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Academic literature on the topic 'Tie2'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Tie2"

1

Leppänen, Veli-Matti, Pipsa Saharinen, and Kari Alitalo. "Structural basis of Tie2 activation and Tie2/Tie1 heterodimerization." Proceedings of the National Academy of Sciences 114, no. 17 (April 10, 2017): 4376–81. http://dx.doi.org/10.1073/pnas.1616166114.

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The endothelial cell (EC)-specific receptor tyrosine kinases Tie1 and Tie2 are necessary for the remodeling and maturation of blood and lymphatic vessels. Angiopoietin-1 (Ang1) growth factor is a Tie2 agonist, whereas Ang2 functions as a context-dependent agonist/antagonist. The orphan receptor Tie1 modulates Tie2 activation, which is induced by association of angiopoietins with Tie2 in cis and across EC–EC junctions in trans. Except for the binding of the C-terminal angiopoietin domains to the Tie2 ligand-binding domain, the mechanisms for Tie2 activation are poorly understood. We report here the structural basis of Ang1-induced Tie2 dimerization in cis and provide mechanistic insights on Ang2 antagonism, Tie1/Tie2 heterodimerization, and Tie2 clustering. We find that Ang1-induced Tie2 dimerization and activation occurs via the formation of an intermolecular β-sheet between the membrane-proximal (third) Fibronectin type III domains (Fn3) of Tie2. The structures of Tie2 and Tie1 Fn3 domains are similar and compatible with Tie2/Tie1 heterodimerization by the same mechanism. Mutagenesis of the key interaction residues of Tie2 and Tie1 Fn3 domains decreased Ang1-induced Tie2 phosphorylation and increased the basal phosphorylation of Tie1, respectively. Furthermore, the Tie2 structures revealed additional interactions between the Fn 2 (Fn2) domains that coincide with a mutation of Tie2 in primary congenital glaucoma that leads to defective Tie2 clustering and junctional localization. Mutagenesis of the Fn2–Fn2 interface increased the basal phosphorylation of Tie2, suggesting that the Fn2 interactions are essential in preformed Tie2 oligomerization. The interactions of the membrane-proximal domains could provide new targets for modulation of Tie receptor activity.
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Saharinen, Pipsa, Katja Kerkelä, Niklas Ekman, Marie Marron, Nicholas Brindle, Gyun Min Lee, Hellmut Augustin, Gou Young Koh, and Kari Alitalo. "Multiple angiopoietin recombinant proteins activate the Tie1 receptor tyrosine kinase and promote its interaction with Tie2." Journal of Cell Biology 169, no. 2 (April 25, 2005): 239–43. http://dx.doi.org/10.1083/jcb.200411105.

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The Tie1 receptor tyrosine kinase was isolated over a decade ago, but so far no ligand has been found to activate this receptor. Here, we have examined the potential of angiopoietins, ligands for the related Tie2 receptor, to mediate Tie1 activation. We show that a soluble Ang1 chimeric protein, COMP-Ang1, stimulates Tie1 phosphorylation in endothelial cells with similar kinetics and angiopoietin dose dependence when compared with Tie2. The phosphorylation of overexpressed Tie1 was weakly induced by COMP-Ang1 also in transfected cells that do not express Tie2. When cotransfected, Tie2 formed heteromeric complexes with Tie1, enhanced Tie1 activation, and induced phosphorylation of a kinase-inactive Tie1 in a ligand-dependent manner. Tie1 phosphorylation was also induced by native Ang1 and Ang4, although less efficiently than with COMP-Ang1. In conclusion, we show that Tie1 phosphorylation is induced by multiple angiopoietin proteins and that the activation is amplified via Tie2. These results should be important in dissecting the signal transduction pathways and biological functions of Tie1.
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Moore, Jason O., Mark A. Lemmon, and Kathryn M. Ferguson. "Dimerization of Tie2 mediated by its membrane-proximal FNIII domains." Proceedings of the National Academy of Sciences 114, no. 17 (April 10, 2017): 4382–87. http://dx.doi.org/10.1073/pnas.1617800114.

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Tie1 and Tie2, members of the tyrosine kinase family with immunoglobulin and EGF homology domains, are receptor tyrosine kinases found primarily in endothelial cells with key roles in development and maintenance of the vasculature and in angiogenesis. They are attractive targets for therapeutic intervention in tumor angiogenesis, inflammation, and sepsis. Tie2 is regulated directly by the multimeric angiopoietin (Ang) ligands, with Ang1 being its primary activator. Structural studies have shown how Angs bind to the Tie2 ligand-binding region, but do not explain Tie2 activation and suggest a passive role for the Tie2 extracellular region (ECR) in ligand-induced receptor dimerization. Here we show that the Tie2 ECR forms strong dimers even in the absence of bound ligand. Dimerization is mediated by membrane-proximal fibronectin type III (FNIII) domains that were omitted in previous structural studies. We describe a 2.5-Å resolution X-ray crystal structure of the membrane-proximal three Tie2 FNIII domains, Tie2(FNIIIa–c), revealing two possible dimerization modes that primarily involve the third FNIII domain, FNIIIc. Mutating these dimer interfaces implicates one of them (dimer 1) in soluble Tie2 (sTie2) dimerization in solution but suggests that both could play a role in Ang1-induced Tie2 activation, possibly modulated by Tie1. Through small-angle X-ray scattering studies of sTie2 dimers in solution and modeling based on crystal structures, we suggest that Ang1 binding may cross-link Tie2 dimers into higher-order oligomers, potentially explaining how Tie2 is differentially clustered following ligand engagement in different cellular contexts. Our results also firmly implicate FNIII domain-mediated interactions in Tie2 activation, identifying a potential Achilles’ heel for therapeutic inhibition.
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Singh, Harprit, Tariq A. Tahir, Deborah O. A. Alawo, Eyad Issa, and Nicholas P. J. Brindle. "Molecular control of angiopoietin signalling." Biochemical Society Transactions 39, no. 6 (November 21, 2011): 1592–96. http://dx.doi.org/10.1042/bst20110699.

