Jessica Cooley
Boston Children's Hospital
22 Papers
400 Citations
Jessica Cooley is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Neutrophil elastase & Elastase. The author has an hindex of 16, co-authored 22 publications. Previous affiliations of Jessica Cooley include Harvard University.
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Papers
The serpin MNEI inhibits elastase-like and chymotrypsin-like serine proteases through efficient reactions at two active sites.
Jessica Cooley,Thomas K. Takayama,Steven D. Shapiro,Norman M. Schechter,Eileen Remold-O'Donnell +4 more
TL;DR: MNEI has a broader specificity, efficiently inhibiting proteases with elastase- and chymotrypsin-like specificities, and plays a regulatory role at extravascular sites to limit inflammatory damage due to proteases of cellular origin.
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Linkage of neutrophil serine proteases and decreased surfactant protein-A (SP-A) levels in inflammatory lung disease
TL;DR: The findings strongly suggest that the neutrophil serine proteases cathepsin G and/or elastase and/ or proteinase-3 contribute to degradation of SP-A and thereby diminish innate pulmonary antimicrobial defence.
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Comparison of human chromosome 6p25 with mouse chromosome 13 reveals a greatly expanded ov-serpin gene repertoire in the mouse.
Dion Kaiserman,Susan Knaggs,Katrina L Scarff,Anneliese Gillard,Ghazala Mirza,Matthew Cadman,Richard McKeone,Paul Denny,Jessica Cooley,Charaf Benarafa,Eileen Remold-O'Donnell,Jiannis Ragoussis,Phillip I. Bird +12 more
TL;DR: Compared with human, this larger mouse serpin repertoire probably reflects the need to regulate a larger proteinase repertoire arising from differing evolutionary pressures on the reproductive and immune systems.
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Characterization of Four Murine Homologs of the Human ov-serpin Monocyte Neutrophil Elastase Inhibitor MNEI (SERPINB1)
TL;DR: The data demonstrate that the four murine homologs of MNEI have met different evolutionary fates, and that EIA is the mouse ortholog of M NEI.
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•Journal Article
Variable expression of WASP in B cell lines of Wiskott-Aldrich syndrome patients.
Eileen Remold-O'Donnell,Jessica Cooley,Anna Shcherbina,T L Hagemann,Sau-Ping Kwan,Dianne M. Kenney,Fred S. Rosen +6 more
TL;DR: The findings suggest that the clinical variability of the Wiskott-Aldrich syndrome can partially be explained by the level of WASP protein in the patient's cells.
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