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Bapta am

Manufactured by Cayman Chemical
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BAPTA-AM is a calcium chelator and cell-permeant form of the calcium-binding compound BAPTA. It is used in research applications to study the role of calcium signaling in cellular processes.

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Lab products found in correlation

Gw4869, by Merck Group (3 mentions) Digitonin, by Merck Group (2 mentions) Doxycycline, by Merck Group (2 mentions) Lysotrackertm red dnd 99, by Thermo Fisher Scientific (2 mentions) Ionomycin, by Merck Group (2 mentions) Sodium taurocholate hydrate, by Merck Group (2 mentions) Pfr luc, by Agilent Technologies (2 mentions) Pm vector, by Takara Bio (2 mentions) 1 oleyl rac glycerol, by Merck Group (2 mentions) Mg132, by Merck Group (2 mentions) Celltiter 96 non radioactive cell proliferation assay, by Promega (2 mentions) Lovastatin, by AG Scientific (2 mentions) Caco 2 cell, by American Type Culture Collection (2 mentions) 1 2 3h n cholesterol, by PerkinElmer (2 mentions) Bapta am, by Thermo Fisher Scientific (1 mentions) Eht1864, by Cayman Chemical (1 mentions) Actin, by Santa Cruz Biotechnology (1 mentions) Beta3 tubulin, by Cell Signaling Technology (1 mentions) Dithiobis succinimidyl propionate, by Thermo Fisher Scientific (1 mentions) Myriocin, by Merck Group (1 mentions)

19 protocols using bapta am

1

Neutrophil Inhibition Prior to Yersinia Infection

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BAPTA-AM (Life Technologies) and EHT 1864 (Cayman Chemical Company) were reconstituted in dimethyl sulfoxide (DMSO) and added to the designated neutrophil wells for final concentrations of 50 μM (EHT 1864) and 25 μM (BAPTA-AM) after allowing the freshly isolated neutrophils to rest at 37°C for 30 min. After adding the inhibitors, neutrophils were incubated at 37°C for an additional 30 min prior to inoculation with Y. pestis.
Eichelberger K.R., Jones G.S, & Goldman W.E. (2019). Inhibition of Neutrophil Primary Granule Release during Yersinia pestis Pulmonary Infection. mBio, 10(6), e02759-19.
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2

Ferroptosis Inhibitors and Protein Analysis

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Erastin (cat. no. E7781), ferrostatin‐1 (Fer‐1; cat. SML0583), and liproxstatin‐1 (Lpx‐1; cat. SML1414) were purchased from Sigma‐Aldrich (Saint Louis, MO, USA). (1S,3R)‐RSL3 (cat. HY‐100218A) was purchased from MedChem Express (Monmouth Junction, NJ, USA). EGTA‐AM (cat. 20401) and BAPTA‐AM (cat. 15551) were from Cayman Chemical (Ann Arbor, MI, USA). Antibodies against MNX1 (Hb9) were from Developmental Studies Hybridoma Band (cat. 81.5C10) (Iowa City, IA, USA), beta3‐tubulin was from Cell Signaling Technology (cat. 5568) (Danvers, MA, USA), and actin was from Santa Cruz Biotechnology (cat. no. sc‐1616‐R) (Dallas, TX, USA). Antibodies against choline acetyltransferase (ChAT) and GPx4 were from Abcam (cat. ab178859 and ab125066, respectively) (Cambridge, MA, USA). Secondary antibodies against mouse IgG and rabbit IgG were from LI‐COR Biotechnology (cat. 925‐68070 and 925‐68071) (Lincoln, NE, USA).
Martinez A.M., Kim A., Flores C.A., Rahman D.F, & Yang W.S. (2023). Mouse embryonic stem cell‐derived motor neurons are susceptible to ferroptosis. FEBS Open Bio, 13(3), 419-433.
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3

Leucine Stimulation in Cultured Cells

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Almost confluent cultures in 6-well plates were washed once with leucine-free low glucose DMEM (US Biological), incubated in leucine-free DMEM for 3 hr, and stimulated with 52 μg/ml leucine for 10 min. For those cells treated with calmidazolium (CMDZ, Cayman Chemical) or BAPTA-AM (Cayman Chemical), compounds were added 1 hr prior to cell harvesting. Cells were processed for biochemical assays as described below.
Li R.J., Xu J., Fu C., Zhang J., Zheng Y.G., Jia H, & Liu J.O. (2016). Regulation of mTORC1 by lysosomal calcium and calmodulin. eLife, 5, e19360.
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4

