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M

M. Gabriela Bowden

Researcher at Texas A&M University

Publications -  18
Citations -  3273

M. Gabriela Bowden is an academic researcher from Texas A&M University. The author has contributed to research in topics: Panton–Valentine leukocidin & Staphylococcus aureus. The author has an hindex of 14, co-authored 18 publications receiving 2901 citations. Previous affiliations of M. Gabriela Bowden include Texas A&M University System & University of Lyon.

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A Novel Mechanism of Rapid Nuclear Neutrophil Extracellular Trap Formation in Response to Staphylococcus aureus

TL;DR: A new mechanism of NET release that is very rapid and contributes to trapping and killing of S. aureus through a novel process of NET formation that did not require neutrophil lysis or even breach of the plasma membrane.
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Staphylococcus aureus Panton-Valentine Leukocidin Causes Necrotizing Pneumonia

TL;DR: It is shown that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell wall–anchored staphylococcal proteins, including the lung inflammatory factor staphlyococcal protein A (Spa).
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A “dock, lock, and latch” Structural Model for a Staphylococcal Adhesin Binding to Fibrinogen

TL;DR: Analysis of the crystal structures, along with mutational studies of both the protein and of the peptide, reveals that SdrG binds to its ligand with a dynamic "dock, lock, and latch" mechanism that represents a general mode of ligand binding for structurally related cell wall-anchored proteins of gram-positive bacteria.
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Identification and preliminary characterization of cell-wall-anchored proteins of Staphylococcus epidermidis

TL;DR: Analysis of primary sequences of the Staphylococcus epidermidis surface (Ses) proteins indicates that they have a structural organization similar to the previously described cell-wall-anchored proteins from S. aureus and other Gram-positive cocci, and western blot analyses of early-logarithmic and late-stationary in vitro cultures suggest that different regulatory mechanisms control the expression of the Ses proteins.