Sentences with phrase «receptor tyrosine kinases in»

In 1995, I began graduate studies on signal transduction by growth factors and receptor tyrosine kinases in the laboratory of Graeme Guy at the Institute of Molecular and Cell Biology (IMCB) in Singapore, obtaining my PhD in 2000.

Sina Koch (Ehninger, TUD)-- «Aberrant subcellular localization as a potential mechanism contributing to the abnormal signaling of the mutant Flt3 - ITd receptor tyrosine kinase in acute myeloid leukemia» (2007)

In addition to causing the functional inactivation of these phosphatases, low concentrations of H2O2 or an oxidative shift in the GSH: GSSH redox status strongly increases the activity of the basic insulin receptor tyrosine kinase in the absence of insulin.

Not exact matches

The Janus tyrosine kinases (Jaks) play a central role in signaling through cytokine receptors.

These receptors, called receptor tyrosine kinases (RTKs), transmit instructions through the cell wall and down through a cascade of reactions to a target gene in the nucleus.

Among patients with advanced non-small cell lung cancer without a mutation of a certain gene (EGFR), conventional chemotherapy, compared with treatment using epidermal growth factor receptor tyrosine kinase inhibitors, was associated with improvement in survival without progression of the cancer, but not with overall survival, according to a study in the April 9 issue of JAMA.

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are the preferred treatment option for patients with advanced non-small cell lung cancer (NSCLC) who have mutations in the EGFR gene.

They found higher levels of JAK1 in resistant tumors, which caused increased expression of epidermal growth factor receptor (EGFR)-- a receptor tyrosine kinase that promotes cell proliferation.

PDGFRα is a cell surface tyrosine kinase receptor involved in organ development and tumor progression, it is present in multiple cell types such as mesenchymal cells, neurons, astrocytes, megakaryocytes and oligodendrocyte progenitor.

Approximately 10 - 15 % of Caucasian and 30 - 35 % of Asian patients with NSCLC have a mutation in the epidermal growth factor receptor (EGFR), which can be successfully targeted with EGFR inhibitors called tyrosine kinase inhibitors (TKI), such as erlotinib, gefitinib and afatinib.

And, indeed, previous research has shown that receptor tyrosine kinases, e.g. insulin receptors, and cytokine receptors, e.g. growth hormone receptors, exist in dimeric form even in the absence of ligands.

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.

The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in mechanisms of resistance to tyrosine kinase inhibitor (TKI) drugs that target the Epidermal Growth Factor Receptor (EGFR) mutation that drive some cases of non-small cell lung cancer (NSCLC).

Gene expression in papillary thyroid carcinomas, with special reference to tyrosine kinase receptors and growth factors.

In 2005, Cagan's team created a general fly model of a human thyroid tumor caused by mutations in the Ret receptor tyrosine kinase gene, then screened a panel of drugs including a kinase inhibitor called vandetanib that suppressed the tumor (Cancer Res, 65:3538 - 41, 2005In 2005, Cagan's team created a general fly model of a human thyroid tumor caused by mutations in the Ret receptor tyrosine kinase gene, then screened a panel of drugs including a kinase inhibitor called vandetanib that suppressed the tumor (Cancer Res, 65:3538 - 41, 2005in the Ret receptor tyrosine kinase gene, then screened a panel of drugs including a kinase inhibitor called vandetanib that suppressed the tumor (Cancer Res, 65:3538 - 41, 2005).

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.

Expression of the receptor tyrosine kinase Tie2 in neoplastic glial cells is associated with integrin beta1 - dependent adhesion to the extracellular matrix.

AXL encodes a receptor tyrosine kinase that promotes breast cancer bone metastasis in mouse models (41).

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.

Also, genes that code for receptor tyrosine kinases, a family of receptors on the surface of cells, may rearrange to form multiple distinct gene fusion partners, as evidenced in an article by Kulkarni, et al, on a translational study involving a patient who developed a BRAF fusion following treatment with a BRAF inhibitor1.

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 unknowin 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 unknowin 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 unknowIn 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 unknowin 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 unknowin 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 unknowin 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 unknowin 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 unknowin a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin 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.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.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.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.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.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.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.in AML and breast cancer patients.10

In addition, at least some Eph receptors can also signal through non-canonical mechanisms that are independent of ligand binding and kinase activity, for example through interplay with other receptor tyrosine kinase families and with serine / threonine kinases.

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

For example, our past work showed that two conserved tyrosine phosphorylation sites in the juxtamembrane segment of the Eph receptors not only mediate association with binding partners but also regulate receptor kinase activity.

They found that certain GBM tumors — particularly those deficient in PTEN — had multiple co-activated receptor tyrosine kinases (RTKs).

Twelve - hour exposure of 3T3 - L1 adipocytes to H (2) O (2) or TNF - alpha resulted in the increase of c - Jun NH (2)- terminal kinase (JNK) activation and insulin receptor substrate 1 (IRS1) serine 307 phosphorylation, concomitantly with the decrease in insulin - stimulated IRS1 tyrosine phosphorylation and cellular glucose uptake.

METHODS: We treated 3T3 - L1 adipocytes with 2.5 mmol / l R (+) alpha - lipoic acid for 2 to 60 min, followed by assays of: 2 - deoxyglucose uptake; glucose transporter 1 and 4 (GLUT1 and GLUT4) subcellular localization; tyrosine phosphorylation of the insulin receptor or of the insulin receptor substrate - 1 in cell lysates; association of phosphatidylinositol 3 - kinase activity with immunoprecipitates of proteins containing phosphotyrosine or of insulin receptor substrate - 1 using a in vitro kinase assay; association of the p85 subunit of phosphatidylinositol 3 - kinase with phosphotyrosine proteins or with insulin receptor substrate - 1; and in vitro activity of immunoprecipitated Akt1.

«In the near future, we'll likely see more medications specifically targeting receptors on cells involved in allergic reactions, such as tyrosine kinase inhibitors (mast cells), for dermatologic use.&raquIn the near future, we'll likely see more medications specifically targeting receptors on cells involved in allergic reactions, such as tyrosine kinase inhibitors (mast cells), for dermatologic use.&raquin allergic reactions, such as tyrosine kinase inhibitors (mast cells), for dermatologic use.»

Investigated TAM family receptor tyrosine kinase gene expression in response to small molecule inhibitors in glioblastoma multiforme