Institution
Victor Chang Cardiac Research Institute
Nonprofit•Sydney, New South Wales, Australia•
About: Victor Chang Cardiac Research Institute is a nonprofit organization based out in Sydney, New South Wales, Australia. It is known for research contribution in the topics: Mechanosensitive channels & Heart failure. The organization has 708 authors who have published 1599 publications receiving 70035 citations.
Papers published on a yearly basis
Papers
More filters
••
TL;DR: The human uterus has no pacemaker or motor innervation, yet develops rhythmic, powerful contractions that increase intrauterine pressure to dilate the cervix and force the fetus through the pelvis.
45 citations
••
TL;DR: GPCR–CoINPocket is a novel contact-informed neighboring pocket metric of GPCR binding-site similarity that is informed by patterns of ligand–residue interactions observed in crystallographically characterized GPCRs and accurately captures known pharmacological relationships between G PCRs, even those undetected by phylogeny.
Abstract: Understanding the pharmacological similarity of G protein-coupled receptors (GPCRs) is paramount for predicting ligand off-target effects, drug repurposing, and ligand discovery for orphan receptors. Phylogenetic relationships do not always correctly capture pharmacological similarity. Previous family-wide attempts to define pharmacological relationships were based on three-dimensional structures and/or known receptor-ligand pairings, both unavailable for orphan GPCRs. Here, we present GPCR-CoINPocket, a novel contact-informed neighboring pocket metric of GPCR binding-site similarity that is informed by patterns of ligand-residue interactions observed in crystallographically characterized GPCRs. GPCR-CoINPocket is applicable to receptors with unknown structure or ligands and accurately captures known pharmacological relationships between GPCRs, even those undetected by phylogeny. When applied to orphan receptor GPR37L1, GPCR-CoINPocket identified its pharmacological neighbors, and transfer of their pharmacology aided in discovery of the first surrogate ligands for this orphan with a 30% success rate. Although primarily designed for GPCRs, the method is easily transferable to other protein families.
44 citations
••
TL;DR: Evaluated the involvement of NADPH oxidases (NOX) in the oxidative damage and progression of ALS neuropathology and treated SOD1(G93A) mice with broad-spectrum NOX inhibitors perphenazine and thioridazine, which induced an immediate and temporary enhancement of motor performance (rotarod) but its precise mode of action needs further investigation.
44 citations
••
TL;DR: Functional studies indicated that induction of 14-3-3 binding to EDC3 causes morphological changes in processing body structures, inhibition of microRNA-mediated mRNA post-transcriptional regulation, and alterations in the protein- protein interactions of EDC 3.
44 citations
••
TL;DR: It is shown that in 8- to 14-week old mice, heme oxygenase-1 deficiency adversely affects steady-state erythropoiesis in the bone marrow, and the extent of anemia in these mice may be ameliorated by the prolonged lifespan of their oxidatively stressed erythrocytes.
Abstract: Heme oxygenase-1 is critical for iron recycling during red blood cell turnover, whereas its impact on steady-state erythropoiesis and red blood cell lifespan is not known. We show here that in 8- to 14-week old mice, heme oxygenase-1 deficiency adversely affects steady-state erythropoiesis in the bone marrow. This is manifested by a decrease in Ter-119+-erythroid cells, abnormal adhesion molecule expression on macrophages and erythroid cells, and a greatly diminished ability to form erythroblastic islands. Compared with wild-type animals, red blood cell size and hemoglobin content are decreased, while the number of circulating red blood cells is increased in heme oxygenase-1 deficient mice, overall leading to microcytic anemia. Heme oxygenase-1 deficiency increases oxidative stress in circulating red blood cells and greatly decreases the frequency of macrophages expressing the phosphatidylserine receptor Tim4 in bone marrow, spleen and liver. Heme oxygenase-1 deficiency increases spleen weight and Ter119+-erythroid cells in the spleen, although α4β1-integrin expression by these cells and splenic macrophages positive for vascular cell adhesion molecule 1 are both decreased. Red blood cell lifespan is prolonged in heme oxygenase-1 deficient mice compared with wild-type mice. Our findings suggest that while macrophages and relevant receptors required for red blood cell formation and removal are substantially depleted in heme oxygenase-1 deficient mice, the extent of anemia in these mice may be ameliorated by the prolonged lifespan of their oxidatively stressed erythrocytes.
44 citations
Authors
Showing all 728 results
Name | H-index | Papers | Citations |
---|---|---|---|
Bruce D. Walker | 155 | 779 | 86020 |
Stefanie Dimmeler | 147 | 574 | 81658 |
Matthias W. Hentze | 110 | 319 | 41879 |
Roland Stocker | 92 | 331 | 34364 |
Richard P. Harvey | 83 | 403 | 27060 |
Michael F. O'Rourke | 81 | 451 | 35355 |
Robert Terkeltaub | 80 | 284 | 21034 |
Robert M. Graham | 69 | 319 | 16342 |
Sunil Gupta | 69 | 440 | 33856 |
Anne Keogh | 64 | 337 | 20268 |
Filip K. Knop | 61 | 437 | 13614 |
Peter S. Macdonald | 57 | 455 | 12988 |
Boris Martinac | 56 | 245 | 14121 |
Carolyn L. Geczy | 55 | 187 | 8987 |
Christopher J. Ormandy | 54 | 131 | 8757 |