After verifying that the recombinant plasmid could express GCase in COS7
cells [Figure 1]a, we further investigated the effect of the mutation through other group tests.
We tested these activators and chlorothalonil in Cos7 cells using transient transfection assays and found that only 4 out of 21 chemicals (spirodiclofen, zoxamide, triphenyltin, and triflumizole) activated GAL-PPAR[gamma] (Figure 1A).
ToxCast[TM] Adipogenesis (b) chemical (a) Chemical name 3T3-L1 Triphenyltin (d) Positive Fluazinam (d) Negative Niclosamide Not tested Pyraclostrobin Not tested Zoxamide Positive Acetochlor Negative Butachlor Not tested Triflumizole Positive Prochloraz Not tested Spirodiclofen Positive Alachlor Negative Tebufenpyrad (d) Not tested Dimethenamid Not tested Tebufenozide Not tested Quinoxyfen (e) Not tested Indoxacarb Not tested Fenpyroximate (Z,E) (d) Not tested S-Bioallethrin Not tested Dimethomorph Not tested Cyazofamid (d) Not tested Chlorothalonil Not tested ToxCast[TM] Activation (c) chemical (a) Chemical name COS7 [AC.
Overexpression of MARCH5 in CoS7 cells leads to the formation of elongated mitochondria, which was overcome by coexpressing a dominant negative mutant of MFN2 that lacked the transmembrane domains.
When the isoforms were expressed in COS7 cells, MARCH10a formed a complex with microtubules (confirmed by treating the cells with nocodazole, a microtubule-depolymerizing agent), while MARCH10b was dispersed in the cytoplasm.
For investigating the pathogenesis of glaucoma induced by mutant MYOC gene, we established an in vitro model in which COS7
cells stably expressed either wild-type MYOC ( wtMYOC ) or mMYOC according to our previous procedure.
In the PPAR[gamma]/RXR[alpha] Cos7
cell reporter assay, TPP significantly induced PPAR[gamma]-driven reporter activity at concentrations [greater than or equal to] 10 [micro]M, with an [EC.
A similar significant synergistic cytotoxicity occurred both in HeLa and Cos7 cells by combining the [alpha]-pinene, thymol and menthol with the saponins.
We used haemolysis of erythrocytes as a model for the physical membrane effects and cytotoxicity against the two cancer cell lines HeLa and Cos7 to monitor the effects on living cells.
4]-luciferase reporter plasmids (per 96-well plate) into COS7 cells using Lipofectamine 2000 reagent (Invitrogen; Life Technologies, Carlsbad, CA) following the manufacturer's recommended protocol.
We tested the ability of ROSI, BADGE, BPA, and LG-268 (control RXR agonist) to activate PPARy (GAL4-hPPAR[gammar]) or RXRa (GAL4-hRXR[alpha]) LBD constructs in transient transfection assays in COS7 cells.
were cultivated in DMEM supplemented with 10% FBS.