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Chemical Compound Review

rhod-2     [2-[2-[2- (bis(carboxymethyl)amino)- 5...

Synonyms: Rhod 2-AM, AC1L3X2S, 132523-91-2, Rhod 2 fluorescent dye
This record was replaced with 123670.
 
 
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Disease relevance of [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium

 

High impact information on [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium

  • We imaged the activity of astrocytes labeled with the calcium (Ca(2+))-sensitive indicator rhod-2 in somatosensory cortex of adult mice [4].
  • In addition, we find that rhod-2 labels mitochondria in T cells, and it reports changes in Ca2+ levels that are consistent with its localization in the TG-insensitive store [5].
  • We used the action potential voltage-clamp technique on ventricular myocytes loaded with indo 1 or rhod 2, both Ca2+ indicators, to study the relation between action potential duration, ICa-L, and cell shortening (inotropic effect) [6].
  • Measurement of [Ca2+]i by use of rhod 2 showed that changes in the rate of rise of the [Ca2+]i transient (which in rat ventricle is due to the rate of Ca2+ release from the sarcoplasmic reticulum) were closely correlated with changes in the magnitude and the time course of ICa-L.(ABSTRACT TRUNCATED AT 400 WORDS)[6]
  • Successful transfection was verified in single cells by detection of GFP, and intracellular Ca2+ ([Ca]i) changes were simultaneously monitored with rhod-2 [7].
 

Biological context of [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium

 

Anatomical context of [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium

  • Applying imaging and single-cell photometric methods, we find that the probe rhod-2 selectively localizes to mitochondria and uses its responses to quantify mitochondrial free [Ca2+] (Cam) [13].
  • We used SEER (shifted excitation and emission ratioing of fluorescence) of SR-trapped mag-indo-1 and confocal imaging of fluorescence of cytosolic rhod-2 to image Ca2+ sparks while reversibly changing and measuring [Ca2+] in the SR ([Ca2+]SR) of membrane-permeabilized frog skeletal muscle cells [14].
  • 1. The Ca(2+)-sensitive fluorescent indicator rhod-2 was used to monitor mitochondrial Ca2+ concentration ([Ca2+]m) in gastric smooth muscle cells from Bufo marinus [15].
  • IL-6 induced an increase in inner mitochondrial membrane polarisation and increased mitochondrial Ca2+ loading (rhod-2 fluorescence) at baseline, but prevented the reperfusion-induced changes in mitochondrial function [16].
  • 1. The Ca2+-sensitive fluorescent indicator rhod-2 was used to measure mitochondrial [Ca2+] ([Ca2+]m) in single smooth muscle cells from the rat pulmonary artery, while simultaneously monitoring cytosolic [Ca2+] ([Ca2+]i) with fura-2 [17].
 

Associations of [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium with other chemical compounds

  • Using Calcium Green-1 and rhod-2 as optical measures of cytoplasmic and mitochondrial free Ca(2+), we show that mitochondria sequester Ca(2+) and tune the frequency of [Ca(2+)](cyt) oscillations in rat gonadotropes [18].
  • In parallel, monitoring of mitochondrial Ca(2+) during stress, via the specific indicator rhod-2, revealed a significant attenuation of Ca(2+) accumulation in mitochondria overexpressing K(+) channels [19].
  • Luminometry of healthy fibroblasts expressing either aequorin or luciferase in the mitochondrial matrix showed that rhod-2 dose dependently decreased the Bk-induced increase in [Ca2+]M and [ATP]M by maximally 80 and 90%, respectively [20].
  • The effects of uncouplers were investigated in perfused mouse hearts labeled with rhod-2/AM or 4-[beta-[2-(di-n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) to map [Ca(2+)](i) transients (emission wavelength = 585 +/- 20 nm) and action potentials (APs) (emission wavelength > 610 nm; excitation wavelength = 530 +/- 20 nm) [21].
  • Exposing cells to ouabain (1 mM) evoked mitochondrial Ca2+ overload and increased the intensity of rhod-2 fluorescence to 180+/-15% of baseline ( p<0.001) [22].
 

