Institution
University of Maryland Biotechnology Institute
About: University of Maryland Biotechnology Institute is a based out in . It is known for research contribution in the topics: Gene & Population. The organization has 1565 authors who have published 2458 publications receiving 171434 citations. The organization is also known as: UMBI.
Topics: Gene, Population, Protein structure, Receptor, Peptide sequence
Papers published on a yearly basis
Papers
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TL;DR: It is demonstrated that a 24 h exposure to AGEs induced apoptosis in both cell lines, suggesting that AGE-receptors may play important roles in the bone alterations described in aging and diabetic patients.
Abstract: Advanced glycation end products (AGEs) have been proposed as the pathological mechanisms underlying diabetic chronic complications. They may also play a role in the pathogenesis of diabetic osteopenia, although their mechanisms of action remain unclear. We investigated the protein (immunofluorescence) and gene expression (realtime RT-PCR) of two receptors for AGEs, RAGE and galectin-3, as well as their regulation by AGEs, and the apoptotic effect on osteoblast-like cells (UMR106 and MC3T3E1) in culture. AGEs up-regulated the expression of RAGE and galectin-3 in both cells lines. These effects were accompanied by an increase in the corresponding mRNA in the non-tumoral MC3T3E1 but not in the osteosarcoma UMR106 cells. Finally, we demonstrated that a 24 h exposure to AGEs induced apoptosis in both cell lines. Thus, AGEs-receptors may play important roles in the bone alterations described in aging and diabetic patients.
76 citations
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TL;DR: The role of zooplankton as hosts of vibrios in the environment is confirmed, and it is suggested that smaller sized plankton may serve as an important reservoir of these bacteria.
76 citations
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TL;DR: Mechanisms of mitochondrial fusion and fission in mammalian cells, the mitochondrial morphogenesis proteins that may be involved in these processes and role of these processes in cell viability are discussed.
Abstract: Mitochondria are highly dynamic organelles that constantly change shape and structure in response to different stimuli and metabolic demands of the cell. Mitochondrial structure in the cell is predominantly regulated by cycles of fusion and fission. These two processes are tightly regulated and under physiological conditions, mitochondrial fusion is evenly counterbalanced by fission. During apoptosis, mitochondria undergo extensive fragmentation, which precedes caspase activation, whereas inhibition of the mitochondrial fission machinery blocks or delays cell death. Aberrant mitochondrial fusion and fission have also emerged as important mechanisms in the development of disease.
76 citations
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TL;DR: The data further support the idea that vGPCR contributes to the pathogenesis of KS by a paracrine mechanism and, in addition, provide the first evidence of collaboration between an HIV-1 protein and an HHV-8 protein.
Abstract: Human herpesvirus 8 (HHV-8), the etiologic agent of Kaposi's sarcoma (KS), encodes a chemokine receptor homologue, the viral G protein-coupled receptor (vGPCR), that has been implicated in KS pathogenesis. Expression of vGPCR constitutively activates several signaling pathways, including NF-κB, and induces the expression of proinflammatory and angiogenic factors, consistent with the inflammatory hyperproliferative nature of KS lesions. Here we show that vGPCR also constitutively activates the nuclear factor of activated T cells (NF-AT), another transcription factor important in regulation of the expression of inflammatory cytokines and related factors. NF-AT activation by vGPCR depended upon signaling through the phosphatidylinositol 3-kinase-Akt-glycogen synthetase kinase 3 (PI3-K/Akt/GSK-3) pathway and resulted in increased expression of NF-AT-dependent cell surface molecules (CD25, CD29, Fas ligand), proinflammatory cytokines (interleukin-2 [IL-2], IL-4), and proangiogenic factors (granulocyte-macrophage colony-stimulating factor GMCSF and TNFα). vGPCR expression also increased endothelial cell-T-cell adhesion. Although infection with HHV-8 is necessary to cause KS, coinfection with human immunodeficiency virus type 1 (HIV-1), in the absence of antiretroviral suppressive therapy, increases the risk of KS by many orders of magnitude. NF-AT and NF-κB activation by vGPCR was greatly increased by the HIV-1 Tat protein, although Tat alone had little effect on NF-AT. The enhancement of NF-AT by Tat appears to be mediated through collaborative stimulation of the PI3-K/Akt/GSK-3 pathway by vGPCR and Tat. Our data further support the idea that vGPCR contributes to the pathogenesis of KS by a paracrine mechanism and, in addition, provide the first evidence of collaboration between an HIV-1 protein and an HHV-8 protein.
76 citations
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TL;DR: The crystal structure of ADI is determined from Pseudomonas aeruginosa by the multi-wavelength anomalous diffraction method at 2.45 Å resolution and the assumption that the substrate binding mode is similar to that of DDAH, an ADI catalytic mechanism is proposed.
76 citations
Authors
Showing all 1565 results
Name | H-index | Papers | Citations |
---|---|---|---|
Stanley B. Prusiner | 168 | 745 | 97528 |
Robert C. Gallo | 145 | 825 | 68212 |
Thomas J. Smith | 140 | 1775 | 113919 |
J. D. Hansen | 122 | 975 | 76198 |
Stephen Mann | 120 | 669 | 55008 |
Donald M. Bers | 118 | 570 | 52757 |
Jon Clardy | 116 | 983 | 56617 |
Rita R. Colwell | 115 | 781 | 55229 |
Joseph R. Lakowicz | 104 | 850 | 76257 |
Patrick M. Schlievert | 90 | 444 | 32037 |
Mitsuhiko Ikura | 89 | 316 | 34132 |
Jeremy Thorner | 87 | 234 | 29999 |
Lawrence E. Samelson | 87 | 209 | 27398 |
Jacques Ravel | 86 | 323 | 45793 |
W. J. Lederer | 79 | 213 | 25509 |