1
We found that this drug inhibits Kir4.1 channels heterologously expressed in HEK-293 cells.
2
The studies were carried out in hOAT4-expressing human kidney HEK-293 cells and human placenta BeWo cells.
3
Expression of the C-terminus truncated receptor for advanced glycation end products (RAGE) resulted in a reduction of HEK-293-MAP kinase activation.
4
Protein expression of the three subunits was verified by performing western blots of total lysates and cell membrane fractions of HEK-293 cells.
5
Excision footprints obtained from HEK-293 cells contained small insertions and deletions consistent with a hAT-type repair mechanism of hairpin formation and non-homologous end-joining.
6
Protocols for production of AAV vectors in a helper virus-free system are available and are based on transient transfection of HEK-293 cells with multiple plasmids.
7
These inward rectifier potassium channels were transfected in HEK-293 cells and macroscopic currents were recorded in the whole-cell and inside-out configurations of the patch-clamp technique.
8
Blocking of RAGE by an antagonistic antibody and expression of C-terminally truncated RAGE resulted in a reduced Caco-2- and HEK-293-MAP kinase activation.
9
Expression of arrestin-3 proteins containing amino acids 1-320 or 201-409 resulted in the inhibition of beta2-adrenergic receptor internalization in HEK-293 cells by approximately 40%.