Gene context of [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium

  • Individual mitochondria of rhod-2 loaded acinar cells showed heterogeneous matrix Ca(2+) concentration increases in response to oscillatory and maximal levels of cholecystokinin octapeptide [23].
  • Moreover, CCK did not affect NMDA-induced Ca2+ influx measured with rhod-2, a fluorescent Ca2+ indicator [24].
  • Staining of calcium stores with rhod-2 showed a TMT-induced [Ca2+]i-decrease in the stores followed by an increase of the calcium concentration in the nuclei of the two cell lines tested [3].
 

Analytical, diagnostic and therapeutic context of [2-[2-[2-(bis(carboxymethyl)amino)-5-methyl-phenoxy]ethoxy]-4-[3,6-bis(dimethylamino)xanthen-9-ylidene]-1-cyclohexa-2,5-dienylidene]-bis(carboxymethyl)ammonium

  • Mitochondrial [Ca2+] (measured with rhod-2 and confocal microscopy) increased during repeated tetanic stimulation in CK-/- but not in wild-type FDB fibres [25].
  • (3) Isolated rabbit hearts were subjected to I/R, and [Ca(2+)](i) was recorded by surface rhod-2 spectrofluorometry [26].
  • 8. Changes in [Ca(2+)](i) in an acidic medium were determined in hippocampal slices by microfluorometry using rhod-2 acetoxymethyl ester as a Ca(2+) marker, and the effects of dexamethasone (240 microg/l) was evaluated [27].
  • In 16 slices loaded with rhod-2 through the perfusion medium, tetanic stimulation of theta-burst type was applied to layer IV of the cortex and changes in Ca2+ concentration were analyzed in layer II/III from which field potentials to test stimulation of layer IV were recorded simultaneously [2].

