Sentences with phrase «tyrosine kinase activity»

The product of the resulting BCR - ABL fusion oncogene possesses ABL's so - called tyrosine kinase activity — the ability to add phosphate chemical groups to the amino acid tyrosine — but fails to turn off appropriately.

To cite a few instances, polymerase chain reaction (PCR), a molecular method developed over three decades ago, has been widely applied in disease diagnosis, disease mechanism deciphering, and prognosis prediction; the elucidation of tyrosine kinase activity in cancer cells has led to the development of novel drugs for cancer treatment; and the identification of proteins and genetic molecules by molecular methods as biomarkers for disease diagnosis and prognosis has been drawing great interest.

Not exact matches

An approach often used in treating CML is to block the Bcr - Abl activity using tyrosine kinase inhibitors (TKIs).

Transmission of signals in a cell is controlled by the coordinated activity of two families of enzymes: protein tyrosine kinases, which add a phosphate group to proteins, and protein tyrosine phosphatases, which remove them.

RET is a type of receptor tyrosine kinase, and mutations that kick its activity into overdrive are linked to certain kinds of cancer.

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).

Disruption of Ca2 + - dependent cell - matrix adhesion enhances c - Src kinase activity, but causes dissociation of the c - Src / FAK complex and dephosphorylation of tyrosine - 577 of FAK in carcinoma cells.

In addition to being integral to cell biology, tyrosine kinases also present targets for new anticancer therapies: One of the most highly touted, rationally designed anticancer compounds, Gleevec, inhibits an oncogenic tyrosine kinase whose aberrant activity fuels the rampant growth of cells in patients with chronic myeloid leukemia.

Binding to ephrin ligands on the surface of neighboring cells induces canonical signaling involving receptor clustering, autophosphorylation on tyrosine residues, and kinase activity - dependent downstream signaling.

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

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.

RIPK2 inhibitor 2 appears to inhibit 38 % of the activity of SNARK and 27 % of the activity of FGFR2, GSK3 - β, JNK1, CSNK1G2 (casein kinase 1), and MET tyrosine kinase.

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.

The LIM / Homeodomain Protein Islet1 Recruits Janus Tyrosine Kinases and Signal Transducer and Activator of Transcription 3 and Stimulates Their Activities

Researchers have known for years that abnormal activity of tyrosine kinases can hasten the development of certain forms of cancer.

This reagent, an antibody that detects the phosphotryosine product of the tyrosine kinase reaction, proved crucial to Lydon's enzyme - activity measurements in cells.

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.

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.