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Merck
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資料

安全性情報

481990

Sigma-Aldrich

Nigericin, Sodium Salt, Streptomyces hygroscopicus

Disrupts the membrane potential and stimulates ATPase activity in mitochondria.

別名:

Nigericin, Sodium Salt, Streptomyces hygroscopicus, Antibiotic K178

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About This Item

実験式(ヒル表記法):
C40H67O11 · Na
CAS番号:
分子量:
746.94
MDL番号:
UNSPSCコード:
12352200
NACRES:
NA.77

品質水準

アッセイ

≥98% (TLC)

形状

lyophilized

メーカー/製品名

Calbiochem®

保管条件

OK to freeze

溶解性

chloroform: soluble
ethanol: soluble
ethyl acetate: soluble

輸送温度

ambient

保管温度

2-8°C

InChI

1S/C40H68O11.Na/c1-21-11-12-28(46-33(21)26(6)36(42)43)17-29-18-30(45-10)27(7)40(48-29)25(5)19-38(9,51-40)32-13-14-37(8,49-32)35-23(3)16-31(47-35)34-22(2)15-24(4)39(44,20-41)50-34;/h21-35,41,44H,11-20H2,1-10H3,(H,42,43);/q;+1/p-1/t21-,22-,23-,24+,25?,26?,27+,28+,29+,30+,31+,32?,33?,34-,35?,37?,38?,39-,40+;/m0./s1

InChI Key

MOYOTUKECQMGHE-KKCUGXASSA-M

詳細

A monocarboxylate that catalyzes the electroneutral exchange of an alkali metal for H+ (antiport). Transports monovalent cations across membranes with the following specificities: K+>Rb+>Cs+>>Na+. An antibiotic that kills bacteria by facilitating the diffusion of ions across membranes. Disrupts the membrane potential and stimulates mitochondrial ATPase activity.
Disrupts the membrane potential and stimulates ATPase activity in mitochondria. Transports monovalent cations across membranes with the following specificity: K+>Rb+>Cs+>>Na+.

生物化学的/生理学的作用

Cell permeable: no
Primary Target
Disrupts the membrane potential and stimulates ATPase activity in mitochondria.
Product does not compete with ATP.
Reversible: no

警告

Toxicity: Toxic (F)

再構成

Following reconstitution, aliquot and freeze. Stock solutions are stable for 1 month at -20°C.

その他情報

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.
Moriyama, Y., et al. 1994. J. Biochem.115, 213.
Eytan, G.D., et al. 1990. J. Biol. Chem.265, 12949.
Alonso, M.A., and Carrasco, L. 1981. FEBS Lett.127, 112.

法的情報

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

ピクトグラム

Skull and crossbones

シグナルワード

Danger

危険有害性情報

危険有害性の分類

Acute Tox. 3 Oral - Eye Irrit. 2

保管分類コード

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3


適用法令

試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。

Jan Code

481990-10MG:
481990-1.1ML:
481990-5MG:
481990-MG:


試験成績書(COA)

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文書ライブラリにアクセスする

Sandip Ghosh et al.
Biosensors & bioelectronics, 155, 112115-112115 (2020-03-29)
Fluorescence based intracellular pH nanoprobes have been developed that overcomes the limitations imposed by shallow penetration depth of ultraviolet excitation, photostability, phototoxicity, and interference from background autofluorescence. In this study, we have constructed a Förster Resonance Energy Transfer (FRET) based
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Cell death and differentiation, 28(4), 1418-1433 (2020-11-20)
Hepatocyte cell death and liver inflammation have been well recognized as central characteristics of nonalcoholic steatohepatitis (NASH), however, the underlying molecular basis remains elusive. The kinase receptor-interacting protein 1 (RIP1) is a multitasking molecule with distinct functions in regulating apoptosis
Juan Ma et al.
The EMBO journal, 40(18), e108249-e108249 (2021-07-24)
SARS-CoV-2 is an emerging coronavirus that causes dysfunctions in multiple human cells and tissues. Studies have looked at the entry of SARS-CoV-2 into host cells mediated by the viral spike protein and human receptor ACE2. However, less is known about
Pan Pan et al.
Nature communications, 12(1), 4664-4664 (2021-08-04)
Excessive inflammatory responses induced upon SARS-CoV-2 infection are associated with severe symptoms of COVID-19. Inflammasomes activated in response to SARS-CoV-2 infection are also associated with COVID-19 severity. Here, we show a distinct mechanism by which SARS-CoV-2 N protein promotes NLRP3

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