References

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  2. Long-term depression in rat visual cortex is associated with a lower rise of postsynaptic calcium than long-term potentiation. Yasuda, H., Tsumoto, T. Neurosci. Res. (1996) [Pubmed]
  3. Modulation of intracellular calcium homeostasis by trimethyltin chloride in human tumour cells: neuroblastoma SY5Y and cervix adenocarcinoma HeLa S3. Florea, A.M., Splettstoesser, F., Dopp, E., Rettenmeier, A.W., Büsselberg, D. Toxicology (2005) [Pubmed]
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  5. Mitochondrial regulation of store-operated calcium signaling in T lymphocytes. Hoth, M., Fanger, C.M., Lewis, R.S. J. Cell Biol. (1997) [Pubmed]
  6. Effects of action potential duration on excitation-contraction coupling in rat ventricular myocytes. Action potential voltage-clamp measurements. Bouchard, R.A., Clark, R.B., Giles, W.R. Circ. Res. (1995) [Pubmed]
  7. Identification of the erythropoietin receptor domain required for calcium channel activation. Miller, B.A., Barber, D.L., Bell, L.L., Beattie, B.K., Zhang, M.Y., Neel, B.G., Yoakim, M., Rothblum, L.I., Cheung, J.Y. J. Biol. Chem. (1999) [Pubmed]
  8. Kainate receptor-mediated inhibition of presynaptic Ca2+ influx and EPSP in area CA1 of the rat hippocampus. Kamiya, H., Ozawa, S. J. Physiol. (Lond.) (1998) [Pubmed]
  9. Cytosolic Ca2+ triggers early afterdepolarizations and Torsade de Pointes in rabbit hearts with type 2 long QT syndrome. Choi, B.R., Burton, F., Salama, G. J. Physiol. (Lond.) (2002) [Pubmed]
  10. Simultaneous maps of optical action potentials and calcium transients in guinea-pig hearts: mechanisms underlying concordant alternans. Choi, B.R., Salama, G. J. Physiol. (Lond.) (2000) [Pubmed]
  11. Two-photon molecular excitation imaging of Ca2+ transients in Langendorff-perfused mouse hearts. Rubart, M., Wang, E., Dunn, K.W., Field, L.J. Am. J. Physiol., Cell Physiol. (2003) [Pubmed]
  12. Sperm mobility: deduction of a model explaining phenotypic variation in roosters (Gallus domesticus). Froman, D.P., Wardell, J.C., Feltmann, A.J. Biol. Reprod. (2006) [Pubmed]
  13. Mitochondrial participation in the intracellular Ca2+ network. Babcock, D.F., Herrington, J., Goodwin, P.C., Park, Y.B., Hille, B. J. Cell Biol. (1997) [Pubmed]
  14. The changes in Ca2+ sparks associated with measured modifications of intra-store Ca2+ concentration in skeletal muscle. Launikonis, B.S., Zhou, J., Santiago, D., Brum, G., Ríos, E. J. Gen. Physiol. (2006) [Pubmed]
  15. Mitochondrial Ca2+ homeostasis during Ca2+ influx and Ca2+ release in gastric myocytes from Bufo marinus. Drummond, R.M., Mix, T.C., Tuft, R.A., Walsh, J.V., Fay, F.S. J. Physiol. (Lond.) (2000) [Pubmed]
  16. IL-6 induces PI 3-kinase and nitric oxide-dependent protection and preserves mitochondrial function in cardiomyocytes. Smart, N., Mojet, M.H., Latchman, D.S., Marber, M.S., Duchen, M.R., Heads, R.J. Cardiovasc. Res. (2006) [Pubmed]
  17. Release of Ca2+ from the sarcoplasmic reticulum increases mitochondrial [Ca2+] in rat pulmonary artery smooth muscle cells. Drummond, R.M., Tuft, R.A. J. Physiol. (Lond.) (1999) [Pubmed]
  18. Mitochondria shape hormonally induced cytoplasmic calcium oscillations and modulate exocytosis. Kaftan, E.J., Xu, T., Abercrombie, R.F., Hille, B. J. Biol. Chem. (2000) [Pubmed]
  19. Targeted expression of Kir6.2 in mitochondria confers protection against hypoxic stress. Ljubkovic, M., Marinovic, J., Fuchs, A., Bosnjak, Z.J., Bienengraeber, M. J. Physiol. (Lond.) (2006) [Pubmed]
  20. Ca2+-mobilizing agonists increase mitochondrial ATP production to accelerate cytosolic Ca2+ removal: aberrations in human complex I deficiency. Visch, H.J., Koopman, W.J., Zeegers, D., van Emst-de Vries, S.E., van Kuppeveld, F.J., van den Heuvel, L.W., Smeitink, J.A., Willems, P.H. Am. J. Physiol., Cell Physiol. (2006) [Pubmed]
  21. Effects of mechanical uncouplers, diacetyl monoxime, and cytochalasin-D on the electrophysiology of perfused mouse hearts. Baker, L.C., Wolk, R., Choi, B.R., Watkins, S., Plan, P., Shah, A., Salama, G. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  22. Nicorandil attenuates the mitochondrial Ca2+ overload with accompanying depolarization of the mitochondrial membrane in the heart. Ishida, H., Higashijima, N., Hirota, Y., Genka, C., Nakazawa, H., Nakaya, H., Sato, T. Naunyn Schmiedebergs Arch. Pharmacol. (2004) [Pubmed]
  23. Role of mitochondria in Ca(2+) oscillations and shape of Ca(2+) signals in pancreatic acinar cells. Camello-Almaraz, C., Salido, G.M., Pariente, J.A., Camello, P.J. Biochem. Pharmacol. (2002) [Pubmed]
  24. Mechanisms of cholecystokinin-induced protection of cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity. Tamura, Y., Sato, Y., Akaike, A., Shiomi, H. Brain Res. (1992) [Pubmed]
  25. Mitochondrial function in intact skeletal muscle fibres of creatine kinase deficient mice. Bruton, J.D., Dahlstedt, A.J., Abbate, F., Westerblad, H. J. Physiol. (Lond.) (2003) [Pubmed]
  26. Cytosolic calcium in the ischemic rabbit heart: assessment by pH- and temperature-adjusted rhod-2 spectrofluorometry. Stamm, C., Friehs, I., Choi, Y.H., Zurakowski, D., McGowan, F.X., del Nido, P.J. Cardiovasc. Res. (2003) [Pubmed]
  27. Suppression of sodium pump activity and an increase in the intracellular Ca2+ concentration by dexamethasone in acidotic mouse brain. Namba, C., Adachi, N., Liu, K., Yorozuya, T., Arai, T. Brain Res. (2002) [Pubmed]
 
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