Sentences with phrase «activated tyrosine kinase»

Western blot analysis of of extracts from cells expressing different activated tyrosine kinase proteins, using Phospho - PDGF Receptor (Tyr754)(23B2) Rabbit.

We believe these observations warrant a comprehensive search for activated tyrosine kinases in MPD and AML, as there are likely additional unidentified genetic events with biologic and therapeutic significance.

Not exact matches

EGFR tyrosine kinase inhibitor (TKI) therapy is approved for EGFR activating mutation positive patients with advanced NSCLC, but the standard for determining mutation status is with DNA derived directly from tumor tissue, which can be limited or not available.

For example, Capsaspora activated transcription factors and a tyrosine - kinase signaling system in different stages to regulate protein formation.

Regorafenib is one of a new generation of anti-cancer therapies that attack tyrosine kinases — enzymes that activate other proteins.

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.

Ari Hashimoto and colleagues found that the MVP promotes the recruitment of Arf6 to the plasma membrane, where it can be activated by receptor tyrosine kinases.

The activity of tyrosine kinases is typically regulated in an auto - inhibitory fashion, but the BCR - Abl fusion gene codes for a protein that is «always on» or continuously activated leading to unregulated cell division (i.e. cancer).

Receptor Tyrosine Kinases and TLR / IL1Rs Unexpectedly Activate Myeloid Cell PI3K [gamma], A Single Convergent Point Promoting Tumor Inflammation and Progression.

STAT5 is also activated by the oncogenic breakpoint cluster region (BCR)-- ABL tyrosine kinase and contributes to the transformation of leukemia cells (45).

Druker also led the original clinical development of Gleevec, which inhibits a biological switch called a tyrosine kinase that is abnormally activated in CML.

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.

In 2005, the identification of an activating mutation in JAK2 (the V617F mutation) as a STAT5 - activating and disease - causing genetic alteration in a significant proportion of patients with myeloproliferative neoplasms (MPNs) has emphasized the oncogenic role of the JAK tyrosine kinases in hematologic malignancies.2 — 5 JAK2 is a member of the Janus tyrosine kinase family comprising three other mammalian non-receptor tyrosine kinases (JAK1, JAK3 and TYK2) that associate with cytokine receptors lacking intrinsic kinase activity to mediate cytokine - induced signal transduction and activation of STAT transcription factors.6 All JAKs share a similar protein structure and contain a tyrosine kinase domain at the C - terminus flanked by a catalytically inactive pseudokinase domain with kinase - regulatory activity, by an atypical SH2 domain and by a FERM domain that mediates association to the membrane - proximal region of the cytokine receptors.7, 8 Soon after the discovery of JAK2 V617F, we and others described that activating JAK1 mutations are relatively common in adult patients with T - cell acute lymphoblastic leukemia (ALL) and participate in ALL development allowing for constitutive activation of STAT5.9 — 11 Several STAT5 - activating JAK1 mutations were also reported in AML and breast cancer patients.10

Abbreviations: ACVR2A, activin A receptor type IIA; BMP, bone morphogenetic protein; BMPR, BMP receptor, type II; CNS, Central nervous system; DA, dopaminergic; DMEM / F12, Dulbecco's modified Eagle's medium nutrient mixture F - 12; E, embryonic day; GDF, growth differentiation factor; GO, gene ontology; KEGG, Kyoto encylopedia of genes and genomes; MAPK, Mitogen - activated protein kinase; mDA, midbrain dopaminergic; PD, Parkinson's disease; RIPA, radioimmunoprecipitation assay; SN, Substantia nigra; TGF - β, transforming growth factor - β; TH, tyrosine hydroxylase; VM, ventral midbrain / mesencephalon; Zeb2, Zinc finger E-box-binding homoeobox 2

Recently, we and others identified a recurrent somatic activating mutation in the JAK2 tyrosine kinase in polycythemia vera (PV), essential thrombocythemia (ET), and myeloid metaplasia with myelofibrosis (MMM).9 - 13 This mutation results in a valine to phenylalanine substitution at codon 617 within the Jak homology domain 2 (JH2) pseudokinase domain of Janus kinase 2 (JAK2).

Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.

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

Activating mutations in tyrosine kinases have been identified in hematopoietic and nonhematopoietic malignancies.

32) Kubo T, Yamamoto H, Lockwood WW, Fujii T, Ouchida M, Soh J, Takigawa J, Kiura K, Shimizu K, Date H, Minna JD, Lam WL, Gazdar AF, Toyooka S (2009) MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR tyrosine kinase inhibitors.

Some time later, Joseph Schlessinger identified how these tyrosine kinases were activated.

CONCLUSION / INTERPRETATION: These results indicate that R (+) alpha - lipoic acid directly activates lipid, tyrosine and serine / threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor.

Engagement of the Insulin - sensitive Pathway in the Stimulation of Glucose Transport by Alpha - lipoic Acid in 3T3 - L1 Adipocytes Diabetologia 2000 (Mar); 43 (3): 294 — 303 These results indicate that R (+) alpha - lipoic acid directly activates lipid, tyrosine and serine / threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor.