol. Chem.269, 8786.
Demaurex, N., et al. 1992. J. Biol. Chem.267, 2318.
Low, A.M., et al. 1992. Am. J. Physiol.262, H31.
Kurebayashi, N., and Ogawa, Y. 1991. J. Muscle Res. Cell Motil.12, 355.
Mason, M.J., et al. 1991. J. Biol. Chem.266, 20856.
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.

Informations légales

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Pictogrammes

Skull and crossbones

Mention d'avertissement

Danger

Mentions de danger

Classification des risques

Acute Tox. 2 Oral

Code de la classe de stockage

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Mia S Geromella et al.
STAR protocols, 4(1), 101987-101987 (2023-01-06)
This protocol employs the indo-1 Ca2+ fluorophore to quantify Ca2+ uptake by the sarco(endo)plasmic reticulum Ca2+ ATPase pump in murine muscle homogenates and allows for real-time kinetic measurement of Ca2+ mobilization within the muscle homogenate. This protocol can be easily
Mehmet Şerif Aydın et al.
iScience, 26(10), 107715-107715 (2023-09-13)
Trauma, vascular events, or neurodegenerative processes can lead to axonal injury and eventual transection (axotomy). Neurons can survive axotomy, yet the underlying mechanisms are not fully understood. Excessive water entry into injured neurons poses a particular risk due to swelling
Hepatic SEL1L-HRD1 ER-associated degradation regulates systemic iron homeostasis via ceruloplasmin.
Thepsuwan, et al.
Proceedings of the National Academy of Sciences of the USA, 120, e2212644120-e2212644120 (2023)

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