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The angiopoietins act through the endothelial receptor tyrosine kinase Tie2 to regulate vessel maturation in angiogenesis and control quiescence and stability of established vessels. The activating ligand, Ang1 (angiopoietin-1), is constitutively expressed by perivascular cells, and the ability of endothelial cells to respond to the ligand is controlled at the level of the Ang1 receptor. This receptor interacts with the related protein Tie1 on the cell surface, and Tie1 inhibits Ang1 signalling through Tie2. The responsiveness of endothelium to Ang1 is determined by the relative levels of Tie2 and the inhibitory co-receptor Tie1 in the cells. Tie1 undergoes regulated ectodomain cleavage which is stimulated by a range of factors including VEGF (vascular endothelial growth factor), inflammatory cytokines and changes in shear stress. Ectodomain cleavage of Tie1 relieves inhibition of Tie2 and enhances Ang1 signalling. This mechanism regulates Ang1 signalling without requiring changes in the level of the ligand and allows Ang1 signalling to be co-ordinated with other signals in the cellular environment. Regulation of signalling at the level of receptor responsiveness may be an important adaptation in systems in which an activating ligand is normally present in excess or where the ligand provides a constitutive maintenance signal.
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SHYU, Kou-Gi, Chih-Chuan CHANG, Bao-Wei WANG, Peiliang KUAN, and Hang CHANG. "Increased expression of angiopoietin-2 and Tie2 receptor in a rat model of myocardial ischaemia/reperfusion." Clinical Science 105, no. 3 (September 1, 2003): 287–94. http://dx.doi.org/10.1042/cs20030025.

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The angiopoietins and Tie receptors are involved in blood vessel formation. The role of the angiopoietin/Tie receptor system in myocardial ischaemia/reperfusion is not well known. To investigate the participation of angiopoietins and Tie receptors in myocardial ischaemia/reperfusion, adult Wistar rats were studied in which the left coronary artery was ligated for 30 min, followed by reperfusion. Angiopoietin-1 (Ang1), angiopoietin-2 (Ang2), Tie1 and Tie2 were measured immediately after relief of occlusion, and 1, 6, 24 and 72 h after reperfusion, by Northern blot, Western blot and immunohistochemical staining. Ang2 mRNA was increased significantly at 24 h and 48 h after reperfusion, and returned to baseline levels at 72 h, in the jeopardized myocardium. Tie2 mRNA increased 3.4-fold immediately after the relief of occlusion, reached a maximum 8-fold increase at 24 h after reperfusion and remained elevated up to 72 h. Ang2 protein levels also increased after reperfusion, reaching a maximum 2.2-fold increase at 48 h after reperfusion. Tie2 protein increased immediately after relief of ischaemia, and showed a significant increase from 6 h to 72 h after reperfusion as compared with the sham control. Ang1 and Tie1 mRNA and protein did not show significant changes after ischaemia/reperfusion. Immunohistochemical studies also showed increased immunoreactivity of Ang2 and Tie2 in the jeopardized myocardium after ischaemia/reperfusion. In conclusion, expression of both Ang2 and Tie2 increased after ischaemia/reperfusion in the rat ventricular myocardium, while the expression of Ang1 and Tie1 did not.
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Winski, Shannon L., LouAnn Cable, Grant Hogeland, Suzy Brown, Dan Weaver, Jenn Garrus, Susan Rhodes, et al. "Role of p38 MAPK and Tie2 in the Pathogenesis of MDS and Their Inhibition by Dual Inhibitor ARRY-614." Blood 120, no. 21 (November 16, 2012): 2825. http://dx.doi.org/10.1182/blood.v120.21.2825.2825.

