Sentences with phrase «kinases in»

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.

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.

I am a motivated medical writer with over 12 years of research experience in multiple labs, working on a variety of biochemical topics, centering on the role of kinases in hypertension, angiogenesis and tumor development.

«The availability of the human genome sequence allows scientists to scan sequences to identify kinases, and the increased speed with which DNA can be sequenced enables us to rapidly search for mutations in those kinases in human cancers,» said Markowitz.

The starting point for the studies was a detailed catalog of all kinases in the cell, similar to one published in December 2002 in the journal Science.

Finally, we show that inactivation of DNA damage checkpoint kinases in senescent cells can restore cell - cycle progression into S phase.

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

Rapid Avr 9 - and Cf - 9 Dependent Activation of MAP Kinases in Tobacco Cell Cultures and Leaves: Convergence of Resistance Gene, Elicitor, Wound, and Salicylate Responses

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.

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

At that time researchers had only just begun to understand the 58 tyrosine kinases in the human proteome, of which EGFR is one.

As lethal toxin treatment led to reduced levels of MEK1 / 2 and MKK3 / 6 and reduced phosphorylation of ERK1 / 2 and p38, we examined the role of these two MAPK kinases in IL - 22 production in ILC3s.

Depletion of ABL kinases in breast cancer cells decreased IL - 6 concentrations and was accompanied by increased OPG expression in osteoblasts.

Depletion of ABL kinases in breast cancer cells also decreased the abundance of MMP1, a protease that cleaves fibrillar collagens and promotes the proteolytic release of bound growth factors (32).

To examine the functional role of ABL kinases in these cells, we depleted endogenous ABL kinases with previously characterized short hairpin RNAs (shRNAs) specific against ABL1 and ABL2 (20).

In another project, I studies the role (s) of kinases in induced pluripotent stem cell (iPSC) generation.

We found that inactivation of the ABL kinases in breast cancer cells also decreased STAT5A mRNA and downstream expression of STAT5 target genes, including TNC (Fig. 6D).

The adenosine triphosphate (ATP)-- competitive kinase inhibitors imatinib (STI571; trade name: Gleevec), dasatinib, and nilotinib inhibit multiple tyrosine kinases in addition to ABL1 and ABL2 (5).

Expression of a constitutively active STAT5A mutant (STAT5A *) reversed the reduction in MMP1, IL - 6, and TNC abundance induced by depletion of both ABL kinases in breast cancer cells (Fig. 7, E and F, and fig.

Here, we uncovered a role for the ABL kinases in promoting breast cancer bone metastasis through the regulation of distinct pathways required for tumor colonization and survival in the bone microenvironment.

Moreover, we found that treatment with a selective allosteric inhibitor of the ABL kinases or simultaneous depletion of both ABL kinases in breast cancer cells impaired breast cancer bone metastases and decreased osteoclast activation in vitro and osteolysis in vivo.

These findings reveal a function for ABL kinases in the regulation of breast cancer bone metastasis and tumor - induced osteolysis in vivo.

The allosteric inhibitors specific for ABL kinases (which are currently in clinical trials) provide a potentially useful tool for selectively targeting ABL kinases in metastatic breast cancer types with an increase in the ABL pathway signature (58).

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.

Regardless, our data support a role for ABL kinases in the regulation of TAZ protein abundance and activity in breast cancer cells.

We showed that inactivation of the ABL kinases in breast cancer cells resulted in decreased expression of genes in the JAK / STAT and cytokine / cytokine receptor pathway signatures, which may be due to decreased STAT5A mRNA expression and reduced STAT5 phosphorylation in ABL1 / ABL2 - depleted breast cancer cells.

Here, we uncovered a critical role for ABL kinases in the regulation of breast cancer metastasis to bone.

We found that depletion of ABL kinases in breast cancer cells decreased STAT5A mRNA expression (Fig. 6D) without decreasing total STAT5 protein abundance as measured by Western blotting with antibodies that detect both STAT5A and STAT5B (Fig. 7D and fig.

Activation of SKN - 1 by novel kinases in Caenorhabditis elegans.

An InCytes from MBC Selection: Regulation of Cell Polarity through Phosphorylation of Bni4 by Pho85 G1 Cyclin - dependent Kinases in Saccharomyces cerevisiae.

Miniaturizing each individual experiment allows us to print whole libraries on a single plate, for instance gRNA / siRNA targeting all kinases in the human genome are printed on approximately 2.06 cm2 (0.32 sq. in.).

Regulation of cell polarity through phosphorylation of Bni4 by Pho85 G1 cyclin - dependent kinases in Saccharomyces cerevisiae.

Rapid regulation of dopamine transporters by tyrosine kinases in rat neuronal preparations.

The roles of two IκB kinase - related kinases in lipopolysaccharide and double stranded RNA signaling and viral infection.

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.

There are about 500 kinases in the human genome, each of which represents a potentially important drug target.

The prevailing view has been that multiple kinases in a network had to be disabled in order to restore normal function.

There are an estimated 400 - 500 kinases in the human genome, with literally dozens being activated during disease processes.

«There are more than 500 kinases in the human body; and many of them are essential building - blocks of life,» Laufer explains.

The onset of M phase requires the activation of the pp34 protein kinase in all eukaryotes thus far examined.

These results not only show promise on a new targeted therapy to treat this malignancy, as PI3K inhibitors are already used in the clinical practice, but also unravel a new function of the PI3K kinase in cancer biology through its role in promoting metastasis.

Our results suggest that frequent overexpression of Aurora Kinase in cancer may reduce RUNX3 transcription activity, leading to cell division and formation of tumours.

Enhancement of the glutamate response by cAMP - dependent protein kinase in hippocampal neurons

Platelet - activating factor - mediated endosome formation causes membrane translocation of p67phox and p40phox that requires recruitment and activation of p38 MAPK, Rab5a, and phosphatidylinositol 3 - kinase in human neutrophils.

Distinct roles of a mitogen - activated protein kinase in cytokinesis between different life cycle forms of Trypanosoma brucei.

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)

University of California - San Francisco Combination therapy against EGFR and PI3 - kinase in glioma

This leads to activation of a kinase; a very important kinase in metabolism called PI3 - Kinase, standing for phosphoinositide or 3 - Kinase.

Inhibitory role of alpha6beta 4 - associated erbB - 2 and phosphoinositide 3 - kinase in keratinocyte haptotactic migration dependent on alpha3beta1 integrin.

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).