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The restricted expression of met tg in neurons was also observed in Nes-R26 Met adult spinal cords, where it was found in dorsal horn neurons, intermediate lateral neurons, and MNs, but not in GFAP-positive astrocytes.
In addition to regulation by the Wnt pathway, expression of MET could therefore be regulated by other signalling pathways.
This was done by introducing miR-34c and investigating whether ectopic expression of MET could rescue the phenotype in DU145 cells.
We determined expression of MET in formalin-fixed paraffin-embedded surgical specimens of TNBC by immunohistochemistry. Recurrence-free and overall survival was analysed with Cox models adjusted for clinical and pathological factors.
As in the PC experiment, the BC OVOL-expressing cell lines demonstrated a stable transition to the MET phenotype and appropriate expression of MET and EMT related genes.
ENCODE array analysis of 5' capped RNA showed decreased expression of MET in hepatitis C cirrhotic liver (fold change −1.8, p = 0.015, Figure S2A).
Expression of MET was examined blinded to clinical data of the patients.
There was expression of MET in all (100%) lung cancer tissues examined (n=32).
We also examined the expression of MET in this cohort (Table 1).
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Expression of Met-TDP-35 in primary motor neurons resulted in the formation of Met-TDP-35-positive cytoplasmic aggregates and motor neuron death.
Interestingly, Met-TDP-35 antibody labeling was specific to TDP-43 pathology in motor neurons, suggesting that the event leading to expression of Met-TDP-35 may be motor neuron specific.
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