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Abstract Abstract 2825 Myelodysplastic syndromes (MDS) are a heterogeneous collection of disorders characterized by dysfunctional bone marrow progenitors leading to peripheral cytopenias. The molecular mechanisms underlying MDS pathophysiology are unclear, but emerging data support a role for both p38 MAPK (p38) and TEK (Tie2). Over-activation of the p38 pathway and increased apoptosis have been reported in the bone marrow of MDS patients, and dysregulation of Tie2 signaling, a potential regulator of hematopoiesis via maintenance of normal hematopoietic stems cell (HSC) quiescence, is associated with worse outcome. To better understand the role of Tie2 in hematopoiesis, CD34+ cells from human cord blood were separated by multi-parameter flow cytometry and cell sorted into HSCs (i.e., CD34+, CD38−) or the more differentiated common myeloid progenitors (CMPs; i.e., CD38+, IL-3Rαlo, CD45RA−), myeloid erythroid progenitors (MEPs; i.e., CD38+, IL-3Rα−, CD45RA−), and granulocyte myeloid progenitors (GMPs; i.e., CD38+, IL-3Rαlo, CD45RA+). Expression of Tie2, Tie1, Ang-1 (Tie2 agonist) and Ang-2 (Tie2 antagonist) was determined by qPCR. The data showed that Tie2, Tie1, and Ang-1 were expressed in CD34+ cells and appeared to be regulated during differentiation, with reduced Tie2 expression observed in the GMP population. To further understand the roles of p38 and Tie2 in MDS, bone marrow and plasma samples were analyzed from a Phase 1 clinical study conducted with ARRY-614, a p38/Tie2 inhibitor, in patients with IPSS Low/Int-1 Risk MDS. At baseline, 65% (13/20) of the MDS patients showed aberrant p38 activation (≥5% phospho-p38 positive cells). Following treatment with ARRY-614, the median percent of cells positive for phospho-p38 was decreased by 85% through up to 4 cycles of treatment (∼112 days). Apoptosis in patient bone marrow samples was reduced as well (monitored by cleaved caspase-3). In cell-based assays, ARRY-614 inhibits both p38-mediated HSP27 phosphorylation (IC50 = 1 nM) and Tie2-dependent AKT phosphorylation (IC50 = 13 nM). Cellular IC50 values, corrected for plasma protein binding, and preliminary pharmacokinetic parameters were used to predict inhibition of these targets in patients. Analysis of the highest administered dose (1200 mg QD) of ARRY-614 as a powder-in-capsule (PiC) formulation in the Phase 1 clinical study predicted robust suppression of phospho-p38 (≥ 50% for 24 hours), consistent with bone marrow and plasma biomarker findings. However, partial inhibition of Tie2 (≥ 50% for 17.1 hours) was predicted. In a second Phase 1 clinical study, an optimized ARRY-614 formulation has demonstrated decreased intra- and inter-patient variability and increased peak plasma concentrations. With this new formulation, peak plasma concentrations of the 400 mg QD cohort were ∼50% higher than those of the 1200 mg QD PiC formulation cohort, possibly affording more extensive Tie2 inhibition. In summary, these observations suggest that inhibition of both p38 and Tie2 may be important for the effects of ARRY-614 in MDS patients. The ongoing Phase 1 dose escalation trial of the optimized ARRY-614 formulation may further our understanding of the contributions of these targets to the pathogenesis of MDS. Disclosures: Winski: Array Biopharma Inc.: Employment. Cable:Array Biopharma Inc.: Employment. Hogeland:Array Biopharma Inc.: Employment. Brown:Array Biopharma Inc.: Employment. Weaver:Array Biopharma Inc.: Employment. Garrus:Array Biopharma Inc.: Employment. Rhodes:Array Biopharma Inc.: Employment. Maloney:Array Biopharma Inc.: Employment. Ptaszynski:Array BioPharma: Consultancy. Chantry:Array Biopharma Inc.: Employment.
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Fonseca, J. A., I. Tomada, N. Tomada, H. Almeida, and D. Neves. "Immunofluorescent detection of Tie1 in the endothelium of the Rat and Human corpus cavernosum during aging." Microscopy and Microanalysis 19, S4 (August 2013): 39–40. http://dx.doi.org/10.1017/s1431927613000810.

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Vasculogenic erectile dysfunction (ED) is an age-related disease partially dependent on vascular growth factors availability and their specific endothelium receptors activation. Among these, angiopoietins-tyrosine kinase with immunoglobulin and EGF homology domain-2 (Tie2) system seems to be particularly dependent on aging, both in rat and in human corpus cavernosum (CC). Angiopoietins (Ang)1 and 2 are produced by pericytes and endothelial cells respectively, and bind with the same affinity to Tie2 receptor. Ang1 was shown to act as an obligatory agonist inducing Tie2 phosphorylation, which promotes cell-cell and cell-extracellular matrix interactions. On the other hand, Ang2 acts in a context-dependent fashion in the increment or, otherwise, destabilization of pre-existent vasculature.Interestingly, it has been demonstrated that activation of Tie2 receptor could also be modulated by Tie1, an additional member of the Tie family of receptor tyrosine kinases, and that co-expression of Tie2 is required for Tie1 activation. Indeed, Tie1 similarly to Tie2 is involved in the maintenance of the vascular integrity. Nevertheless, its role in Angiopoietins-Tie system regulation remains poorly understood, and the identification of a true ligand has remained elusive. In the present study, we aim to demonstrate the expression of Tie1 in the endothelium of aged CC in the Rat and Human species.Twenty-five male Wistar rats were divided in five groups (n=5) and sacrificed by decapitation when they reached the ages of study (6, 12, 18, 24 and 36 months). The penises were excised and immediately fixed in formalin solution. Human CC fragments were obtained from organ donors without known risk factors for ED and divided in two groups: young (16–35 years) and aged (59–74 years). Paraffin embedded sections were deparaffinized, rehydrated and submitted to epitope retrieval with heated Tris-EDTA pH 9.0 buffer before dual-immunolabeling of Tie1 (rabbit anti-Tie1 antibody -abcam) and specific markers of endothelium and smooth muscle cell (goat- anti-PECAM-1 and mouse anti-m-actin antibodies, Santa Cruz Biotechnology Inc. and Millipore, respectively). Appropriate secondary antibodies were employed (anti-rabbit labelled with Alexa 488 with anti-mouse, or, anti –goat labelled with Alexa 568). Nuclei counterstaining was achieved with 4´-6-diamino-2-phenylindole. Images were observed in an Apotome microscope (Carl Zeiss System, Göttingen, Germany) using the filter sets, 01 to DAPI, 09 to Alexa 488 and 31 to Alexa 568, and acquired with Axio Vision 3.0 program (Carl Zeiss System).Tie1 was detected in the endothelium in the CC of Rat, co-localizing with PECAM-1 (Figure 1a) but not with w-actin (Figure 1b). The intensity of Tie1 immunolabeling was higher in the older animals (24 and 36 months). Tie1 was also detected in Human CC endothelium, suggesting an up-regulation in samples obtained from older individuals (Figure 2a and 2b).The present results demonstrate for the first time the expression of Tie1 in the endothelium of CC in Rat and Human, which appears to exhibit an age-dependent up-regulation. Ongoing research employing molecular studies will clarify this aspect.
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Leppänen, Veli-Matti, Pascal Brouillard, Emilia A. Korhonen, Tuomas Sipilä, Sawan Kumar Jha, Nicole Revencu, Veerle Labarque, et al. "Characterization of ANGPT2 mutations associated with primary lymphedema." Science Translational Medicine 12, no. 560 (September 9, 2020): eaax8013. http://dx.doi.org/10.1126/scitranslmed.aax8013.

