The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

SureCN1374716     2- [acetyloxymethoxycarbonylmethy l-[2-[2-[2...

Synonyms: AC1MHY51, LS-187588, 139890-68-9
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of BAPTA-AM

  • Activation of NF-kappaB is attenuated by pertussis toxin and inhibitors of protein kinase C, and it is completely blocked by the Ca2+ chelator BAPTA-AM [1].
  • Further examinations revealed that TRPV1-induced toxicity was accompanied by increases in intracellular Ca(2+), and mitochondrial damage; these effects were inhibited by capsazepine, I-RTX, and the intracellular Ca(2+) chelator BAPTA-AM [2].
  • The exit of vesicular stomatitis virus G from a pre-Golgi compartment and the exit of Shiga toxin from an endosomal compartment are sensitive to the membrane-permeant calcium chelator 1,2-bis(2-amino phenoxy)ethane-N,N,N',N'-tetraacetic acid-tetrakis (acetoxymethyl ester) (BAPTA-AM) [3].
  • Hypoxia to ECs increased ERK phosphorylation within 10 min and which was abolished by administration of PD98095, calphostin C, and BAPTA/AM [4].
  • 2. STDs and SWs persisted in the presence of tetrodotoxin, nifedipine and ryanodine, and upon brief exposure to Ca2+-free Cd2+-containing solutions; they were enhanced by ACh and blocked by BAPTA AM, cyclopiazonic acid and caffeine [5].

High impact information on BAPTA-AM


Chemical compound and disease context of BAPTA-AM

  • METHODS: To resolve the mechanism of TG induced growth arrest, rat AT3.1 prostatic cancer cells were analyzed for RNA and protein expression of the growth arrest gene, gadd153, intracellular free Ca2+ levels (Cai), and cell cycle distribution on exposure to TG alone and in combination with Ca2+ chelation induced by BAPTA-AM or BAPTA-AM/EGTA [11].
  • Calcium ions play an important role in veratridine-induced chromaffin cell death because the cell permeant Ca(2+) chelator BAPTA-AM and extracellular Ca(2+) removal completely prevented veratridine-induced toxicity [12].
  • Both DNA synthesis and phosphorylation of MAPK in response to SP were attenuated by pretreatment with pertussis toxin, genistein, D609, U73122, staurosporine, removal of Ca(2+) by BAPTA/AM plus EGTA, PD98059, and SB202190 [13].
  • The effect of the membrane-permeant calcium chelator 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA/AM) on ionomycin-induced cellular calcium overload was studied in single differentiated NH15-CA2 neuroblastoma x glioma hybrid cells [14].
  • Glucose deprivation and hypoxia decreased (Na(+)+K+)-ATPase activity in the absence of extracellular Ca2+, but the effects were blocked by 1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid tetra-acetomethyl ester (BAPTA-AM), a chelator of intracellular Ca2+ [15].

Biological context of BAPTA-AM

  • Cotreatment of growth plate chondrocytes with RA and BAPTA-AM, a cell permeable Ca2+ chelator, inhibited the up-regulation of annexin gene expression and mineralization of these cultures [16].
  • This effect was largely overcome by loading cells with BAPTA-AM, highlighting the importance of mitochondrial Ca2+ buffering in shaping the release kinetics [17].
  • An interesting finding was that acute treatment of cells with BAPTA-AM activated capacitative Ca2+ entry at the plasma membrane, due to its efficient hydrolysis in the stores, and the ensuing decrease in the endoplasmic reticulum [Ca2+] [18].
  • Buffering the Ca(2+) increase with the cytoplasmic Ca(2+) chelator BAPTA-AM [1,2-bis(2-aminophenoxy)ethane-N,N,N1,N-tetraacetic acid] blocks RC3-induced apoptosis, indicating that the rise in intracellular Ca(2+) is required for apoptotic death [19].
  • This increase in permeability was inhibited completely by chelation of intracellular calcium ions by BAPTA-AM and inhibition of calmodulin activity and myosin light chain (MLC) phosphorylation [20].

