Sentences with phrase «abl expression»

BCR / ABL expression of myeloid progenitors increases beta1 - integrin mediated adhesion to stromal cells.

In a study recently published in the journal Experimental Haematology, the group demonstrate that is wide variation in BCR - ABL expression levels in the cell model and the stickier cells have a higher level of BCR - ABL expression.

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.

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.

To evaluate whether altered expression of the ABL genes is associated with breast cancer progression and metastasis, we examined the expression of ABL1 and ABL2 in normal and invasive breast tumor specimens using published TCGA (The Cancer Genome Atlas) data sets (14 — 16).

ABL kinases regulate the expression of genes in the JAK / STAT and Hippo pathway signatures in metastatic breast cancer cells.

Abl kinases are required for vascular function, Tie2 expression, and angiopoietin - 1 — mediated survival

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.

Inactivation of ABL kinases inhibited the expression of the TAZ target gene AXL, which shows increased expression in several human cancers and correlates with poor prognosis, increased invasiveness and metastasis, and enhanced drug resistance (53, 54).

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).

Further, we identified a role for ABL kinases in promoting the expression of multiple pro — bone metastasis genes such as AXL (which encodes a receptor tyrosine kinase), IL6 (which encodes interleukin - 6), MMP1 (which encodes matrix metalloproteinase 1), and TNC (which encodes tenascin - C) through TAZ - and signal transducer and activator of transcription 5 (STAT5)-- mediated signaling.

Expression of a constitutively active STAT5A mutant (STAT5A *) reversed the reduction in MMP1, IL - 6, and TNC abundance induced by depletion of both ABL kinases in breast cancer cells (Fig. 7, E and F, and fig.

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).

To identify key molecular mediators of the ABL kinases implicated in the regulation of the ABL1 / ABL2 - dependent pathways, we analyzed the expression of individual genes for transcripts altered by loss of the ABL kinases.

However, we can not rule out the possibility that ABL kinases might regulate YAP1 - mediated expression of other target genes in breast cancer cells.

Depletion of ABL kinases in breast cancer cells decreased IL - 6 concentrations and was accompanied by increased OPG expression in osteoblasts.