Sentences with phrase «specific tyrosine kinase»

Another focus was the differential sensitivity of different mutations towards inhibition with specific tyrosine kinase inhibitors (5).

Not exact matches

During the early years of my PhD studies, I was very fascinated by the exciting discoveries in the field of signal transduction, in particular how receptor tyrosine kinases are activated to transmit their signals and how protein complexes are formed through defined protein folds (domains) interacting with specific cellular targets.

We are focusing on a few key molecular pathways including; 1) Polycomb - mediated epigenetic gene silencing in the tumor initiation, maintenance, and invasion, 2) c - Met (receptor tyrosine kinase) signal transduction pathways in stemness and migration of these tumor cells, 3) Novel mitogenic signaling pathways that are specific to GSCs, and 4) Identification of radio - and chemo - sensitizing pathway to maximize therapeutic efficacy.

These events occur when specific extracellular molecules bind to receptor proteins in the plasma membrane known as receptor tyrosine kinases and heterotrimeric G - protein - coupled receptors.

The initial model for STAT signaling involves a specific cytokine binding to its cognate receptor and promoting the transphosphorylation of receptor associated tyrosine kinases from the Janus - activated kinase family (JAK).

These mutant kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.

Activated JAK kinases in turn phosphorylate - specific tyrosine motifs found in receptor domains, which then recruit the specific monomeric STATs to the receptor complex.