BAPTA AM

1 -phenylene)]bis [N- [2- [(acetyloxy)methoxy]-2-ox-oethyl]-, l,l -bis[(acetyloxy)methyl] ester Other Names l,2-Bis(2-aminophenoxy)ethane-A,A,A, A -tetraacetic acid tetrakis(acetoxymethyl ester) Glycine, A, A - [ 1,2-ethanediylbis(oxy-2,1 -phenylene)]bis [A- [2-[(acetyloxy)methoxy]-2-oxoethyl]-, bis[(acetyloxy)meth-yl] ester BAPTA-AM 

Staining Applications Calcium ions fungi motor neurons  

Biological Applications Calcium indicators treating cancer, chronic bacterial infection, glaucoma, ocular hypertension, HTV-associated conditions, infectious diseases, neurodegenerative disorders, neurological conditions, psychiatric conditions Industrial Applications Not reported 

Safety/Toxicity Cytotoxicity neurotoxicity renal toxicity 

Preparation and properties of calcium-specific, long-wavelength indicator dyes. Eur. Pat. Appl. EP 314480 1989 Chem. Abstr. 1990, 112, 135620. 

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Many of these intracellular events are critical to the prohferative effects of CXCL12. For example, the CXCL12-induced effect on proliferation is dependent on calcium. Pre-treatment of pituitary adenoma cells with BAPTA-AM abohshes the CXCL12-induced increase in prohferation (Florio et al. 2006). The increase in proliferation also requires activation of Erk 1/2, as pre-treatment with PD98059, a MEK inhibitor, blocks the proliferative effect of CXCL12, and this is correlated with a decrease in Erk 1/2 phosphorylation. Similarly, the proliferative effects of... 

BAPTA-AM l,2-Bis(0-aminophenoxy)ethane-N, MI Af -tetraacetic acid tetra(acetoxymethyl) ester... 

Figure 2 Effect of removal of intracellular and extracellular calcium on induction of tyrosine hydroxylase mRNA in PC12 cells by hypoxia, (a) Cells were exposed to normoxia (C, 21% O2, 6 hr) or hypoxia (H, 5% O2, 6 hr) in normal serum-free medium or to hypoxia in Ca -free medium supplemented with 1 mM EGTA. (b) Same experiment as in panel a except, in addition, cells were preloaded with the indicated amount of BAPTA-AM for 40 min prior to hypoxia exposure to chelate intracellular calcium.

Figure 8 CREB phosphorylation by hypoxia does not require Ca, PCK, RSK-2, MAPK, or p38. Cells were pretreated with various drugs or vehicle (0.1% dimethyl sulfoxide) as indicated. Cells were then exposed to either normoxia (C, 21% O2) or hypoxia (H, 5% O2) for 6 hr, and whole-cell lysates were immunoblotted with an antibody specific for Ser phospho-CREB. (a) Cells were preincubated for 40 min in serum-fi ee medium in the presence of Ca and vehicle (—) or in serum-iree medium formulated without Ca and supplemented with 1 mM EGTA-I-100 pM BAPTA-AM (-h). The medium was then replaced (minus drug or vehicle) and cells were exposed to either normoxia or hypoxia, (b) Cells were pretreated for 40 min in serum-free medium with either vehicle (—) or 20 pM chelerythrine chloride, an inhibitor of PKC (CHL -P), and exposed to either normoxia or hypoxia, (c) Cells were pretreated for 40 min in serum-fi ee medium with either vehicle (—) or 0.3 pM Ro 31-8220, an inhibitor of RSK and p70 S6 kinase (-P), and exposed to either normoxia or hypoxia, (d) Cells were pretreated for 40 min in serum-lree medium with either vehicle (—) or 50 pM PD098059, an inhibitor of MEKl and the downstream MAPKS (-P), and exposed to either normoxia or hypoxia, (e) Cells were pretreated for 1 hr in serum-fiee medium with either vehicle (—) or 10 nM rapamycin, an inhibitor of p70 S6 kinase (-P), and exposed to either normoxia or hypoxia, (f) Cells were pretreated for 1 hr in serum-fiee medium with either vehicle (—) or 20 pM SB203580, an inhibitor of p38a kinase and MAPKAP kinase (-P), and then exposed to either normoxia or hypoxia. In all of these experiments, hypoxia did not alter the total levels of CREB.

The influence of Cd on physiological Ca " signaling has been reviewed elsewhere [460] and the role of Ca in Cd -induced ceU death is detailed in Section 5.5.4.2. Many groups have reported the release of Ca " following Cd " treatment but these data have to be taken with care as Cd Nbinding fluorescent dyes, or inhibitors, such as Fura-2 or BAPTA-AM, were employed. Cd " can increase cytosolic Ca by inactivating the SERCA pump and calmodulin-dependent Ca " ATPases. In addition, Cd is well known to interact with calmodulin to activate CaMKII [481] as well as affect calreticulin-mediated signaling [482]. 

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