Log In Sign up
The largest database of trusted experimental protocols

Bafilomycin a1

Manufactured by Avantor
Visit Supplier

Bafilomycin A1 is a macrolide antibiotic that functions as a selective and potent inhibitor of vacuolar-type H+-ATPases (V-ATPases). It is commonly used as a research tool in cell and molecular biology studies.

Automatically generated - may contain errors

Lab products found in correlation

Monensin, by Merck Group (1 mentions) Brefeldin a, by Merck Group (1 mentions) Atglistatin, by Merck Group (1 mentions) Gsk2606414, by MedChemExpress (1 mentions) Gsk2850163, by Merck Group (1 mentions) Cay10566, by MedChemExpress (1 mentions) Ceapin a7, by Merck Group (1 mentions) Thapsigargin, by Merck Group (1 mentions) Tunicamycin, by Merck Group (1 mentions)

4 protocols using bafilomycin a1

1

Investigating Exocytosis Mechanisms

Check if the same lab product or an alternative is used in the 5 most similar protocols
The role of exocytosis (e.g., vesicular exocytosis) mechanisms was studied by administering monensin (Sigma Chemical Co., St. Louis, MO), which interferes with vesicle formation from the Golgi formation 4 (link), 39 (link), bafilomycin A1 (VWR International, Brisbane CA), an inhibitor of vacuolar H+-ATPases that produce proton gradients in endoplasmic reticulum thereby reducing the driving force for uptake of ATP into the vesicle 20 and brefeldin A (Sigma Chemical Co) which blocks the activation of a subset of ADP-ribosylation factors and thereby inhibiting vesicle trafficking 38 (link).
Joseph E.K., Green P.G, & Levine J.D. (2014). ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia. The journal of pain : official journal of the American Pain Society, 15(7), 771-777.
+ Open protocol
+ Expand
2

Autophagy Regulation in Cortical Neurons

Check if the same lab product or an alternative is used in the 5 most similar protocols
Cortical neurons were cultured onto 6-well dishes at a density of 80,000 per well and maintained in neuronal maintenance media as described. At DIV-8, cells were treated with 100 nM bafilomycin A1 (VWR, 196,000), in conditioned maintenance media, or additionally with 250 nM rapamycin (Cayman Biotech, 53,123–88-9) for durations as indicated. EBSS conditions were first washed once with EBSS (to remove excess serum form maintenance media) followed by addition of EBSS + bafilomycin A1. After treatment, cells were washed once in EBSS and collected directly by addition of sample buffer. Samples were sonicated, boiled and subjected to SDS-PAGE and western blotting as described.
Ivankovic D., Drew J., Lesept F., White I.J., López Doménech G., Tooze S.A, & Kittler J.T. (2019). Axonal autophagosome maturation defect through failure of ATG9A sorting underpins pathology in AP-4 deficiency syndrome. Autophagy, 16(3), 391-407.
+ Open protocol
+ Expand
3

Autophagy Inhibition by Bafilomycin A1

Check if the same lab product or an alternative is used in the 5 most similar protocols
Bafilomycin A1 (100nM; cat# 200003–360, CAS# 88899-55-2, VWR) was used to block autophagy in experimental cells, four hours prior to lysis. This was then followed by comparison of LC3-II levels normalized to β-Actin between Bafilomycin A1 treated and untreated cells obtained from western blot imaging as previously described (Klionsky et al., 2012 (link)).
Rahman A.A., Soto-Avellaneda A., Jin H.Y., Stojkovska I., Lai N.K., Albright J.E., Webb A.R., Oe E., Valarde J.P., Oxford A.E., Urquhart P.E., Wagner B., Brown C., Amado I., Vasquez P., Lehning N., Grozdanov V., Pu X., Danzer K.M, & Morrison B.E. (2020). Enhanced hyaluronan signaling and autophagy dysfunction by VPS35 D620N. Neuroscience, 441, 33-45.
+ Open protocol
+ Expand
4

Modulation of Lipid Metabolism Pathways

Check if the same lab product or an alternative is used in the 5 most similar protocols
TAG formation was inhibited using the DGAT1 inhibitor T863 (MedChemExpress, #HY-32219) and the DGAT2 inhibitor PF 06424439 (Bio-Techne, #6348/5). Import of fatty acids into mitochondria was blocked by CPT1 inhibitor etomoxir (Calbiochem, #236020). Desaturation of fatty acids was inhibited by the SCD1 inhibitor CAY10566 (MedChemExpress, #HY-15823-1mg). Lipolysis was inhibited by treating the cells with the ATGL inhibitor atglistatin (Sigma-Aldrich, #SML1075). The ER stress response branches were inhibited individually using the PERK inhibitor GSK2606414 (MedChemExpress, #HY-18072), the IRE1a inhibitor GSK2850163 (Sigma-Aldrich, #1684), and the ATF6 inhibitor Ceapin-A7 (Sigma-Aldrich, #SML2330). ER stress was chemically induced with tunicamycin (Sigma-Aldrich, #5045700001) and thapsigargin (Sigma-Aldrich, #586005). Autophagosome-lysosome fusion was blocked using the V-ATPase inhibitor bafilomycin A1 (VWR, #J61835.MX). The concentration of each treatment is indicated in the figure legends.
Pérez-Martí A., Ramakrishnan S., Li J., Dugourd A., Molenaar M.R., De La Motte L.R., Grand K., Mansouri A., Parisot M., Lienkamp S.S., Saez-Rodriguez J, & Simons M. (2022). Reducing lipid bilayer stress by monounsaturated fatty acids protects renal proximal tubules in diabetes. eLife, 11, e74391.
+ Open protocol
+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Sign up for free.
Registration takes 20 seconds.
Available from any computer
No download required

Sign up now

Revolutionizing how scientists
search and build protocols!