- ￥789
- Sigma-Aldrich
- 进口
- 47036-50G-F
- 2025年09月17日
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- 详细信息
- 文献和实验
- 技术资料
- 保存条件：
常温
- 保质期：
根据瓶身LOT号查询
- 英文名：
Saponin
- 库存：
有现货
- 供应商：
浙江羽翔生物科技有限公司
- CAS号：
8047-15-2
- 规格：
50G
属性
等级
Molecular Biology
质量水平
200
分子量
1000-2000 g/mol
组成
Sapogenin, 8-25%
技术
HPLC: suitable
protein quantification: suitable
CMC
0.001-0.01%
密度
1.015-1.020 g/mL at 20 °C (5% in H2O)(lit.)
异质活性
DNase, RNase, Protease, Phosphatase, none detected
SMILES字符串
C[C@]1(CCC23COC4([C@H]2C1)CC[C@@H]5[C@]6(CC[C@@H](C(C6CC[C@]5([C@@]4(C[C@H]3O)C)C)(C)C)O[C@H]7[C@@H]([C@H]([C@H](CO7)O[C@H]8[C@@H]([C@H]([C@@H](CO8)O)O)O)O[C@@H]9[C@@H]([C@H]([C@@H]([C@H](O9)CO)O)O)O)O[C@H]1[C@@H]([C@H]([C@@H]([C@H](O1)CO)O)O)O[C@@H]1[C@@H]([C@H]([C@@H]([C@H](O1)CO)O)O)O)C)C=O
InChI
1S/C58H94O27/c1-52(2)29-7-11-55(5)30(8-12-58-31-15-53(3,22-62)13-14-57(31,23-77-58)32(64)16-56(55,58)6)54(29,4)10-9-33(52)82-50-46(85-51-45(40(71)37(68)27(19-61)80-51)84-49-43(74)39(70)36(67)26(18-60)79-49)44(83-48-42(73)38(69)35(66)25(17-59)78-48)28(21-76-50)81-47-41(72)34(65)24(63)20-75-47/h22,24-51,59-61,63-74H,7-21,23H2,1-6H3/t24-,25-,26-,27-,28+,29?,30-,31+,32-,33+,34+,35-,36-,37-,38+,39+,40+,41-,42-,43-,44+,45-,46-,47+,48-,49-,50+,51+,53-,54+,55-,56+,57?,58?/m1/s1
InChI key
MAEBCGDGGATMSC-OSHGGGOQSA-N
一般描述
应用
- 作为磷酸缓冲液(PBS)组分，处理细胞用于免疫细胞化学和共聚焦显微镜分析
- 透化细胞，用于测定线粒体总质量
- 作为内参试剂，用于黑乳海参皂苷提取
生化/生理作用
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文献和实验Blood autophagy defect causes accelerated non-hematopoietic organ aging.
Autophagy has been well studied in regulating aging; however, the impact of autophagy in one organ on the aging of other organs has not been documented. In this study, we used a mouse model with deletion of an autophagy-essential gene Atg7 in hematopoietic system to evaluate the intrinsic role of hematopoietic autophagy on the aging of non-hematopoietic organs. We found that autophagy defect in hematopoietic system causes growth retardation and shortened lifespan, along with aging-like phenotypes including hypertrophic heart, lung and spleen, but atrophic thymus and reduced bone mineral density at organismal level. Hematopoietic autophagy defect also causes increased oxidative stress and mitochondrial mass or aging gene expression at cellular level in multiple non-hematopoietic organs. The organ aging in the Atg7-deleted mice was reversed by anatomic connection to wild-type mice with intact blood autophagy via parabiosis, but not by injection of blood cell-free plasma. Our finding thus highlights an essential role of hematopoietic autophagy for decelerating aging in non-hematopoietic organs.
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