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Rhod-2 (sodium salt)

目录号 : GC44828

A red fluorescent calcium indicator

Rhod-2 (sodium salt) Chemical Structure

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1mg
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产品描述

Rhod-2 (sodium salt) is a water-soluble, red fluorescent calcium indicator. It exhibits a significant shift in fluorescence intensity upon calcium binding (ex max = 549 nm; calcium-free v. ex/em max = 552/581 nm; calcium-bound). [1][2] Unlike the UV-excitable indicators fura-2 and indo-1 , there is no accompanying spectral shift.

Reference:
[1]. Paredes, R.M., Etzler, J.C., Watts, L.T., et al. Chemical calcium indicators. Methods 46(3), 143-151 (2008).
[2]. Minta, A., Kao, J.P., and Tsien, R.Y. Fluorescent indicators for cytosolic calcium based on rhodamine and fluorescein chromophores. The Journal of Biological Chemisty 264(14), 8171-8178 (1989).

Chemical Properties

Cas No. SDF
化学名 2,2'-((2-(2-(2-(bis(carboxylatomethyl)amino)-5-(6-(dimethylamino)-3-(dimethyliminio)-3H-xanthen-9-yl)phenoxy)ethoxy)-4-methylphenyl)azanediyl)diacetate, trisodium salt
Canonical SMILES CN(C)C(C=C1)=CC2=C1C(C3=CC=C(N(CC([O-])=O)CC([O-])=O)C(OCCOC4=C(N(CC([O-])=O)CC([O-])=O)C=CC(C)=C4)=C3)=C(C=C/5)C(O2)=CC5=[N+](C)\C.[Na+].[Na+].[Na+]
分子式 C40H39N4O11•3Na 分子量 820.7
溶解度 moderately soluble in water 储存条件 Store at -20°C
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1 mM 1.2185 mL 6.0924 mL 12.1847 mL
5 mM 0.2437 mL 1.2185 mL 2.4369 mL
10 mM 0.1218 mL 0.6092 mL 1.2185 mL
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Research Update

Mode of mitochondrial Ca2+ clearance and its influence on secretory responses in stimulated chromaffin cells

Cell Calcium 2006 Jan;39(1):35-46.PMID:16257445DOI:10.1016/j.ceca.2005.09.001.

To study the role of mitochondrial Ca(2+) clearance in stimulated cells, changes in free Ca(2+) concentration in the cytosol, [Ca(2+)](c) and that in mitochondria, [Ca(2+)](m) along with secretory responses were observed using chromaffin cells co-loaded with Fura-2 and Rhod-2 in the perfused rat adrenal medulla. When the cells were stimulated with 40 mM K(+) in the perfusate, the duration of [Ca(2+)](m) response markedly increased with prolongation of the stimulation period, exhibiting a mean half-decay time of 21 min with 30s stimulation, whereas its amplitude was not altered with stimulations of 10-30s. A computer simulation analysis showed that such a mode of [Ca(2+)](m) response can be produced if excess Ca(2+) taken up by mitochondria precipitates as calcium phosphate (Pi) salt. In the presence of 5 microM rotenone plus 10 microM oligomycin, a decrease in the duration of [Ca(2+)](m) response and a slight but significant increase (24%) in the secretory response to 30s stimulation with 40 mM K(+) were observed. Simulation analyses suggested that this effect of rotenone may be due to reduction in mitochondrial Ca(2+) uptake induced by rotenone-elicited partial depolarization of the mitochondrial membrane potential. In chromaffin cells transsynaptically stimulated through the splanchnic nerve, the intensity of NAD(P)H autofluorescence changed with time courses similar to those of [Ca(2+)](m) responses. The temporal profiles of those two responses were prolonged in a similar manner by application of an inhibitor of mitochondrial Na(+)/Ca(2+) exchanger, CGP37157. Thus, due to the unique Ca(2+) buffering mechanism, [Ca(2+)](m) responses associated with massive mitochondrial Ca(2+) uptake may occur within a limited concentration range in which Ca(2+)-sensitive dehydrogenases are activated to control the mitochondrial redox state in stimulated chromaffin cells.

Mitochondrial Ca2+ uptake and release influence metabotropic and ionotropic cytosolic Ca2+ responses in rat oligodendrocyte progenitors

J Physiol 1998 Apr 15;508 ( Pt 2)(Pt 2):413-26.PMID:9508806DOI:10.1111/j.1469-7793.1998.413bq.x.

1. Many physiologically important activities of oligodendrocyte progenitor cells (O-2A cells), including proliferation, migration and differentiation, are regulated by cytosolic Ca2+ signals. However, little is known concerning the mechanisms of Ca2+ signalling in this cell type. We have studied the interactions between Ca2+ entry, Ca2+ release from endoplasmic reticulum and Ca2+ regulation by mitochondria in influencing cytosolic Ca2+ responses in O-2A cells. 2. Methacholine (MCh; 100 microM) activated Ca2+ waves that propagated from several initiation sites along O-2A processes. 3. During a Ca2+ wave evoked by MCh, mitochondrial membrane potential was often either depolarized (21 % of mitochondria) or hyperpolarized (20 % of mitochondria), as measured by changes in the fluorescence of 5,5',6,6'-tetrachloro-1,1',3, 3'-tetraethylbenzimidazole carbocyanine iodide (JC-1). 4. Stimulation with kainate (100 microM) evoked a slowly rising, sustained cytosolic Ca2+ elevation in O-2A cells. This also, in some cases, resulted in either a depolarization (15 % of mitochondria) or hyperpolarization (12 % of mitochondria) of mitochondrial membrane potential. 5. Simultaneous measurement of cytosolic (fluo-3 AM) and mitochondrial (Rhod-2 AM) Ca2+ responses revealed that Ca2+ elevations in the cytosol evoked by either MCh or kainate were translated into long-lasting Ca2+ elevations in subpopulations of mitochondria. In some mitochondria, Ca2+ signals appeared to activate Ca2+ release into the cytosol. 6. Inhibition of the mitochondrial Na+-Ca2+ exchanger by CGP-37157 (25 microM) decreased kainate Ca2+ response amplitude and increased the rate of return of the response to basal Ca2+ levels. 7. Thus, both ionotropic and metabotropic stimulation evoke changes in mitochondrial membrane potential and Ca2+ levels in O-2A cells. Ca2+ uptake into some mitochondria is activated by Ca2+ entry into cells or release from stores. Mitochondrial Ca2+ release appears to play a key role in shaping kainate-evoked Ca2+ responses.