CALCIUM CARBONATE-13C - CAS 287389-46-2
Catalog number: 287389-46-2
Category: Main Product
Molecular Formula:
CCaO3
Molecular Weight:
101.1
COA:
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Purity:
95%
Synonyms:
CALCIUM CARBONATE-13C; CALCIUM CARBONATE-13C, 99 ATOM % 13C
MSDS:
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Quantity:
Data not available, please inquire.
Melting Point:
825ºC(lit.)
InChIKey:
VTYYLEPIZMXCLO-YTBWXGASSA-L
InChI:
InChI=1S/CH2O3.Ca/c2-1(3)4;/h(H2,2,3,4);/q;+2/p-2/i1+1;
Canonical SMILES:
C(=O)([O-])[O-].[Ca+2]
1.Successful Treatment of Sodium Oxalate Induced Urolithiasis with HelichrysumFlowers.
Onaran M1, Orhan N2, Farahvash A1, Ekin HN2, Kocabıyık M3, Gönül İI4, Şen İ1, Aslan M5. J Ethnopharmacol. 2016 Apr 13. pii: S0378-8741(16)30194-5. doi: 10.1016/j.jep.2016.04.003. [Epub ahead of print]
ETHNOPHARMACOLOGICAL RELEVANCE: Helichrysum (Asteraceae) flowers, known as "altın otu, yayla çiçeği, kudama çiçeği", are widely used to remove kidney stones and for their diuretic properties in Turkey.
2.Influence of metabolic dysfunction on cardiac mechanics in decompensated hypertrophy and heart failure.
Tewari SG1, Bugenhagen SM2, Vinnakota KC1, Rice JJ3, Janssen PM4, Beard DA5. J Mol Cell Cardiol. 2016 Apr 13. pii: S0022-2828(16)30069-4. doi: 10.1016/j.yjmcc.2016.04.003. [Epub ahead of print]
Alterations in energetic state of the myocardium are associated with decompensated heart failure in humans and in animal models. However, the functional consequences of the observed changes in energetic state on mechanical function are not known. The primary aim of the study was to quantify mechanical/energetic coupling in the heart and to determine if energetic dysfunction can contribute to mechanical failure. A secondary aim was to apply a quantitative systems pharmacology analysis to investigate the effects of drugs that target cross-bridge cycling kinetics in heart failure-associated energetic dysfunction. Herein, a model of metabolite- and calcium-dependent myocardial mechanics was developed from calcium concentration and tension time courses in rat cardiac muscle obtained at different lengths and stimulation frequencies. The muscle dynamics model accounting for the effect of metabolites was integrated into a model of the cardiac ventricles to simulate pressure-volume dynamics in the heart.
3.α-Syntrophin is involved in the survival signaling pathway in myoblasts under menadione-induced oxidative stress.
Lim JA1, Choi SJ1, Moon JY1, Kim HS2. Exp Cell Res. 2016 Apr 13. pii: S0014-4827(16)30069-6. doi: 10.1016/j.yexcr.2016.04.001. [Epub ahead of print]
Dystrophin-deficient muscle is known to be more vulnerable to oxidative stress, but not much is known about the signaling pathway(s) responsible for this phenomenon. α-Syntrophin, a component of the dystrophin-glycoprotein complex, can function as a scaffold protein because of its multiple protein interaction domains. In this study, we investigated the role of α-syntrophin in C2 myoblasts under menadione-induced oxidative stress. We found that the protein level of α-syntrophin was elevated when cells were exposed to menadione. To investigate the function of α-syntrophin during oxidative stress, we established α-syntrophin-overexpressing and knockdown cell lines. The α-syntrophin-overexpressing cells were resistant to the menadione-induced oxidative stress. In addition, survival signalings such as protein kinase B (Akt) phosphorylation and the Bcl-2/BAX ratio were increased in these cells. On the other hand, apoptotic signals such as cleavage of caspase-3 and poly ADP ribose polymerase (PARP) were increased in the α-syntrophin knockdown cells.
4.Deoxycholic acid mediates non-canonical EGFR-MAPK activation through the induction of calcium signaling in colon cancer cells.
Centuori SM1, Gomes CJ2, Trujillo J2, Borg J1, Brownlee J1, Putnam CW3, Martinez JD4. Biochim Biophys Acta. 2016 Apr 13. pii: S1388-1981(16)30100-7. doi: 10.1016/j.bbalip.2016.04.006. [Epub ahead of print]
Obesity and a western diet have been linked to high levels of bile acids and the development of colon cancer. Specifically, increased levels of the bile acid deoxycholic acid (DCA), an established tumor promoter, has been shown to correlate with increased development of colorectal adenomas and progression to carcinoma. Herein we investigate the mechanism by which DCA leads to EGFR-MAPK activation, a candidate mechanism by which DCA may promote colorectal tumorigenesis. DCA treated colon cancer cells exhibited strong and prolonged activation of ERK1/2 when compared to EGF treatment alone. We also showed that DCA treatment prevents EGFR degradation as opposed to the canonical EGFR recycling observed with EGF treatment. Moreover, the combination of DCA and EGF treatment displayed synergistic activity, suggesting DCA activates MAPK signaling in a non-canonical manner. Further evaluation showed that DCA treatment increased intracellular calcium levels and CAMKII phosphorylation, and that blocking calcium with BAPTA-AM abrogated MAPK activation induced by DCA, but not by EGF.
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