Lipid Reconstitution and Protein Labeling

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N-ethyl maleimide (NEM), dithiothreitol (DTT) and myriocin were from Sigma-Aldrich, 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC), 1,2-dioleoyl-sn-glycero-3-phosphoethanol-amine (DOPE) and 1-palmitoyl-2-{6-[(7-nitro-2-1,3-benzoxadiazol-4-yl)amino]hexanoyl}-sn-glycero-3-phosphoethanolamine (NBD-PE) from Avanti Polar Lipids, and dithiobis(succinimidyl-propionate) (DSP), mouse monoclonal anti-HA agarose beads, C6-NBD-ceramide and N3-Alexa-Fluor647 from Thermo Fischer Scientific. Curcumin and thapsigargin were from Enzo Life Sciences, tamoxifen, fuminosin B1 and BAPTA-AM from Cayman, z-VAD-fmk from Merck Millipore, and L-arabinose from Carl Roth. Mouse monoclonal anti-V5 agarose beads were from Bethyl Laboratories and Ni-NTA agarose from Qiagen.
Cabukusta B., Kol M., Kneller L., Hilderink A., Bickert A., Mina J.G., Korneev S, & Holthuis J.C. (2017). ER residency of the ceramide phosphoethanolamine synthase SMSr relies on homotypic oligomerization mediated by its SAM domain. Scientific Reports, 7, 41290.
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5

Elucidating IGF-II Signaling Pathways in Senescence

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IGF-II signal transduction may occur through different pathways (Figure 5a). We determined which of these could be associated with senescence. In particular, the MSC cultures were incubated at 37°C for 30 min with each of the following drugs, separately: 100 nM Pertussis toxin (PTX, BMLG101-0050 Enzo Biochem, NY, USA) for the Gαi kinase, 1 μM YM-254890 (YM, 10–1590 Focus Biomolecules, PA, USA) to block Gαq/11, 50 μM D609 (sc201403, Santa Cruz Biotechology, CA, USA) to inhibit PLCβ, 10 μM BAPTA-AM (BPT) (15551 Cayman, MI, USA) and 10 mM 1,2,3,4-tetrahydrostaurosporine (STP, ab143861, Abcam, UK) for PKCα kinase inhibition, 5 nM PKCβi (Santa Cruz Biotech, TX, USA) for PKCβ inhibition, and 100 mM chlorpromazine (CPZ, sc-357313, Santa Cruz) to block endocytosis. Subsequently, we added 25 ng/ml IGF-II, and the samples were further incubated for 24 hr, and the senescence assays were performed. For each drug, we evaluated the inhibitory effect at the concentration we used (Figure 7—figure supplement 1).
Alessio N., Squillaro T., Di Bernardo G., Galano G., De Rosa R., Melone M.A., Peluso G, & Galderisi U. (2020). Increase of circulating IGFBP-4 following genotoxic stress and its implication for senescence. eLife, 9, e54523.
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6

Neutrophil Inhibitor Evaluation for Candida

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Neutrophils were pre-treated with indicated inhibitors 30 min before addition of C. albicans. Inhibitors SkyI (for Syk), BAPTA-AM (a selective chelator of Ca2+), Ro 318220 (for total PKC), Rottlerin (for PKCδ), BB-CI-Amidine (for PAD1-4), GSK484 (for PAD4) were all purchased from Cayman. Ro 6976 (for PKCα+β1), LY 333531 (for PKCβ) were from Millipore.
Wu S.Y., Weng C.L., Jheng M.J., Kan H.W., Hsieh S.T., Liu F.T, & Wu-Hsieh B.A. (2019). Candida albicans triggers NADPH oxidase-independent neutrophil extracellular traps through dectin-2. PLoS Pathogens, 15(11), e1008096.
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7