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Primary lymphedema is caused by developmental and functional defects of the lymphatic vascular system that result in accumulation of protein-rich fluid in tissues, resulting in edema. The 28 currently known genes causing primary lymphedema can explain <30% of cases. Angiopoietin 1 (ANGPT1) and ANGPT2 function via the TIE1-TIE2 (tyrosine kinase with immunoglobulin-like and epidermal growth factor–like domains 1 and 2) receptor complex and α5β1 integrin to form an endothelial cell signaling pathway that is critical for blood and lymphatic vessel formation and remodeling during embryonic development, as well as for homeostasis of the mature vasculature. By screening a cohort of 543 individuals affected by primary lymphedema, we identified one heterozygous de novo ANGPT2 whole-gene deletion and four heterozygous ANGPT2 missense mutations. Functional analyses revealed three missense mutations that resulted in decreased ANGPT2 secretion and inhibited the secretion of wild-type (WT)–ANGPT2, suggesting that they have a dominant-negative effect on ANGPT2 signaling. WT-ANGPT2 and soluble mutants T299M and N304K activated TIE1 and TIE2 in an autocrine assay in human lymphatic endothelial cells. Molecular modeling and biophysical studies showed that amino-terminally truncated ANGPT subunits formed asymmetrical homodimers that bound TIE2 in a 2:1 ratio. The T299M mutant, located in the dimerization interphase, showed reduced integrin α5 binding, and its expression in mouse skin promoted hyperplasia and dilation of cutaneous lymphatic vessels. These results demonstrate that primary lymphedema can be associated with ANGPT2 mutations and provide insights into TIE1 and TIE2 activation mechanisms.
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CHANG, Hang, Bao-Wei WANG, Peiliang KUAN, and Kou-Gi SHYU. "Cyclical mechanical stretch enhances angiopoietin-2 and Tie2 receptor expression in cultured human umbilical vein endothelial cells." Clinical Science 104, no. 4 (March 20, 2003): 421–28. http://dx.doi.org/10.1042/cs1040421.

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Endothelial cells are essential for neovascularization. Angiopoietins and Tie receptors are required for a normal vasculature. How cyclical mechanical stretch affects the expression of components of the angiopoietin system is not known. In this study, we investigated the regulation of angiopoietins and Tie receptors by cyclical mechanical stretch in cultured human umbilical vein endothelial cells (HUVECs). HUVECs grown on a flexible membrane base were stretched by vacuum to 20% elongation, at 60cycles/min. The levels of angiopoietin-2 protein began to increase as early as 2h after stretch was initially applied, reached a maximum of 2.7-fold over the control value by 6h. The Tie2 receptor protein showed the same pattern as Ang-2. These increases in angiopoietin-2 and Tie2 receptor proteins at 6h were blocked by the addition (30min before stretch) of the protein kinase C inhibitor Gö6976 (16nM) or the tyrosine kinase inhibitor herbimycin A (24µM). Similar to protein expression, the levels of angiopoietin-2 and Tie2 receptor mRNAs in HUVECs increased 3.1-fold and 2.5-fold respectively after stretch for 6h. These increases were also blocked by Gö6976 or herbimycin A. Cyclical mechanical stretch increased (and Gö6976 or herbimycin A abrogated these increases) the immunohistochemical labelling of angiopoietin-2 and Tie2 receptor after a 6h stretch. The levels of angiopoietin-1 and Tie1 receptor proteins, mRNAs and immunohistochemical staining were unaffected by cyclical mechanical stretch. Thus cyclical mechanical stretch activates the expression of angiopoietin-2 and the Tie2 receptor, but not angiopoietin-1 or the Tie1 receptor, in cultured HUVECs. This mechanical effect is probably mediated by the tyrosine kinase and protein kinase C pathways.
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Wuitschick, Jeffrey D., Paul R. Lindstrom, Alison E. Meyer, and Kathleen M. Karrer. "Homing Endonucleases Encoded by Germ Line-Limited Genes in Tetrahymena thermophila Have APETELA2 DNA Binding Domains." Eukaryotic Cell 3, no. 3 (June 2004): 685–94. http://dx.doi.org/10.1128/ec.3.3.685-694.2004.

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ABSTRACT Three insertion elements were previously found in a family of germ line-limited mobile elements, the Tlr elements, in the ciliate Tetrahymena. Each of the insertions contains an open reading frame (ORF). Sequence analysis of the deduced proteins encoded by the elements suggests that they are homing endonucleases. The genes are designated TIE1-1, TIE2-1, and TIE3-1 for Tetrahymena insertion-homing endonuclease. The endonuclease motif occupies the amino terminal half of each TIE protein. The C-terminal regions of the proteins are similar to the APETELA2 DNA binding domain of plant transcription factors. The TIE1 and TIE3 elements belong to families of repeated sequences in the germ line micronuclear genome. Comparison of the genes and the deduced proteins they encode suggests that there are at least two distinct families of homing endonuclease genes, each of which appears to be preferentially associated with a specific region of the Tlr elements. The TIE1 and TIE3 elements and their cognates undergo programmed elimination from the developing somatic macronucleus of Tetrahymena. The possible role of homing endonuclease-like genes in the DNA breakage step in developmentally programmed DNA elimination in Tetrahymena is discussed.
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Dissertations / Theses on the topic "Tie2"

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Seegar, Tom CM. "TIED TOGETHER: A MOLECULAR ROLE FOR TIE1 IN ANGIOPOIETIN TIE2 SIGNALING." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2122.

