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In an initial molecular characterization of mouse pancreatic CTCs, we undertook RNA sequencing (RNA-seq) of CTC-enriched populations, identifying activation of noncanonical WNT signaling as a recurrent event, potentially contributing to the anoikis resistance of circulating epithelial cells (Yu et al., 2012).
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These studies identify activation of Cdc42 and inhibition of GSK-3β as novel strategies for correcting abnormalities associated with VEGF-driven angiogenesis, and they suggest new approaches for achieving improved therapeutic neovascularization with VEGF.
We here identify activation of STAT3 as a novel pathway targeted by PPARβ/δ.
In addition, phospho-protein levels may identify activation of specific signaling pathways.
We also identified activation of JNK and elevated expression of cleaved caspase-3 in ceramide-treated ACCs.
We recently identified activation of astrocytic Nrf2 as a contributor to endogenous neuroprotective responses in the context of ischaemic preconditioning.
We identified activation of caspase-3 as well as PARP cleavage in the malignant lymphoma cell lines.
Subsequent experiments (Fig. 1E) identified activation of GCN2 (sensor of uncharged tRNA) and PERK (sensor of ER stress) as candidate upstream kinases responsible for eIF2α activation.
Our results identifies activation of the PKA/pCREB downstream of β1-ADR in MeA as responsible signaling cascade for learning of social cues in MeA.
Analysis of transduced JURKAT cells overexpressing either MSX2 or oncogenic TLX1 and NKX2-5 identified activation of NOTCH3-signaling, including bHLH target gene HEY1.
Indeed, comparison of the Pol II signals at 10dpp and 16dpp clearly identified activation of pachytene piRNAs after 10dpp (Additional file 1: Figure S13).
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