Anatomical context of BAPTA-AM

  • Furthermore, we show that L1- and K+(-)dependent neurite outgrowth can be specifically inhibited by a reduction in extracellular calcium to 0.25 microM, and by pretreatment of cerebellar neurons with the intracellular calcium chelator BAPTA/AM [21].
  • Additionally, the response could be fully inhibited by preloading PC12 cells with BAPTA/AM which buffers changes in intracellular calcium [22].
  • Both responses were significantly reduced by pre-treatment with sarco-endoplasmic reticulum Ca(2+) ATPase (SERCA) pump inhibitors or with the intracellular Ca(2+) chelator BAPTA-AM [23].
  • Pretreatment of myocytes with the intracellular Ca2+ chelator BAPTA-AM prevented the ATP-stimulated increase in cytosolic Ca2+ and attenuated the ATP-stimulated increase in c-fos expression [24].
  • Omission of Ca2+ from the incubation medium or loading synaptosomes with the Ca2+ chelator BAPTA-AM (20 and 100 mumol/L) prevented NE release, indicating a Ca(2+)-dependent mechanism [25].

Associations of BAPTA-AM with other chemical compounds


Gene context of BAPTA-AM

  • Akt activation is abolished by the phospholipase C-gamma inhibitor U-73122, by the intracellular calcium chelator BAPTA-AM, and by the specific calmodulin antagonist W-7 [30].
  • GnRH-induced JNK activity was reduced after treatment with the intracellular calcium chelator BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester), whereas activation of ERK was not affected [31].
  • Moreover, the effect of this compound on CYP1A1 was strongly abolished in the presence of BAPTA-AM, a well known chelator of intracellular calcium, and 2-aminoethyl diphenylborate, an inhibitor of store-operated calcium channels [32].
  • An increase in intracellular calcium with the calcium ionophore A23187 or intracellular calcium chelation by BAPTA-AM had no effect on either basal or FXa-induced VEGF secretion, suggesting that the calcium signaling pathway was not sufficient to induce VEGF secretion [33].
  • Intracellular Ca(2+) chelator BAPTA/AM or cyclic adenosine monophosphate (cAMP)-dependent protein kinase inhibitor H-89 partially blocked the inhibitory effects of PGE(2) on CCL27 production and NF-kappaB activity, and the addition of both completely abrogated the inhibition [34].