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The primary function of the vascular system is the maintenance of oxygen homeostasis for all metazoan tissue. Angiogenesis, the remodeling and maintenance of new blood vessels from an existing vessel, is primarily controlled through the endothelial specific receptor tyrosine kinase Tie2, and the orphan receptor tyrosine kinase, Tie1. Although these receptors share highly conserved, genetic and biochemical analysis has shown these receptors have distinct and essential roles in angiogenesis. Tie2 activation typically results in vessel stability and quiescences and has further been shown to interact with all four sub-types of the angiopoietin signaling factors, Ang1-4. Conversely, Tie1 is involved in vascular remodeling and has no known ligands. The aim of this study is to resolve the molecular mechanism in which Tie1 modulates Angiopoietin-induced Tie2 signaling. Using biophysical, structural, and biochemical assays we show Tie1 directly interacts with Tie2 via electrostatic interactions housed within the extracellular domains. The binding of Tie1 to Tie2 attenuates Tie2 phosphorylation. We further show the constitutive agonist of Tie2, Ang-1, is capable of excluding Tie1 initiating Tie2 activation. Whereas the antagonist, Ang-2, is in incapable of excluding Tie1. Finally, we identify a region within the angiopoietin receptor-binding domain that is capable of including or excluding Tie1 from Tie2. Based upon the available data, we provide a model for Angiopoietin-induced Tie2 signaling.
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Dalton, Annamarie. "Regulation of Tie2 Extracellular Complex Formation in Angiogenesis." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3780.

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Pathological angiogenesis is an essential component of tumor growth, development, and metastasis for which few effective therapeutic options exist. Though many cancer therapies target the function of cell surface receptors, mechanisms regulating membrane receptor crosstalk remain unclear. Two important families of receptors in angiogenesis, the Ties and Integrins, respond to the extracellular environment via outside-in and, in the case of Integrins, also inside- out signaling. Recent reports showed that the endothelial specific tyrosine kinase receptor, Tie2, forms complexes with two of the endothelial Integrin heterodimers, α5β1 and αVβ3, providing a convenient mechanism for the integration of extracellular stimuli. Our data confirm the interaction between Integrins and Tie2 and additionally indicate an interaction with the orphan co-receptor Tie1. To elucidate the biological role of these macromolecular complexes, biochemical and biophysical methods including co-immunoprecipitation, FRET microscopy, and cellular based assays were used to follow receptor/Integrin association in response to the Tie2 ligands Angiopoietin-1 and -2 as well as the Integrin ligand fibronectin. Furthermore, structural analysis by small angle x-ray scattering of Tie2-ligand complexes and specific Integrin and Tie complexes are being used to identify the basis for growth factor receptor and Integrin signal transduction.
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Forget, Mary A. "Tumor Angiogenesis is all Tied up in Tie2-Expressing Macrophages." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1356032077.

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Nyamay'Antu, Alengo. "Elucidating the mechanism of angiopoeitin-mediated Tie2 signalling." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/elucidating-the-mechanism-of-angiopoeitinmediated-tie2-signalling(4269f3c3-fc71-455d-ae5b-4bc47dda78ca).html.

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Research on angiogenesis has been focused on developing anti-angiogenic therapies to target endothelial cell-specific signalling pathways, as a mean to limit tumour outgrowth and metastasis. One of the main targets is the endothelial cell-specific Tie2 receptor and its ligands, the angiopoietins, which controls the later stages of angiogenesis. Although the angiopoietin/Tie2 signalling pathways have been well characterized, the molecular mechanism by which the ligands regulate Tie2 activity remains unclear. To address this question, we determined whether the activation mechanism of Tie2 is induced by dimerisation alone, or whether subsequent relative rotation of the kinase domain is required. Here we employed a coiled-coiled based protein engineering approach to identify the relative orientations of the kinase domains that are optimal for Tie2 activation. By replacing the extracellular domain of Tie2 with the dimeric parallel coiled-coil motif Put3cc, we generated ligand-independent homodimers of the kinase domains Put3cc-Tie2 I-VII that have distinct orientations. We show that dimerisation is sufficient to induce Tie2 activation and downstream activation of Akt, and that varying the interface of the kinase domain in Tie2 dimers can increase its catalytic efficiency. In addition we examined for the presence of potential dimerisation within the transmembrane and intracellular domain of Tie2. We show that the KD and potentially the TM contain dimerisation motifs that stabilise Tie2 in the inactive and active conformations. In addition, we show that deletion of the potential coiled-coil motif in the JM does not disrupt dimerisation but decreases the catalytic efficiency of Tie2. Finally, we propose that the activation mechanism of Tie2 may be similar to the previously described asymmetric dimer formation of EGFR and FGFR receptors.
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Park, Eun-Hee 1971. "Mechanisms of translation initiation of receptor tyrosine kinase Tie2." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=102690.