Crustacean Neuromuscular Signaling Modulators

Cited 1 time
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Tetrodotoxin (TTX), myristoylated PKI(14–22) and calcineurin autoinhibitory peptide (CiP) were purchased from Tocris Bioscience (Bristol, UK). BAPTA-AM, ryanodine and xestospongin C were from Cayman Chemical (Ann Arbor, MI). All other chemicals were purchased from Sigma-Aldrich (St. Louis, MI). DA was made fresh every 30min to minimize oxidation. PKI is an effective blocker of the PKA catalytic subunit in crustaceans [43 (link),46 (link),47 (link)]. CiP and FK506 block calcineurin activity in crustacean neurons at the indicated dosages [48 (link)–50 (link)]. In the spiny lobster, BAPTA, ryanodine and xestospongin C disrupt Ca2+ dynamics at the indicated dosages by chelating Ca2+, blocking ryanodine receptor function and inhibiting IP3 receptor function, respectively [51 (link)].
Krenz W.D., Rodgers E.W, & Baro D.J. (2015). Tonic 5nM DA Stabilizes Neuronal Output by Enabling Bidirectional Activity-Dependent Regulation of the Hyperpolarization Activated Current via PKA and Calcineurin. PLoS ONE, 10(2), e0117965.
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8

Comprehensive Reagent Acquisition Protocol

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All chemicals or reagents were obtained from Sigma-Aldrich unless specified otherwise. PJ34 was from Santa Cruz, DPQ from Calbiochem, Ac-DVED-CMK, GKT137831, BAPTA-AM and U0126 from Cayman Chemical, CTC and PF431396 from Tocris.
Mortadza S.S., Sim J.A., Stacey M, & Jiang L.H. (2017). Signalling mechanisms mediating Zn2+-induced TRPM2 channel activation and cell death in microglial cells. Scientific Reports, 7, 45032.
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9

Investigating Calcium-Dependent Platelet Activation

Cited 2 times
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To evaluate the effect of calcium depletion on SMPA, GFP were treated with calcium chelators binding extracellular (EDTA) or intracellular (BAPTA-AM) calcium pools in platelets. Chosen concentrations of calcium chelators were shown to inhibit platelet membrane scrambling in previous studies. Specifically, non-recalcified GFP (20,000 platelets/uL) were treated with 1 mM EDTA (Sigma-Aldrich, St. Louis, MO) for 10 min31 (link),32 (link) and subjected to shear stress of 30 and 70 dynes/cm2 in the HSD or sonication. Then, activated GFP were recalcified with 2.5 mM CaCl2 and processed to detect annexin V binding as described below. Alternatively, non-recalcified GFP (100,000 platelets/uL) were loaded with 20 uM BAPTA-AM (Cayman Chemical, Ann Arbor, MI) for 30 min with minimal agitation on orbital shaker at room temperature33 (link). Residual solution-phase BAPTA was washed via second gel-filtration of BAPTA-treated GFP. Then, BAPTA-loaded GFP was diluted and recalcified to undergo shear exposure in the HSD or sonication as described above.
Roka-Moiia Y., Walk R., Palomares D.E., Ammann K.R., Dimasi A., Italiano J.E., Sheriff J., Bluestein D, & Slepian M.J. (2020). Platelet Activation Via Shear Stress Exposure Induces A Differing Pattern Of Biomarkers Of Activation Versus Biochemical Agonists. Thrombosis and haemostasis, 120(5), 776-792.
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10

Neurochemical Modulation Protocols

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Methamphetamine (Sigma-Aldrich; St. Louis, Missouri, USA), CdCl2 (Spectrum Chemical; Gardena, CA, USA), 1,2-Bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid tetrakis (acetoxymethyl ester) (BAPTA-AM; Cayman Chemical; Ann Arbor, MI, USA), cyclopiazonic acid (CPA; Cayman Chemical), 2-Aminoethoxydiphenylborane (2-APB; Tocris; Minneapolis, MN, USA), Thapsigargin (Tocris) were dissolved in stock solutions and then diluted into ACSF at specified concentrations.
Yorgason J.T., Hedges D.M., Obray J.D., Jang E.Y., Bills K.B., Woodbury M., Williams B., Parsons M.J., Andres M.A, & Steffensen S.C. (2020). Methamphetamine increases dopamine release in the nucleus accumbens through calcium-dependent processes. Psychopharmacology, 237(5), 1317-1330.
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