In addition to inhibiting STAT5 signaling, we found that depletion of ABL
kinases decreased the expression of the Hippo pathway mediator TAZ and downstream target genes in triple - negative and HER2 + breast cancer cells.
Not exact matches
We found that depletion of ABL
kinases in breast cancer cells
decreased STAT5A mRNA
expression (Fig. 6D) without
decreasing total STAT5 protein abundance as measured by Western blotting with antibodies that detect both STAT5A and STAT5B (Fig. 7D and fig.
We showed that inactivation of the ABL
kinases in breast cancer cells resulted in
decreased expression of genes in the JAK / STAT and cytokine / cytokine receptor pathway signatures, which may be due to
decreased STAT5A mRNA
expression and reduced STAT5 phosphorylation in ABL1 / ABL2 - depleted breast cancer cells.
We found that ~ 90 % knockdown of ABL1 alone resulted in enhanced ABL2
expression and did not produce a significant
decrease in the phosphorylation of CrkL, a reporter for the activation state of the ABL
kinases (Fig. 2K), and did not inhibit metastasis (Fig. 2, L and M).
We found that inactivation of the ABL
kinases in breast cancer cells also
decreased STAT5A mRNA and downstream
expression of STAT5 target genes, including TNC (Fig. 6D).
Further, inactivation of the ABL
kinases resulted in
decreased expression of the genes in the Hippo, Janus
kinase (JAK) / STAT, and cytokine / cytokine receptor pathway signatures (Fig. 6B).
Depletion of ABL
kinases in breast cancer cells
decreased IL - 6 concentrations and was accompanied by increased OPG
expression in osteoblasts.
Of particular note were
decreased mGluR5 and Tyrosine
Kinase c - kit and increased IBA1, CD68, ICAM1, VEGF - D, and TLR4 mRNA
expression in Tsc1GFAPCKO mice.