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Angiogenesis is a process of new blood vessel formation and is the culmination of both mitogenic and tissue remodeling events, resulting in neovascularization. It is a physiological process that is required for, amongst others, normal embryonic development, female reproductive function, and wound healing. Angiogenesis is a tightly regulated process which is balanced by both positive and negative factors. However, in many disease states, including diabetic retinopathy, age-related macular degeneration, rheumatoid arthritis, and several cancers, dysregulation of angiogenesis contributes to disease progression. Previous published reports have implicated the coordinated activities of at least two families of receptor tyrosine kinases (RTKs), the vascular endothelial growth factor receptor (VEGFR) and the Tie receptor families, in this process.
Tie2, an endothelial-specific receptor tyrosine kinase, plays an essential role in normal blood vessel maturation, remodeling, and stability. Tie2 expression is also upregulated in various cancers indicating a role in tumor angiogenesis. The human Tie2 mRNA transcript contains an unusually long (372 nucleotides) 5' untranslated region (UTR) with five upstream open reading frames (uORFs). In this thesis, we demonstrate that the Tie2 5' UTR promotes cap-independent translation, indicating the presence of functional internal ribosome entry site (IRES). In addition, we illustrate that Tie2 IRES activity is maintained, and even slightly stimulated, under hypoxic conditions when cap-dependent protein synthesis is attenuated. We further show that the Tie2 IRES is functional during quiescence, another condition known to compromise cap-dependent translation. These results present how Tie2 mRNA is translated despite a cumbersome structured 5' UTR and how its production is secured under unfavorable environmental conditions.
We define experimental conditions where the Tie2 IRES is not active, allowing us to assess the contribution of cap-dependent translation to Tie2 protein synthesis. We demonstrate evidence that Tie2 mRNA can be translated via both cap-dependent scanning mechanism and internal initiation. Moreover, we show that the presence of the uORFs within the 5' UTR is inhibitory to downstream translation initiation. Our results suggest that the uORFs serve to decrease the proportion of ribosomes competent for reinitiation as they traverse the mRNA 5' UTR and thus minimizing interference with the IRES and/or mediating inefficient translation of the potent protein under normal conditions. Like many other cellular IRESes, the entire Tie2 5' UTR appears to be required for maximum IRES activity.
Taken together, our results underscore the complex mechanisms to control gene expression at the level of translation initiation of the Tie2 mRNA.
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Muhammad, Sharif Ossai. "Characterizing the interaction between VE-PTP, Tie2 and VE-Cadherin." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2869.

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Many signaling pathways have been shown to be involved in the formation of the vascular system. Among them are the endothelial specific receptor families such as VEGF, Ang/Tie, as well as other signaling pathways such as semaphorins, which are also involved, in axonal guidance. It is known that the interaction between receptor tyrosine kinase, Tie2, VE-Cadherin, and VE-PTP mediate endothelial cell quiescence and adhesion. However, the structural basis of these interactions is not well understood. The aim of our study is to characterize the binding interactions between these players. Another important part of our study is describing the cross-talk between vasculature and nervous system by characterizing the Neuropilin/Plexin/Semaphorin system. VE-Cadherin along with neuropilins plays an essential role by directing VEGF signals to the appropriate location and coordinating the activation of downstream molecules. We characterize the interaction between Tie2, VE-PTP and VE-Cadherin by (FRET)-based proximity assay, fluorescence lifetime imaging, and co-immunoprecipitation assays. Our data showed a consistent localization of the protein and FRET signal for Tie2 and VE-PTP prior to ligand recognition. We showed the association between Tie2 and VE-Cadherin complex by co-immunoprecipatation. However, our FRET data was not consistent. The examination of VE-PTP and VE-Cadherin for association and localization of the protein showed a very unique, mutually exclusive localization of the protein. Our study of Neuropilin/Plexin/Semaphorin system showed changes in the protein localization, FRET signal and morphology upon stimulation of HEK293 cells expressing Nrp/plexin with Sema3D. In this system VE-Cadherin along with neuropilins plays an essential role by directing VEGF signals to the appropriate location and coordinating the activation of downstream molecules. The characterization of extracellular binding between Tie2, VE-PTP, and VE-Cadherin, will help to better understand the molecular mechanisms of normal and tumor angiogenesis to develop new anti-angiogeneic therapies.
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Tamagno, Sara. "Characterization of the role of angiopoietin-tie signalling in haematopoietic stem cell development in the murine embryo." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31056.

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Haematopoietic stem cells (HSCs) are capable of self-renewing and multi-lineage reconstitution of the haematopoietic system of irradiated recipient mice. In the mouse embryo, HSCs originate in a step-wise manner from the haematogenic endothelium. The first HSC precursor has been detected at E9.5 in the dorsal aorta, while HSCs emerge in the aorta-gonad-mesonephros (AGM) region around E11. To date, the molecular mechanisms regulating these events are poorly characterized. Through the activating role of Angiopoietin1 (Ang1) on Tie2 receptor, the Ang-Tie signalling pathway plays a critical role in HSC maintenance in the adult bone marrow niche. Tie2 ligand Angiopoietin2 (Ang2) is described as being a Tie2 inhibitor, however its role is unknown. The aim of this thesis was to characterise the role of Ang-Tie signalling pathway in HSC formation in the mouse embryo. First, I used an ex vivo aggregate system to culture with angiopoietins cells derived from the AGM region at stages of development preceding HSC formation (E9.5-E11). Ang2- treated cells were able to reconstitute the peripheral blood of recipient mice to a higher extent compared to control, indicating a role for Ang2 in promoting HSC maturation. Then, I characterized the expression pattern of Ang-Tie molecules in the AGM region. Ang2-expressing cells were identified as perivascular and sub-aortic mesenchymal cells located in the ventral side of the aorta and in proximity of intra-aortic haematopoietic clusters. Finally, I performed an RNA-seq analysis with the aim of unravelling the molecular mechanisms involved in Ang2-mediated HSC maturation. Pre-HSC-I were cultured in presence or absence of Ang2 and their transcriptional profiles were compared, revealing a number of genes and pathways up-regulated or down-regulated in presence of Ang2, which might indicate a role for Ang2 in increasing cell proliferation, favouring cell migration, and regulation of other signalling pathways involved in HSC development. All together, these data support Ang2 as a novel regulator for HSC formation.
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Pucci, Ferdinando. "Gene expression signature and pro-angiogenic function of Tie2-expressing macrophages." Thesis, Open University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527443.

