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Merck

C2618

Sigma-Aldrich

细胞松驰素D

Ready Made Solution, from Zygosporium mansonii, 5 mg/mL in DMSO

别名:

接柄孢菌素A

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About This Item

经验公式(希尔记法):
C30H37NO6
CAS号:
分子量:
507.62
Beilstein:
1632828
MDL號碼:
分類程式碼代碼:
51102829
PubChem物質ID:
NACRES:
NA.85

生物源

Zygosporium mansonii

品質等級

形狀

solution

濃度

5 mg/mL in DMSO

抗生素活性譜

fungi

作用方式

enzyme | interferes

運輸包裝

wet ice

儲存溫度

−20°C

SMILES 字串

[H][C@@]12[C@H](C)C(=C)[C@@H](O)[C@@H]3\C=C\C[C@H](C)C(=O)[C@](C)(O)\C=C\[C@@H](OC(C)=O)[C@@]13C(=O)N[C@H]2Cc4ccccc4

InChI

1S/C30H37NO6/c1-17-10-9-13-22-26(33)19(3)18(2)25-23(16-21-11-7-6-8-12-21)31-28(35)30(22,25)24(37-20(4)32)14-15-29(5,36)27(17)34/h6-9,11-15,17-18,22-26,33,36H,3,10,16H2,1-2,4-5H3,(H,31,35)/b13-9+,15-14+/t17-,18+,22-,23-,24+,25-,26+,29+,30+/m0/s1

InChI 密鑰

SDZRWUKZFQQKKV-JHADDHBZSA-N

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應用

细胞松弛素D是黑僵菌代谢物的同分异构体。细胞松弛素D具有抗菌和抗肿瘤活性。它还会有害于肌动蛋白丝的长时程增强作用(LTP)的维持。它与促进有利于肌动蛋白解聚的条件有关。

生化/生理作用

细胞渗透性真菌毒素;肌动蛋白聚合的有效抑制剂。破坏肌动蛋白微丝并激活p53依赖性通路,引起细胞周期在G1-S过渡期阻滞。抑制平滑肌收缩。抑制胰岛素刺激而非基础的葡萄糖转运。
肌动蛋白聚合的强效抑制剂;可破坏肌动蛋白微丝;激活p53依赖性通路;抑制平滑肌收缩;抑制胰岛素刺激的葡萄糖转运。

其他說明

保持容器密闭,并置于干燥通风处。打开后的容器必须小心重新密封并保持直立以防止泄漏。

儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 2

閃點(°F)

188.6 °F - closed cup - Solvent

閃點(°C)

87 °C - closed cup - Solvent

個人防護裝備

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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The inhibition of sugar transport in chick embryo fibroblasts by cytochalasin B. Evidence for a membrane-specific effect.
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The amounts of actin and myosin in rabbit neutrophils expressed as micrograms/10(6) cells are 5.6 +/- 0.75 and 0.56 +/- 0.08, respectively. The average value of the total actin in rabbit neutrophils under unstimulated conditions is distributed between Triton X-100
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B cells are stimulated to initiate DNA synthesis by modest doses of anti-immunoglobulin antibody in combination with cytochalasin. The ability of these agents to stimulate B cells in a sequential fashion was evaluated. Anti-immunoglobulin prepared cells to respond to subsequently
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Virology, 456-457, 342-352 (2014-06-04)
Cell infection by parvoviruses requires that capsids be delivered from outside the cell to the cytoplasm, followed by genome trafficking to the nucleus. Here we microinject capsids into cells that lack receptors and followed their movements within the cell over
Giovanna Leoni et al.
The Journal of clinical investigation, 125(3), 1215-1227 (2015-02-11)
Epithelial restitution is an essential process that is required to repair barrier function at mucosal surfaces following injury. Prolonged breaches in epithelial barrier function result in inflammation and further damage; therefore, a better understanding of the epithelial restitution process has

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