Exact(1)
Imatinib reduced MMP in BCR-ABL1-expressing cells with concurrent Bax activation, but this activation occurred only when imatinib was in combination with nutlin-3, an inhibitor of Mdm2, a key regulator of p53 [ 33, 34].
Similar(59)
However, the exact molecular mechanisms by which this activation occurred are not yet determined.
This activation occurs extracellularly and is often mediated by activated MMPs [ 11].
This activation occurs upstream of PKCγ and Src mediated potentiation of NMDAR activity, ultimately leading to morphine tolerance.
This activation occurs via alkylation of key cysteine residues on the KEAP1 protein, which blocks KEAP1-dependent proteolysis of Nrf2.
However, there currently exists considerable controversy as to how this activation occurs.
This activation occurs via a Ras/Rac1/Pak1/MKK4 pathway.
Research over the past decade indicates this activation occurs in at least two ways.
However, not all the mechanisms by which this activation occurs are totally known.
150 This activation occurs only in α2-containing heterotrimers, 151 although the reason for this isoform specificity is not known.
This activation occurs through interaction of antigen-presenting cells (APCs)—dendritic cells and macrophages [ 16] with T lymphocytes.
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