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Dunmore, Benjamin John. "Investigations into the involvement of Tie2 in endothelial-mural cell interactions." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/27747.

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The interaction of endothelial cells and mural cells play a critical role in the stabilisation and maturation of the embryonic and postnatal vasculature. Several pathological situations exhibit poor and abnormal endothelial and mural cell association. In this study immunohistochemical analysis revealed dysmorphogenic microvessels within atherosclerotic plaques are lacking mural cells. Similar dysmorphogenic mural cell poor vessels were also observed in human myocardium following laser induced myocardial injury. In both cases elevated VEGF was detected associated with the mural cell poor vessels. To gain insight into the mechanisms controlling mural cell recruitment assays were established to examine directly smooth muscle cell migration and adhesion between smooth muscle cells and endothelial cells in culture. These assays were used to study the involvement of the angiopoietin/Tie2 system in recruitment and retention of mural cells. Ang-l was observed to stimulate endothelial-directed migration of putative mural cell precursors. The ligand also increased adhesion between endothelial cells and smooth muscle cells. To investigate further the possible role of Tie2 in interaction between endothelial cells and mural cells a mutant form of the receptor found in inherited venous malformations (VM) was studied. The form of VM associated with this mutant receptor is characterised by dysmorphogenic, enlarged mural cell vessels. Surprisingly, mutant Tie2 did not inhibit endothelial-induced mural cell migration or adhesion between endothelial cells and mural cells. Taken together these data suggest Tie2 has a role in regulating endothelial:mural cell interaction. Furthermore, the presence of mural cell poor vessels in the atherosclerotic plaque, injured myocardium and inherited VM may reflect escape of these vessels from regression by the presence of survival factors in the case of the plaque and injured myocardium, or constitutive anti-apoptotic signalling from mutant Tie2 in the case of VM.
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Girlalt-Pujol, Marta. "Investigating the regulation of the endocytosis of tyrosine kinase receptor Tie2." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18527/.

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Tie2 receptor is a cell surface tyrosine kinase receptor expressed almost exclusively in endothelial cells, where it is mainly studied for its role in angiogenesis. Indeed, Tie2 has been related to various pathologies with vascular implication such as pulmonary hypertension, diabetes retinopathy and tumour growth. The regulation of Tie2 activation and function is complex, involving multiple factors that are still being investigated. For instance, after activation by the agonistic ligand Angiopoietin-1 (Ang1), Tie2 is internalized in cells by an endocytic mechanism that has yet to be fully characterised. As it has been shown that endocytosis of molecules can play a regulatory role in intracellular signalling in various ways I believe that the endocytosis of Tie2 may also be important in the regulation of its activity and cellular output. Therefore, I decided to characterise the endocytic mechanisms involved in the internalization of Tie2 to determine whether endocytosis can be a regulator of Tie2 signalling. To facilitate the study of Tie2 I created a HeLa cell line with inducible expression of a Tie2FLAG receptor that emulates both expression levels and characteristics of endogenous Tie2 in Human Umbilical Vein Endothelial Cells. To study the endocytosis of Tie2 receptor I developed an immunofluorescence-based assay to quantify the amount of internalized agonistic ligand Ang1 in a high throughput Screening format. I also performed complementary immunofluorescence and western blot analysis to investigate the characteristics of Tie2 internalization.
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Books on the topic "Tie2"

1

Michael, Adam. How to tie ties. New York: Sterling Pub., 1996.

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Johnson, Jean. Threads & ties that bind: Exquisite quilts from tie fabrics. Lincolnwood, Ill., U.S.A: Quilt Digest, 1997.

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Webster, Paul D. The wood crosstie: A 150 year success story : the Railway Tie Association & the National Association of Railroad Tie Producers : a three-quarters of a century history. Gulf Shores, Ala. (P.O. Box 1039, Gulf Shores 36547): Railway Tie Association, 1992.

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1941-, Spark Ron, and Sakai Steve, eds. Fit to be tied: Vintage ties of the forties and early fifties. New York: Abbeville Press, 1987.

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Elwin, Janet B. Ties--ties--ties: Traditional quilts from neckties. Paducah, KY: American Quilter's Society, 1996.

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Tied up, tied down. Macon, GA: Samhain Publishing, Ltd., 2009.

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Ties. New York: Costume & Fashion Press, 1998.

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Ties. London: V&A Publications, 1998.

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Tied. New York: Gallery Books, 2014.

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Tied. North Carolina?]: J. Taylor Publishing, 2013.

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Book chapters on the topic "Tie2"

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Partanen, J., and D. J. Dumont. "Functions of Tie1 and Tie2 Receptor Tyrosine Kinases in Vascular Development." In Current Topics in Microbiology and Immunology, 159–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59953-8_8.

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Niess, Hanno, C. Conrad, R. Huss, I. v. Lüttichau, I. Ischenko, M. Guba, C. Heeschen, K. W. Jauch, C. J. Bruns, and P. Nelson. "Stammzell-basierte Tie2/Tk Suizidgentherapie des fortgeschrittenen Pankreaskarzinoms." In Chirurgisches Forum 2007, 13–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71123-0_5.

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Biswas, Arpita A., and David J. Goldhamer. "FACS Fractionation and Differentiation of Skeletal-Muscle Resident Multipotent Tie2+ Progenitors." In Methods in Molecular Biology, 255–67. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3810-0_18.

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Guha, Prajna P., Sascha A. David, and Chandra C. Ghosh. "Detecting Tie2, an Endothelial Growth Factor Receptor, by Using Immunohistochemistry in Mouse Lungs." In Cytokine Bioassays, 201–8. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0928-5_18.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TIF2." In Encyclopedia of Signaling Molecules, 1852. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101362.

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Irvine, William M. "TiO2." In Encyclopedia of Astrobiology, 2505–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_5119.

