Golgicide A;Golgicide A (GCA);Golgicide A, 10 mM in DMSO;Golgicide A - CAS 1139889-93-2 - Calbiochem;6,8-Difluoro-4-pyridin-3-yl-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinoline;6,8-Difluoro-4-pyridin-3-yl-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinoline USP/EP/BP;rel-(3aR,9bS)-6,8-Difluoro-4-(pyridin-3-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinoline;3H-Cyclopenta[c]quinoline, 6,8-difluoro-3a,4,5,9b-tetrahydro-4-(3-pyridinyl)-, (3aR,9bS)-rel-
A cell-permeable quinoline compound that selectively targets ArfGEF GBF1, but not BIG1/2, and attenuates GBF1-mediated cellular vesicle traffickings in a reversible manner. Phenotypic comparisons in Vero (African Green Monkey Kidney epithelial) cultures reveal that selective blockage of GBF1 function by GCA (10 μM) or by FGB1-E794K dominant-inactive expression affects medial- and cis-Golgi similarly to that seen with BFA (Cat. No. 203729), however, the non-GBF1-specific BFA (10 μg/ml or 35.6 μM) causes additional GBF1-independent morphologic effects on TGN, notably the rapid dispersal of Golgi-associated coat proteins AP-1 and GGA3, which are not seen with GCA treatment. Endocytic/retrograde transport studies using GCA establishes that GBF1 function is not required for the transport of bacterial toxins to the endosomes, however the retrograde transport of StxB (shiga toxin B subunit) from endosomes to TGN and Golgi is GBF1-dependent (100% inhibition of StxB sulfation at 10 μM), accounting for GCA′s (10 μM) ability to completely prevent Vera cells from Stx-induced (up to 100 ng/ml) inhibition of cellular protein synthesis.
6,8-Difluoro-4-pyridin-3-yl-3a,4,5,9b-tetrahydro-3H-cyclopenta[c]quinoline Upstream-Materialien And Downstream Produkte