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Concanamycin AV-type (vacuolar) H+-ATPase inhibitor |
Sample solution is provided at 25 µL, 10mM.
Quality Control & MSDS
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- Purity ≥95.00%
- COA (Certificate Of Analysis)
- MSDS (Material Safety Data Sheet)
- Datasheet
Chemical structure
Related Biological Data
Cell experiment [1,2]: | |
Cell lines | HCT-116, DLD-1, Colo206F, HeLa cells, Androgen-dependent (LNCaP) and androgen-independent (C4-2B) cells. |
Preparation method | This compound is limited soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition | 20 nM, 60 min |
Applications | CCA effectively attenuated the TRAIL-induced activation of caspases in TRAIL-sensitive colorectal cancer cell lines. In CCA-treated Colo206F cells, the number of M30-positive apoptotic cells gradually increased and almost reached the proportion seen in untreated cells within 3–4h after the addition of TRAIL. Treatment with CCA resulted in a lack of apoptosis-related chromatin condensation in DLD-1 cells incubated with TRAIL for 90 min. Treatment with nanomolar concentrations of concanamycin A reduced the in vitro invasion in LNCaP and C4-2B cell types by 80%. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
References: [1]. Horova V, et al., Inhibition of vacuolar ATPase attenuates the TRAIL-induced activation of caspase-8 and modulates the trafficking of TRAIL receptosomes. FEBS J, 2013. 280(14). [2]. Michel V, et al., Inhibitors of vacuolar ATPase proton pumps inhibit human prostate cancer cell invasion and prostate-specific antigen expression and secretion. Int J Cancer. 2013.132(2). |
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Cas No. | 80890-47-7 | SDF | Download SDF |
Synonyms | N/A | ||
Chemical Name | N/A | ||
Canonical SMILES | CCC1C(C(CC(=CC=CC(C(OC(=O)C(=CC(=CC(C1O)C)C)OC)C(C)C(C(C)C2(CC(C(C(O2)C=CC)C)OC3CC(C(C(O3)C)OC(=O)N)O)O)O)OC)C)C)O | ||
Formula | C46H75NO14 | M.Wt | 866.09 |
Solubility | Limited solubility, soluble in DMSO | Storage | Store at -20°C |
Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
Concanamycin A is a specific inhibitor of vacuolar-type ATPase (V-ATPase) with IC50 value of 10 nM [1].
Vacuolar-type ATPase (V-ATPase) is expressed by clear cells to acidify the lumen of the epididymis, which is essential for male fertility; what"s more, it induced proton extrusion into the extracellular medium which contributes to maintaining the intracellular pH under an acidic microenvironment. V-ATPase has also been reported to involve in the process of acidificating microenvironment around/in solid tumors and inducing tumor invasion/multi-drug resistance in several malignant tumors. [2].
Concanamycin A (CMA) is a specific V-ATPase inhibitor and is different from the reported V-ATPase inhibitor SS33410. In oral squamous cell carcinoma (OSCC) OSCC cell lines (MISK81-5, SAS and HSC-4), low-concentration of CMA treatment induced the apoptosis of tumor cells [3]. Pretreated colorectal cancer cell lines with concanamycin A could significantly enhanced the Tumour necrosis factor (TNF) related apoptosis inducing ligand (TRAIL)-induced apoptosis by blocking endosomal acidification by V-ATPase [4]. When tested with prostate cancer cell line C4-2B, inhibition of V-ATPase by concanamycin A reduced 80% invasion in vitro [5].
Concanamycin A also had been reported as a potent inhibitor of CTL cytotoxicity via perforin-mediated cytotoxic pathway [6].
References: [1]. Huss, M., et al., Concanamycin A, the specific inhibitor of V-ATPases, binds to the V(o) subunit c. J Biol Chem, 2002. 277(43): p. 40544-8.[2]. Muroi, M., et al., Folimycin (concanamycin A), a specific inhibitor of V-ATPase, blocks intracellular translocation of the glycoprotein of vesicular stomatitis virus before arrival to the Golgi apparatus. Cell Struct Funct, 1993. 18(3): p. 139-49.[3]. Kiyoshima, T., et al., Chemoresistance to concanamycin A1 in human oral squamous cell carcinoma is attenuated by an HDAC inhibitor partly via suppression of Bcl-2 expression. PLoS One, 2013. 8(11).[4]. Horova V, et al., Inhibition of vacuolar ATPase attenuates the TRAIL-induced activation of caspase-8 and modulates the trafficking of TRAIL receptosomes. FEBS J, 2013. 280(14).[5]. Michel V, et al., Inhibitors of vacuolar ATPase proton pumps inhibit human prostate cancer cell invasion and prostate-specific antigen expression and secretion. Int J Cancer. 2013.132(2).[6]. Benkhoucha M et al., The neurotrophic hepatocyte growth factor attenuates CD8+ cytotoxic T-lymphocyte activity. J Neuroinflammation. 2013, 10.
