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Brefeldin A,20350-15-6,IC-0201281
Brefeldin A (BFA) is a fungal macrocyclic lactone and a potent, reversible inhibitor of intracellular vesicle formation and protein trafficking between the endoplasmic reticulum (ER) and the Golgi apparatus[1][2].Brefeldin A is an ATPase inhibitor with IC50 value of 0.2 µM[9].Brefeldin A and its analogs are promising inhibitors in drug development due to a number of key features such as apoptosis?inducing properties as well as antitumor, antifungal, and antiviral effects [3,6].Brefeldin A is a CRISPR/Cas9 activator. Brefeldin A inhibits HSV-1 and has anti-cancer activity[4].
Perturbation of ER-Golgi trafficking by brefeldin A (BFA) treatment attenuated nucleotide-binding oligomerization domain-like receptor family, pyrin-domain-containing 3 (NLRP3) inflammasome activation in mouse bone marrow-derived macrophages (BMDMs) [5].ADP-ribosylation of BARS is mediated by formation of a conjugate between Brefeldin A and ADPR. BARS shows BAC binding when incubated with the medium from the brefeldin A-treated CD38+ HeLa cells[3].Brefeldin A induces anchorage-independent cell death in MDA-MB-231 breast cancer cells with an EC50 of 0.016 µg/mL, inhibits the formation of MDA-MB-231 colonies in 3D and 2D cultures and inhibits the migration and MMP 9 activity of MDA-MB-231[2].
In tumor-bearing mice, M-brefeldin A can prolong blood circulation, improve tumor accumulation ability, and show effective inhibition of tumor growth, M-brefeldin A 10 mg/kg group showed effective antitumor effect and significantly delayed tumor progression, while M-brefeldin A 5 mg/kg mice did not show significant inhibitory effect[7]. Mice were treated with the Golgi blocker Brefeldin A. Since most cytokines are processed and secreted via the classical secretion pathway through the Golgi, brefeldin A blocks cytokine secretion, leading to their accumulation within immune cells, which are eventually detected by flow cytometry. Thus, treatment of mice with brefeldin A allows in situ assessment of cytokine production without the use of reporter mice [8].-
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Brefeldin A (BFA) is a fungal macrocyclic lactone and a potent, reversible inhibitor of intracellular vesicle formation and protein trafficking between the endoplasmic reticulum (ER) and the Golgi apparatus[1][2].Brefeldin A is an ATPase inhibitor with IC50 value of 0.2 µM[9].Brefeldin A and its analogs are promising inhibitors in drug development due to a number of key features such as apoptosis?inducing properties as well as antitumor, antifungal, and antiviral effects [3,6].Brefeldin A is a CRISPR/Cas9 activator. Brefeldin A inhibits HSV-1 and has anti-cancer activity[4].
Perturbation of ER-Golgi trafficking by brefeldin A (BFA) treatment attenuated nucleotide-binding oligomerization domain-like receptor family, pyrin-domain-containing 3 (NLRP3) inflammasome activation in mouse bone marrow-derived macrophages (BMDMs) [5].ADP-ribosylation of BARS is mediated by formation of a conjugate between Brefeldin A and ADPR. BARS shows BAC binding when incubated with the medium from the brefeldin A-treated CD38+ HeLa cells[3].Brefeldin A induces anchorage-independent cell death in MDA-MB-231 breast cancer cells with an EC50 of 0.016 µg/mL, inhibits the formation of MDA-MB-231 colonies in 3D and 2D cultures and inhibits the migration and MMP 9 activity of MDA-MB-231[2].
In tumor-bearing mice, M-brefeldin A can prolong blood circulation, improve tumor accumulation ability, and show effective inhibition of tumor growth, M-brefeldin A 10 mg/kg group showed effective antitumor effect and significantly delayed tumor progression, while M-brefeldin A 5 mg/kg mice did not show significant inhibitory effect[7]. Mice were treated with the Golgi blocker Brefeldin A. Since most cytokines are processed and secreted via the classical secretion pathway through the Golgi, brefeldin A blocks cytokine secretion, leading to their accumulation within immune cells, which are eventually detected by flow cytometry. Thus, treatment of mice with brefeldin A allows in situ assessment of cytokine production without the use of reporter mice [8].
Perturbation of ER-Golgi trafficking by brefeldin A (BFA) treatment attenuated nucleotide-binding oligomerization domain-like receptor family, pyrin-domain-containing 3 (NLRP3) inflammasome activation in mouse bone marrow-derived macrophages (BMDMs) [5].ADP-ribosylation of BARS is mediated by formation of a conjugate between Brefeldin A and ADPR. BARS shows BAC binding when incubated with the medium from the brefeldin A-treated CD38+ HeLa cells[3].Brefeldin A induces anchorage-independent cell death in MDA-MB-231 breast cancer cells with an EC50 of 0.016 µg/mL, inhibits the formation of MDA-MB-231 colonies in 3D and 2D cultures and inhibits the migration and MMP 9 activity of MDA-MB-231[2].
In tumor-bearing mice, M-brefeldin A can prolong blood circulation, improve tumor accumulation ability, and show effective inhibition of tumor growth, M-brefeldin A 10 mg/kg group showed effective antitumor effect and significantly delayed tumor progression, while M-brefeldin A 5 mg/kg mice did not show significant inhibitory effect[7]. Mice were treated with the Golgi blocker Brefeldin A. Since most cytokines are processed and secreted via the classical secretion pathway through the Golgi, brefeldin A blocks cytokine secretion, leading to their accumulation within immune cells, which are eventually detected by flow cytometry. Thus, treatment of mice with brefeldin A allows in situ assessment of cytokine production without the use of reporter mice [8].
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