Analytical, diagnostic and therapeutic context of BAPTA-AM


  1. Lysophosphatidic acid activates NF-kappaB in fibroblasts. A requirement for multiple inputs. Shahrestanifar, M., Fan, X., Manning, D.R. J. Biol. Chem. (1999) [Pubmed]
  2. Transient Receptor Potential Vanilloid Subtype 1 Mediates Microglial Cell Death In Vivo and In Vitro via Ca2+-Mediated Mitochondrial Damage and Cytochrome c Release. Kim, S.R., Kim, S.U., Oh, U., Jin, B.K. J. Immunol. (2006) [Pubmed]
  3. Selective effects of calcium chelators on anterograde and retrograde protein transport in the cell. Chen, J.L., Ahluwalia, J.P., Stamnes, M. J. Biol. Chem. (2002) [Pubmed]
  4. Endothelial exposure to hypoxia induces Egr-1 expression involving PKCalpha-mediated Ras/Raf-1/ERK1/2 pathway. Lo, L.W., Cheng, J.J., Chiu, J.J., Wung, B.S., Liu, Y.C., Wang, D.L. J. Cell. Physiol. (2001) [Pubmed]
  5. Role of calcium stores and membrane voltage in the generation of slow wave action potentials in guinea-pig gastric pylorus. van Helden, D.F., Imtiaz, M.S., Nurgaliyeva, K., von der Weid, P., Dosen, P.J. J. Physiol. (Lond.) (2000) [Pubmed]
  6. Nitric oxide induces coupling of mitochondrial signalling with the endoplasmic reticulum stress response. Xu, W., Liu, L., Charles, I.G., Moncada, S. Nat. Cell Biol. (2004) [Pubmed]
  7. A novel signaling mechanism between gas and blood compartments of the lung. Kuebler, W.M., Parthasarathi, K., Wang, P.M., Bhattacharya, J. J. Clin. Invest. (2000) [Pubmed]
  8. Native low density lipoprotein-induced calcium transients trigger VCAM-1 and E-selectin expression in cultured human vascular endothelial cells. Allen, S., Khan, S., Al-Mohanna, F., Batten, P., Yacoub, M. J. Clin. Invest. (1998) [Pubmed]
  9. Peptidergic activation of transcription and secretion in chromaffin cells. Cis and trans signaling determinants of pituitary adenylyl cyclase-activating polypeptide (PACAP). Taupenot, L., Mahata, S.K., Wu, H., O'Connor, D.T. J. Clin. Invest. (1998) [Pubmed]
  10. Endothelin (ET)-3 stimulates cyclic guanosine 3',5'-monophosphate production via ETB receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells. Owada, A., Tomita, K., Terada, Y., Sakamoto, H., Nonoguchi, H., Marumo, F. J. Clin. Invest. (1994) [Pubmed]
  11. Mechanism and role of growth arrest in programmed (apoptotic) death of prostatic cancer cells induced by thapsigargin. Lin, X.S., Denmeade, S.R., Cisek, L., Isaacs, J.T. Prostate (1997) [Pubmed]
  12. Veratridine induces apoptotic death in bovine chromaffin cells through superoxide production. Jordán, J., Galindo, M.F., Calvo, S., González-García, C., Ceña, V. Br. J. Pharmacol. (2000) [Pubmed]
  13. Substance P-induced activation of p42/44 mitogen-activated protein kinase associated with cell proliferation in human tracheal smooth muscle cells. Yang, C.M., Hsiao, L.D., Chien, C.S., Lin, C.C., Luo, S.F., Wang, C.C. Cell. Signal. (2002) [Pubmed]
  14. Intracellular calcium chelator BAPTA protects cells against toxic calcium overload but also alters physiological calcium responses. Collatz, M.B., Rüdel, R., Brinkmeier, H. Cell Calcium (1997) [Pubmed]
  15. Glucose and oxygen deprivation induces a Ca(2+)-mediated decrease in (Na(+)+K+)-ATPase activity in rat brain slices. Matsuda, T., Shimizu, I., Murata, Y., Baba, A. Brain Res. (1992) [Pubmed]
  16. Retinoic acid stimulates annexin-mediated growth plate chondrocyte mineralization. Wang, W., Kirsch, T. J. Cell Biol. (2002) [Pubmed]
  17. Ca2+ homeostasis in the agonist-sensitive internal store: functional interactions between mitochondria and the ER measured In situ in intact cells. Landolfi, B., Curci, S., Debellis, L., Pozzan, T., Hofer, A.M. J. Cell Biol. (1998) [Pubmed]
  18. Free [Ca2+] dynamics measured in agonist-sensitive stores of single living intact cells: a new look at the refilling process. Hofer, A.M., Landolfi, B., Debellis, L., Pozzan, T., Curci, S. EMBO J. (1998) [Pubmed]
  19. Transcriptional program of apoptosis induction following interleukin 2 deprivation: identification of RC3, a calcium/calmodulin binding protein, as a novel proapoptotic factor. Devireddy, L.R., Green, M.R. Mol. Cell. Biol. (2003) [Pubmed]
  20. Transient and prolonged increase in endothelial permeability induced by histamine and thrombin: role of protein kinases, calcium, and RhoA. van Nieuw Amerongen, G.P., Draijer, R., Vermeer, M.A., van Hinsbergh, V.W. Circ. Res. (1998) [Pubmed]
