Bafa1

Manufactured by Thermo Fisher Scientific

Sourced in United States

BafA1 is a laboratory equipment designed for scientific research applications. It functions as a tool for analyzing and manipulating biological samples. The core purpose of BafA1 is to facilitate specific research activities, but a detailed description cannot be provided while maintaining an unbiased and factual approach.

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Lab products found in correlation

7 protocols using bafa1

Molecular Probes for Organelle Dynamics

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Reagents and antibodies were purchased from the following suppliers: anti-Giantin (Abcam; ab24586, 1:1000), anti-BiP for immunofluorescence (Abcam ab21685, 1:500), anti-BiP for Western blot (Cell signaling, 3183S, 1:1000), anti-KDEL (Abcam ab176333, 1:1000), anti-GFP (Santa Cruz sc-9996, 1:1000), anti-HA (Cell signaling 3724, 1:1000), anti-GAPDH (Cell signaling 2118, 1:2000), TMP (Sigma), CHX (Sigma), doxycycline (Sigma), fibronectin (EMD Millipore), Hoechst (Thermo Fisher Scientific; 10 mg/ml in H₂O, 1:2000) D/D solubilizer (Clonetech), BafA1 (Alfa Aesar), epoxomicin (EMD Millipore), SNAP-tag ligands (SNAP Cell TMR Star and Oregon Green [New England Biolabs]), HT TMR ligand (Promega), and DSP Crosslinker (Thermo Fisher Scientific). HyT36 and HyT36(-Cl) were previously described (Tae et al., 2012 (link); Serebrenik et al., 2018 (link)).

Hellerschmied D., Serebrenik Y.V., Shao L., Burslem G.M, & Crews C.M. (2019). Protein folding state-dependent sorting at the Golgi apparatus. Molecular Biology of the Cell, 30(17), 2296-2308.

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Comprehensive Chemical Treatments for Cell Assays

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The following chemicals were used for treatment of cells: BafA1 (Alfa Aeser, J61835), 17-AAG (Sigma-Aldrich, A8476), 6-AN (Sigma-Aldrich, A68203), AMI (Sigma-Aldrich, 1019701), BRO (Sigma-Aldrich, 1076501), CEL (Sigma-Aldrich, PZ0008), CLO (Sigma-Aldrich, C7291), ETO (Sigma-Aldrich, E1383), (MET (Sigma-Aldrich, M0605000), PAR (Sigma-Aldrich, P9623), RAP (Tocris, 1292), SMER3 (Tocris, 4375), ABT-737 (Selleckchem, S10002), Tat-B (Anaspec, AS65467), Tat-scr. (Anaspec, AS65468), GOS (Sigma-Aldrich, G8761), HAL (Tocris, 0931), MIN (Sigma-Aldrich, M9511), NIC (Sigma-Aldrich, N3510), PIM (Sigma-Aldrich, P1793), PRT (Tocris, 0610), PER (Sigma-Aldrich, SML0120), PEP (Sigma-Aldrich, P6402), PYR (Sigma-Aldrich, 1592001), RAS (Sigma-Aldrich, SML0124), SEC (Sigma-Aldrich, SML0055), SAL (Sigma-Aldrich, S4526), TAM (Sigma-Aldrich, T5648), TOP (Tocris, 4562), VAL (Sigma-Aldrich, V0627), PHLPPi NSC117079 (GlixxLabs, GLXC-03994), C¹⁴-Valine (Perkin Elmer, NEC291EU050UC), Akti X (Cayman Chemical, 14863) MK-2206 HCl (Cayman Chemical, 11593).

Gassen N.C., Niemeyer D., Muth D., Corman V.M., Martinelli S., Gassen A., Hafner K., Papies J., Mösbauer K., Zellner A., Zannas A.S., Herrmann A., Holsboer F., Brack-Werner R., Boshart M., Müller-Myhsok B., Drosten C., Müller M.A, & Rein T. (2019). SKP2 attenuates autophagy through Beclin1-ubiquitination and its inhibition reduces MERS-Coronavirus infection. Nature Communications, 10, 5770.

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Modulating Inflammation and Autophagy with MIF and Inhibitors

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In in vitro experiments, 1 ng/ml human rMIF was applied. In in vivo experiments, 50 µg of murine rMIF was injected intraperitoneally or subcutaneously. As a negative control, rMIF was heat-denatured at 90°C for 10 min. To inhibit MIF activity, the MIF tautomerase inhibitor ISO-1 (50 µM; Calbiochem, La Jolla, CA) or anti-MIF polyclonal antibodies (10 µg/ml) were mixed with rMIF before treatment. The rabbit anti-MIF polyclonal antibody was purified from rMIF-immunized rabbit serum. To inhibit autophagy, 5 mM 3-MA (Sigma-Aldrich) or 5 mM NAC (Sigma-Aldrich) was used. Rapamycin (Bio Basic Inc., Amherst, NY) was added at 100 nM to induce autophagy. To block autophagy flux, 25 nM Baf A1 (Alfa Aesar, Ward Hill, MA) or 100 µM CQ (Sigma-Aldrich) was applied. The MAPK/ERK inhibitor UO126 (10 µM, Sigma-Aldrich), the ROCK inhibitor Y27632 (50 µM, Santa Cruz Biotechnology, Inc., Dallas, TX), the MLCK inhibitor ML7 (50 µM, Santa Cruz Biotechnology) and the AMPK inhibitor compound C (10 µM, Sigma-Aldrich) were used in both in vitro and in vivo experiments.