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6个元素瓶子分别是:氰化锂、钴、金、钨、盐酸、镓。
其中我们需要的是氰化锂、金。
在楼下的一间屋子里用电脑打开一扇门。里面有个U-238试剂,回到大房间将“U238”放在最右边单独的位置,然后把“氰化锂”和“金”放在左边的两个位置上,打开电脑点第三项执行。然后退出看电脑后面的玻璃墙,会有一件盔甲从传送带上出来,拿起盔甲。
然后这里就有两条路线可走了,一是做出成果来拿给机器人看可以出去,然后机器人把你领到二楼老总办公室可以了解详细内容。二是按照另一个科学家的意思,打开安保系统强行闯出去。看你怎么选咯。
共杂了5张膜,其中两张是升级版的NylonN+,另外两张是Osmonics公司的MAGNA:NylonTransferMembrane,还有一张是之前碱转法杂交过的,结果很好的膜,拿来重复杂交用做阳性对照。
我们按照说明书上用10×SSC转24h,UV焦联800J,洗膜,预杂交6h后用标记了同位素的探针杂交过夜,洗膜40min,用盖格计数器扫描五张膜上计数都很明显,而且膜上不同的部位信号强度不同,当时估计肯定是杂上了,心里挺高兴的。
可是压磷屏24hour后,扫描结果除了五张白白的膜什么也看不到。
现在可以肯定的是:磷屏、同位素和标记试剂盒都没问题(因为用做Northern结果很好)。
这样一来就提出以下几个疑问:
1,如果是转膜的问题,为什么阳性对照那张膜也杂不出来呢?
2,如果是标记探针模板的问题,为什么我们的Marker(λDNA)也杂不出来呢?λDNA做模板应该不会出问题吧。
3,如果是扫描系统的问题为什么别人的都能扫出结果?
4,如果是磷屏坏了,为什么还能看到五张白白的膜,而不是漆黑一片?
5,如果没有杂交上,为什么用计数器扫描时计数都很明显,而且膜上不同的部位信号强度也不同?
6,如果这两种膜不能使用同位素,为什么原来用同位素杂的很好的阳性对照也没有结果呢?
做之前已经仔细的阅读了两种膜的说明书,加之以前的经验,本来感觉是十拿九稳的事。再者说NylonN+和MAGNA:NylonTransferMembrane这两种膜是不同公司生产的,性质上有一定差别,按道理两种膜都杂不出来的可能行应该很小才对。感觉好像就在压磷屏之后可能出了什么问题,明明是有信号的为什么杂不出来呢??
希望有经验的朋友帮助分析一下,发表一下意见,不胜感激!
(1)原发性骨肿瘤及骨肿瘤的软组织和肺转移的早期诊断;
(2)检查原因不明的骨痛;
(3)选择骨骼病理组织学检查部位;
(4)制定放疗计划;
(5)淋巴瘤、乳腺癌、肺癌、前列腺癌等其他系统肿瘤的术前分期及治疗后的随访;
(6)对可疑肿瘤患者进行筛选;
(7)骨骼炎性病变的诊断及随访;
(8)应力性骨折、缺血性骨坏死等骨关节创伤的鉴别诊断;
(9)Paget病的定位诊断及治疗后的随访。向左转|向右转
1:在工业探伤方面的应用
2:在火灾报警方面的应用
3:辐照技术在农业方面的应用
4:钢水液位测定方面的应用
5:安全保卫方面的应用
请尽量详细一点,谢谢!!!
由质子数相同,中子数不同的同种元素,形成同位素。
同位素的概念,仅仅用在元素层次,也就是原子层次。
在分子层次,在化合物的层次上,没有同位素的概念。
②、水是化合物,是由三种元素化合而成,对水来说,没有同位素的概念,
因此也就没有水的同位素的摩尔质量的说法。
③、楼主的问题应该是,水由氢、氧的不同同位素形成时的摩尔质量怎么算?
A、由氕 protium 形成的水是 H₂O,Mr = 18 grams。
B、由氘 deuterium 形成的水是 D₂O,Mr = 20 grams。
B、由氚 Tritium 形成的水是 T₂O,Mr = 22 grams。
上面是氢的最常见的同位素,氢一共有七种同位素。而氧元素,共有13种同位素。
由氢的不同同位素,跟氧的不同同位素,形成的同系物的水,供有91种。
这91种同系物的摩尔质量,比较好算,但是系统特征、性质,还没有人好好地
全部研究一遍。
2、德国人一生只会做几次放射线检查,而中国人高至每次看病都需要放射线检查,中国的国情决定了这样的结局,因为不查或者漏查,一旦发现新的问题,都是首诊医生的责任,患者及家属不答应的同时,严重者可以定性为医疗事故;
3、辐射最大的危害莫过于基因突变而导致的肿瘤,但一般来说一次的射线量不足以导致基因变异,但短时期内重复接受放射线检查无疑是重大危险因素;
4、为了自己和家人的健康,建议还是少做检查。如果就医时医生执意要求检查,可以请高年资医师确定是否有必要,或者根据自己的自身情况判断有无必要性,但这个过程一定是需要签字确认不同意的(中国的国情);
5、年轻人的基因有端粒酶的保护,年长者端粒酶几乎已经耗尽甚至变异,总的来说,不必过于担心,但也不要接受或者主动参与过度医疗。
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