1,721,045 research outputs found
Leucocyte and endothelial cell biology
Prof Mathew A Vadas$AUD 3,566,050.12ProgramProgram Gran
Transcriptional regulation of mouse granulocyte-macrophage colony-stimulating factor/IL-3 locus
Cameron S. Osborne, Mathew A. Vadas, and Peter N. Cockeril
What determines the severity of inflammation
Prof Mathew A Vadas$AUD 253,551.22NHMRC Project GrantsStandard Project Gran
Control of blood cell interaction with vessel walls
Prof Mathew A Vadas$AUD 89,405.75NHMRC Project GrantsStandard Project Gran
Activation of a T cell-specific enhancer upstream of the interleukin-3 gene involves cooperation between overlapping Oct and NFAT motifs and changes in chromatin structure.
Kym N Duncliffe, Andrew G Bert, Mathew A Vadas, Peter N Cockeril
Lumen formation during angiogenesis in vitro involves phagocytic activity, formation and secretion of vacuoles, cell death, and capillary tube remodelling by different populations of endothelial cells.
Geoffrey T. Meyer, Lisa J. Matthias, Leanne Noack, Mathew A. Vadas, Jennifer R. Gambl
Cold shock domain factors activate the granulocyte-macrophage colony-stimulating factor promoter in stimulated Jurkat T cells
Peter Diamond, M. Frances Shannon, Mathew A. Vadas, and Leeanne S. Cole
Letter to the Editor: 1H and 15N chemical shift assignments for domain 4 of the common beta-chain of the IL-3, IL-5 and GM-CSF receptors
Terrence D. Mulhern, Christopher J. Bagley, Craig Gaunt, Angel.F. Lopez, Mathew A. Vadas, Richard J. D'Andrea, Grant W. Booke
Translocation of protein tyrosine phosphatase Pez/PTPD2/PTP36 to the nucleus is associated with induction of cell proliferation
Pez is a non-transmembrane tyrosine phosphatase with homology to the FERM (4.1, ezrin, radixin, moesin) family of proteins. The subcellular localisation of Pez in endothelial cells was found to be regulated by cell density and serum concentration. In confluent monolayers Pez was cytoplasmic, but in cells cultured at low density Pez was nuclear, suggesting that it is a nuclear protein in proliferating cells. This notion is supported by the loss of nuclear Pez when cells are serum-starved to induce quiescence, and the rapid return of Pez to the nucleus upon refeeding with serum to induce proliferation. Vascular endothelial cells normally exist as a quiescent confluent monolayer but become proliferative during angiogenesis or upon vascular injury. Using a 'wound' assay to mimic these events in vitro, Pez was found to be nuclear in the cells that had migrated and were proliferative at the 'wound' edge. TGFbeta, which inhibits cell proliferation but not migration, inhibited the translocation of Pez to the nucleus in the cells at the 'wound' edge, further strengthening the argument that Pez plays a role in the nucleus during cell proliferation. Together, the data presented indicate that Pez is a nuclear tyrosine phosphatase that may play a role in cell proliferation.Carol Wadham, Jennifer R. Gamble, Mathew A. Vadas and Yeesim Khew-Goodal
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