Chen H.R., Chuang Y.C., Chao C.H, & Yeh T.M. (2015). Macrophage migration inhibitory factor induces vascular leakage via autophagy. Biology Open, 4(2), 244-252.

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Chemical Treatments for Cell Studies

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The following chemicals were used for treatment of cells: AICAR (Sigma–Aldrich, A9978), BafA1 (Alfa Aeser, J61835), rapamycin (RAP, Tocris, 1292), niclosamide (NIC, Sigma–Aldrich, Munich, Germany, N3510), valinomycin (VAL, Sigma–Aldrich, V0627), MG132 (Sigma–Aldrich, M8699), MK-2206 HCl (Cayman Chemical, 11593), MRT68921 (Sigma–Aldrich, SML 1644), SMIP004 (Maybridge Chemicals, TL00829SC), DSS (disuccinimidyl suberate, Thermo Fisher Scientific, 21655), SAR405 (Sigma–Aldrich, 5.33063), Spermine (Sigma–Aldrich, S4264-5G), Spermidine (Sigma–Aldrich, 85558-5 G), DFMO (Sigma-Aldrich, D193-25MG).

Gassen N.C., Papies J., Bajaj T., Emanuel J., Dethloff F., Chua R.L., Trimpert J., Heinemann N., Niemeyer C., Weege F., Hönzke K., Aschman T., Heinz D.E., Weckmann K., Ebert T., Zellner A., Lennarz M., Wyler E., Schroeder S., Richter A., Niemeyer D., Hoffmann K., Meyer T.F., Heppner F.L., Corman V.M., Landthaler M., Hocke A.C., Morkel M., Osterrieder N., Conrad C., Eils R., Radbruch H., Giavalisco P., Drosten C, & Müller M.A. (2021). SARS-CoV-2-mediated dysregulation of metabolism and autophagy uncovers host-targeting antivirals. Nature Communications, 12, 3818.

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Modulation of N2a Cell Autophagy

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Treatments of N2a cell cultures included glutocorticoid receptor (GR) stimulation with dexamethasone (Sigma-Aldrich) ranging from 1 to 100 nM for 24 hours, HBSS (Thermo Fisher Scientific)–induced starvation for 4 hours, and inhibition of autophagosome-lysosome fusion by BafA1 (100 nM, 4 hours; Alfa Aesar).

Häusl A.S., Bajaj T., Brix L.M., Pöhlmann M.L., Hafner K., De Angelis M., Nagler J., Dethloff F., Balsevich G., Schramm K.W., Giavalisco P., Chen A., Schmidt M.V, & Gassen N.C. (2022). Mediobasal hypothalamic FKBP51 acts as a molecular switch linking autophagy to whole-body metabolism. Science Advances, 8(10), eabi4797.

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Autophagy Regulation in Fibrosis

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Recombinant human TGF‐β2, 3‐methyladenine (3‐MA) and bafilomycin A1 (Baf‐A1) were purchased from PeproTech and Sigma‐Aldrich, respectively. The GFP‐LC3B plasmid was obtained from Addgene (24920), and adenovirus encoding for mRFP‐GFP‐LC3 was obtained from Hanbio Biotechnology. Rabbit anti‐human LC3B, p62, Atg5‐12, Beclin 1 and GAPDH were from Cell Signaling. Mouse anti‐human α‐SMA was from Sigma‐Aldrich. Rabbit anti‐human fibronectin, collagen IV, p‐KRT8, mouse anti‐human KRT8 and LAMP2 were from Abcam. Goat anti‐rabbit or antimouse horseradish peroxidase (HRP)‐labelled secondary antibodies were from Thermo Fisher Scientific. Mouse IgG isotype control, rabbit IgG isotype control, AlexaFluor488‐conjugated donkey antimouse and AlexaFluor555‐conjugated donkey anti‐rabbit secondary antibodies were from Life Technologies.

Miao Q., Xu Y., Yin H., Zhang H, & Ye J. (2020). KRT8 phosphorylation regulates the epithelial‐mesenchymal transition in retinal pigment epithelial cells through autophagy modulation. Journal of Cellular and Molecular Medicine, 24(5), 3217-3228.

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Establishment of in vitro diabetic nephropathy model

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Bone marrow MSCs were extracted as previously described [33] . Total bone marrow cells were harvested from rats. The cells were then cultured in DMEM/F12 (HyClone, Logan, UT, USA) supplemented with 10% foetal bovine serum (FBS, Gibco, Carlsbad, CA, USA) at 37°C in 5% CO 2 .
Human embryonic kidney epithelial cells (HKCs) were purchased from ATCC (Manassas, VA, USA) and maintained in RPMI-1640 medium (Thermo Fisher Scientific, Waltham, MA, USA) containing 10% FBS, 1% penicillin (Thermo Fisher Scientific) and 1% streptomycin (Thermo Fisher Scientific) at 37°C and 5% CO 2 . To establish an in vitro model of DN, HKCs were treated with high D-glucose (HG, Pepro Tech, Rocky Hill, NJ, USA) at a concentration of 35 mM for 48 h. Furthermore, mannitol, low glucose (LG) and lysosome inhibitor (Baf A1) were obtained from Pepro Tech (Rocky Hill, NJ, USA).

Cai X., Zou F., Xuan R, & Lai X.Y. (2021). Exosomes from mesenchymal stem cells expressing microribonucleic acid-125b inhibit the progression of diabetic nephropathy via the tumour necrosis factor receptor-associated factor 6/Akt axis. Endocrine journal, 68(7).

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