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Harmelink, Cristina, Xianghu Qu, and Scott H. Baldwin. "Tie1." In Encyclopedia of Signaling Molecules, 5425–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101887.

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Rots, Hanne. "Tien." In Jij mág niet lief zijn, 43–45. Houten: Bohn Stafleu van Loghum, 2004. http://dx.doi.org/10.1007/978-90-313-9257-5_10.

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Krebs, Uwe. "Tier." In Handbuch Pädagogische Anthropologie, 621–32. Wiesbaden: Springer Fachmedien Wiesbaden, 2013. http://dx.doi.org/10.1007/978-3-531-18970-3_57.

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Toepfer, Georg. "Tier." In Historisches Wörterbuch der Biologie, 494–509. Stuttgart: J.B. Metzler, 2011. http://dx.doi.org/10.1007/978-3-476-00461-1_26.

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Conference papers on the topic "Tie2"

1

Cescon, David W., Philippe L. Bedard, Sue Chow, Helen Chen, Albiruni Razak, Monika Wizemann, Lillian L. Siu, and David Hedley. "Abstract 4647: Tie2-expressing monocytes (TEMs) as potential biomarkers of angiopoietin-Tie2 (Ang/Tie2) directed therapies: correlative analysis of a phase I study of AMG386 + temsirolimus (T)." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4647.

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Flynn, Daniel L., Michael D. Kaufman, Cynthia B. Leary, Molly M. Hood, Wei-Ping Lu, Benjamin A. Turner, Scott C. Wise, Marc S. Rudoltz, and Bryan D. Smith. "Abstract PR01: Rebastinib, a selective TIE2 kinase inhibitor, decreases TIE2-expressing macrophages, reduces metastasis, and increases survival in murine cancer models." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-pr01.

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Steinberger, Kayla J., Mary Forget, Xiaokui Mo, Randall Evans, Amy Gross, Leni Moldovan, Andrey Bobko, Valery Khramstov, Clay B. Marsh, and Timothy D. Eubank. "Abstract 5207: HIF-1α regulates the Tie2 receptor on Tie2-expressing monocytes in PyMT breast tumors and augments angiogenic function and metastatic potential." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5207.

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Plate, Karl H., Alexander Scholz, Patrick Harter, Michel Mittelbronn, Paul van Slyke, Dan Dumont, and Yvonne Reiss. "Abstract B70: Targeting the Tie2/angiopoietin signaling pathway in glioblastoma." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b70.

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Hossain, Mohammad Belayat, Rehnuma Shifat, Jingyi Li, Yisel Rivera-Mokina, Francisco Puerta Martinez, David G. Johnson, Mark T. Bedford, et al. "Abstract 5854: TIE2-mediated epigenetic marks regulate therapeutic resistance of glioblastoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5854.

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Jayson, Gordon C., Cong Zhou, Alison Backen, Andrew Renehan, Andrew Clamp, Richard Kaplan, and Rosamonde E. Banks. "Abstract IA10: Angiopoietin/Tie2 as predictive biomarkers for bevacizumab in ovarian cancer." In Abstracts: AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; March 5-8, 2015; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-ia10.

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Hossain, Mohammad B., Anupama Gururaj, Nahir Cortes-Santiago, Konrad Gabrusiewicz, Juan Fueyo, and Candelaria Gomez-Manzano. "Abstract 2136: Nuclear trafficking of Tie2 is associated with radioresistance of gliomas." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2136.

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Knific, T., L. Roškar, Š. Smrkolj, and T. Lanišnik Rižner. "EP556 Decreased s-Tie2 plasma concentration in patients with endometrioid endometrial cancer." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.613.

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Jiang, xinguo, Ramesh Natarajan, Mohammad A. khan, Mark Krasnow, Gregg Semenza, and Mark R. Nicolls. "HIF1± And The Repair Of Injured Airway Microvasculature By Recipient-derived Tie2(+) Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1081.

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Min, Yongfen, Xiubao Ren, and Charles Lin. "Abstract 3391: Tie2 signaling regulates osteoclastogenesis and osteolytic bone invasion of breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3391.

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Reports on the topic "Tie2"

1

Metheny-Barlow, Linda J. Regulation of Tie2 During VEGI-Mediated Inhibition of Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada427147.

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Lee, William M. Targeting Tie2 to Increase Breast Cancer Responsiveness to Antiangiogenic Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada439242.

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Lee, William. Targeting Tie2 to Increase Breast Cancer Responsiveness to Antiangiogenic Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada457695.

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Lee, William M. Targeting Tie2 to Increase Breast Cancer Responsiveness to Antiangiogenic Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427176.

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Alesina, Alberto, and Paola Giuliano. Family Ties. Cambridge, MA: National Bureau of Economic Research, April 2013. http://dx.doi.org/10.3386/w18966.

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Shoup, Brian. U.S.-India Security Ties. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434959.

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Laurence, Janice H., Peter F. Ramsberger, and Jane M. Arabian. Education Credential Tier Evaluation. Fort Belvoir, VA: Defense Technical Information Center, May 1997. http://dx.doi.org/10.21236/ada335804.

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Zoppi, Steve, and Ann West. TIER Thematic Requirements / Prioritized. Internet2, April 2016. http://dx.doi.org/10.26869/ti.117.1.

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Babb, James, and Tom Dopirak. TIER Grouper Deployment Guide. Edited by Bill Thompson. Internet2, April 2017. http://dx.doi.org/10.26869/ti.25.1.

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Cohen, Lauren, Andrea Frazzini, and Christopher Malloy. Sell Side School Ties. Cambridge, MA: National Bureau of Economic Research, May 2008. http://dx.doi.org/10.3386/w13973.

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