We also probed cellular response following compressive mechanical stimulation to PDMS substrates of varying stiffness.
We also probed the mechanism by which reduced ER stress response leads to increased neurodegeneration.
We also probed this blot with anti-ATF3 antibody to show the increase of ATF3 expression upon Kdo2-Lipid A treatment in ATF3+/+ MEFs.
We also probed the p53 pathway in hTERT-HME1-derived polyploid cells by treating the cells with daunorubicin followed by western blotting for p53 and p21.
In the present study, we also probed the changes of cytokine profiles as well as lymphocyte compositions in the lymph nodes to determine whether there was a distinct immunological shift in the Th cell functions following DNCB treatments.
We also probed extracts of infected NIH-3T3 by Western blots with the antibodies used for ChIPs, and the results were similar to those obtained with HCT116: only H3K79me2 was slightly reduced (Figure S2, Right Panels).
To verify the efficiency and specificity of our biotinylation procedure, we also probed for GluR1, a well-known cell-surface subunit of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor) receptors.
We also probed inhibition by the local anesthetic proadifen.
We also probed the main effect of distractor during encoding.
For comparison with somatic cell histones we also probed Xenopus S3 cell histones.
We also probed these lysates with phospho-specific antibodies to a number of cellular signalling proteins.