  21. Calcium influx into neurons can solely account for cell contact-dependent neurite outgrowth stimulated by transfected L1. Williams, E.J., Doherty, P., Turner, G., Reid, R.A., Hemperly, J.J., Walsh, F.S. J. Cell Biol. (1992) [Pubmed]
  22. Thy-1 antibody-triggered neurite outgrowth requires an influx of calcium into neurons via N- and L-type calcium channels. Doherty, P., Singh, A., Rimon, G., Bolsover, S.R., Walsh, F.S. J. Cell Biol. (1993) [Pubmed]
  23. Asymmetrical, agonist-induced fluctuations in local extracellular [Ca(2+)] in intact polarized epithelia. Caroppo, R., Gerbino, A., Debellis, L., Kifor, O., Soybel, D.I., Brown, E.M., Hofer, A.M., Curci, S. EMBO J. (2001) [Pubmed]
  24. Extracellular ATP induces immediate-early gene expression but not cellular hypertrophy in neonatal cardiac myocytes. Zheng, J.S., Boluyt, M.O., O'Neill, L., Crow, M.T., Lakatta, E.G. Circ. Res. (1994) [Pubmed]
  25. Role of Ca2+ in metabolic inhibition-induced norepinephrine release in rat brain synaptosomes. Du, X.J., Bobik, A., Little, P.J., Esler, M.D., Dart, A.M. Circ. Res. (1997) [Pubmed]
  26. Role of Ca2+ and protein kinase C in shear stress-induced actin depolymerization and endothelin 1 gene expression. Morita, T., Kurihara, H., Maemura, K., Yoshizumi, M., Nagai, R., Yazaki, Y. Circ. Res. (1994) [Pubmed]
  27. Angiotensin II and other hypertrophic stimuli mediated by G protein-coupled receptors activate tyrosine kinase, mitogen-activated protein kinase, and 90-kD S6 kinase in cardiac myocytes. The critical role of Ca(2+)-dependent signaling. Sadoshima, J., Qiu, Z., Morgan, J.P., Izumo, S. Circ. Res. (1995) [Pubmed]
  28. Insulin inhibits secretin-induced ductal secretion by activation of PKC alpha and inhibition of PKA activity. Lesage, G.D., Marucci, L., Alvaro, D., Glaser, S.S., Benedetti, A., Marzioni, M., Patel, T., Francis, H., Phinizy, J.L., Alpini, G. Hepatology (2002) [Pubmed]
  29. Vasopressin-induced disruption of actin cytoskeletal organization and canalicular function in isolated rat hepatocyte couplets: possible involvement of protein kinase C. Roma, M.G., Stone, V., Shaw, R., Coleman, R. Hepatology (1998) [Pubmed]
  30. Calmodulin-mediated activation of Akt regulates survival of c-Myc-overexpressing mouse mammary carcinoma cells. Deb, T.B., Coticchia, C.M., Dickson, R.B. J. Biol. Chem. (2004) [Pubmed]
  31. Divergent signaling pathways requiring discrete calcium signals mediate concurrent activation of two mitogen-activated protein kinases by gonadotropin-releasing hormone. Mulvaney, J.M., Roberson, M.S. J. Biol. Chem. (2000) [Pubmed]
  32. Transcriptional induction of CYP1A1 by oltipraz in human Caco-2 cells is aryl hydrocarbon receptor- and calcium-dependent. Le Ferrec, E., Lagadic-Gossmann, D., Rauch, C., Bardiau, C., Maheo, K., Massiere, F., Le Vee, M., Guillouzo, A., Morel, F. J. Biol. Chem. (2002) [Pubmed]
  33. Vascular endothelial growth factor production by fibroblasts in response to factor VIIa binding to tissue factor involves thrombin and factor Xa. Ollivier, V., Chabbat, J., Herbert, J.M., Hakim, J., de Prost, D. Arterioscler. Thromb. Vasc. Biol. (2000) [Pubmed]
  34. Prostaglandin E(2) suppresses CCL27 production through EP2 and EP3 receptors in human keratinocytes. Kanda, N., Mitsui, H., Watanabe, S. J. Allergy Clin. Immunol. (2004) [Pubmed]
  35. Processes that remove calcium from the cytoplasm during excitation-contraction coupling in intact rat heart cells. Balke, C.W., Egan, T.M., Wier, W.G. J. Physiol. (Lond.) (1994) [Pubmed]
  36. Calcium dependence of rapid astrocyte death induced by transient hypoxia, acidosis, and extracellular ion shifts. Bondarenko, A., Chesler, M. Glia (2001) [Pubmed]
  37. 1,2-bis(2-Aminophenoxy)ethane-N,N,N',N'-tetraacetic acid induces caspase-mediated apoptosis and reactive oxygen species-mediated necrosis in cultured cortical neurons. Han, K.S., Kang, H.J., Kim, E.Y., Yoon, W.J., Sohn, S., Kwon, H.J., Gwag, B.J. J. Neurochem. (2001) [Pubmed]
  38. Preparation, characterization and utility of a novel antibody for resolving the spatial and temporal dynamics of the calcium chelator BAPTA. Tymianski, M., Sattler, R., Bernstein, G., Jones, O.T. Cell Calcium (1997) [Pubmed]
  39. Activation of deoxycytidine kinase in lymphocytes is calcium dependent and involves a conformational change detectable by native immunostaining. Keszler, G., Spasokoukotskaja, T., Csapo, Z., Talianidis, I., Eriksson, S., Staub, M., Sasvari-Szekely, M. Biochem. Pharmacol. (2004) [Pubmed]
WikiGenes - Universities